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BASIC PREOPERATIVE EVALUATION
The basic evaluation is required for every patient who undergoes open heart surgery. In emergency situations, this information may not be available or obtainable if lifesaving emergency surgery is the only chance for survival. In other patients, the presence of comorbid conditions or the severity of heart disease requires additional information to assess both the potential benefits and risks of operation.
The basic evaluation includes history, physical examination, blood testing, urinalysis, chest x-ray, electrocardiogram, and almost always cardiac catheterization
Each of these components of the basic evaluation should be performed with the planned surgical procedure in mind.
For example, if coronary artery bypass grafting is planned, the history should indicate prior phlebitis or vein stripping; if a mitral prosthesis must be replaced, a previous deep postoperative sternotomy wound infection is relevant.
For some patients, an appropiate indication for operation and information from the basic evaluation are all that are needed to prescribe and carry out the procedure.
These are nearly always patients for whom the operation has a low risk of mortality and morbidity.
For others, much more information is needed, the decision to recommend operation is more complex and difficult, the operation and postoperative course are likely to be more costly, the benefits may be less dramatic, and the risk is higher.
These patients are addressed at the end of this chapter.
The history is an important source of information that usually establishes the indications for operation and the need for studies beyond the basic evaluation.
The reason for having an operation should be elicited from the patient's point of view.
What symptom, threat, or restriction does the patient expect the operation to remove? What quality of lifestyle does the patient expect after surgery?
In addition to information regarding the severity of heart dysfunction, the history provides an inventory of comorbid diseases and compromised organ and system functions.
In elderly patients, heart disease is seldom the only disease.
A thorough history sometimes provides clues to occult disease not previously known (e.g., emphysema, alcoholic liver disease, diabetes, renal insufficiency, arrhythmias, etc.) or reveals long-forgotten events, such as a serious automobile accident, in a patient with a mass lesion over the aortic isthmus.
During the history, the patient should be assessed carefully to determine motivation and ability to care for basic needs.
The principal symptoms of cardiac disease are chest pain or discomfort, dyspnea, fatique, peripheral edema, and syncope.
Symptoms and prior manifestations of the patient's cardiac disease should be described in terms of chronicity and severity.
Episodic aspects of the disease, such as pulmonary congestion, recent chest discomfort, syncope, palpitations, hemoptysis, or infection, should be described in terms of frequency, duration, and severity. Severity of symptoms is described and assessed by a standard classification of severity such as the New York Heart Association functional classification of heart failure or the Canadian Heart Association classification for severity of angina pectoris.
The surgeon should particularly note combinations of symptoms, such as episodic chest pain (angina) and shortness of breath (heart failure), that may be manifestions of one disease process (ischemia) or two (ischemia and valve disease or severe left ventricular dysfunction).
All allergies should be reviewed carefully and recorded prominently in the hospital chart and, when appropiate, on the order sheet. Antibiotic allergies influence choices of prophylactic and therapeutic antibiotics.
Heparin-induced thrombocytopenia occurs in 2 to 5 percent of patients exposed to the drug, and the catastrophic form of the disease, heparin-induced thrombocytopenia and thrombosis, occurs in 0.1 to 0.2 percent.] Fish allergy or use of protamine insulin may indicate a predisposition to a protamine reaction.
Prior cardiac surgery may immunize a patient to bovine thrombin (fibrin glue) or aprotinin ; a second exposure may cause a severe bleeding disorder from factor V deficiency (bovine thrombin) or an anaphylactic reaction (aprotinin).
Medication intolerance may be due to allergy or to side effects. Although allergy is uncommon (see above), undesirable side effects of various cardiovascular drugs are extremely common. In addition, combinations of drugs may produce serious cumulative or adverse effects (e.g., aspirin plus Coumadin). The history should include not only the drugs that the patient is taking but also drugs taken in the past that caused unpleasant side effects. No one can remember all drugs or combination drug side effects, but each physician should be aware of adverse effects of drugs that he or she frequently prescribes. A history that reveals an adverse reaction to a drug commonly used by the surgeon may save the patient discomfort postoperatively. Standard pharmacologic texts, the package inserts of specific drugs, and the Physician's Desk Reference are ready sources of information regarding adverse effects of medications.
Prior hospitalization and illnesses
It is particularly important to record prior procedures, operations, treatments, or radiation involving the thorax or cardiovascular system. Previous radiation for breast cancer may affect a decision to use the ipsilateral internal mammary artery for myocardial revascularization. Diabetes may preclude using both mammary arteries for conduits. Prior gastric resection may render the gastroepiploic artery unavailable for coronary arterial bypass. Steroid dependency for arthritis may predispose to infection. Multiple hospitalizations related to any organ system may be an indication for further investigation. The operating surgeon is in the best position to evaluate the relevance or prior operations and illness on the design of the proposed operation (i.e., are modifications needed?) and on reducing the risk of postoperative complications.
REVIEW OF SYSTEMS
The level of intelligence and general ability of the patient to care for himself or herself independently bear on the decision to operate and on expected benefits of operation. Elderly, frail, and forgetful patients must be interrogated carefully and respectfully. The ability to live alone and care for basic needs independently are good indications of an elderly patient's strength, motivation, and mental state. Elderly patients who require nursing home care or who cannot be trusted at home alone are poor candidates for operation. Patients with substance abuse problems, neglected dental care, or poor hygiene are not good candidates for prosthetic heart valves or other procedures that require careful regulation of postoperative medications, infection prophylaxis, or immunosuppression therapy.
The ambulatory status of the patient is extremely important not only for rapid recovery from operation but also for long-term care and quality of life. To a large extent, recovery from open heart surgery is based on postoperative walking as an economic and effective means to progressively increase exercise tolerance and to prevent complications such as pneumonia and decubitus ulcers. In nonambulatory or morbidly obese patients, operation is associated with a higher risk of morbidity and increased length of stay. ] , Patients should be questioned about their motivation and determination to ambulate quickly postoperatively.
Amaurosis fugax (transient losses of vision) indicates the probable presence of carotid arterial disease of atheroemboli from the aorta and should prompt further investigation by appropriate ultrasonic studies.
Ears, nose, and throat
Occasionally, the pain of angina pectoris is manifest in the throat or ear. Symptoms of cough, purulent sputum production, or hemoptysis raise the suspicion of upper airway bronchitis, infection, or malignancy that needs further evaluation, especially in smokers and abusers of alcohol. A history of difficult endotracheal tube intubation is noteworthy. False teeth, dental caps, and a history of painful teeth or dental abscesses are relevant to anesthesia and to value surgery.
Cough, shortness of breath, sputum production, hemoptysis, unexplained weight loss, chest pain, wheezing, and episodes of infection require further evaluation for primary pulmonary disease. A history of smoking, particularly a long, heavy one, is relevant to the possibility of chronic obstructive pulmonary disease that may exacerbate symptoms of congestive heart failure. The surgeon should carefully evaluate the possibility that the patient may require long-term postoperative intubation and respiratory support because of age, frailty, and intrinsic lung disease. Spirometry, pulse oximetry, and arterial blood gases may provide further information relevant to this risk.
Most of this history is recorded in the present illness. However, a history of hypertension, childhood murmurs, rheumatic fever, syncopal episodes, chest radiation, traumatic myocardial contusion, viral myocarditis, and so on may not be directly related to the patient's present complaint but may be relevant to intraoperative and postoperative assessment and management.
A detailed history of aortic and/or peripheral vascular disease is important as an indication of diffuse atherosclerotic vascular disease and as a potential for complications of vessel cannulation. Patients should be queried for symptoms of aneurysm and peripheral vascular ischemia. Occasional patients are referred for myocardial revascularization when coronary arterial disease is first discovered after an abdominal aortic aneurysm or peripheral vascular disease becomes symptomatic.
Recent change in chronic gastrointestinal (GI) symptoms or recent onset of new symptoms may be an indication for detailed GI evaluation. The patient should be questioned regarding symptoms of or factors predisposing to liver disease. A history of hepatitis requires further evaluation to determine activity and degree of functional impairment. A history of pancreatitis or liver disease may predispose postoperative dysfunction of these organs. A history of GI bleeding from either the upper or lower intestitinal tract may be a determining factor in the choice of a tissue or mechanical cardiac valve prosthesis.
Loss of a kidney, chronic renal disease, or prior treatment for renal insufficiency generally requires further evaluation and estimation of renal functional reserve if laboratory tests are elevated and a complicated operation is planned. Previous urinary tract surgery and symptoms of recurrent urinary tract infection or prostatism may impair insertion of a Foley catheter and predispose to systemic infection. Preoperative evaluation of symptomatic patients by a urologist is often advisable.
A history of stroke, transient ischemic attack, headache, visual disturbance, or change in mental status or personality should be noted and may require further evaluation. Patients with a history of stroke or transient ischemic attack (TIA) are at great risk of intraoperatiave and postoperative stroke, particularly if carotid artery bruits are also present. [12 ] , [13 ]
The patient's functional capacity and strength and the effect of neurologic abnormalities should be described. Elderly patients who are drowsy and sleep a great deal, who are difficult to arouse, who are forgetful or cannot be left alone comfortably, and who are nonambulatory or marginally ambulatory are poor candidates for cardiac surgical procedures. Furthermore, these patients rarely initiate consideration of cardiac surgery; more often the possibility of operation is raised by loving family members or overzealous physicians.
Abnormalities of joint function and muscle strength and function should be described. The possibility that shoulder or neck pain may be muscular or skeletal in origin should be considered carefully. Early symptoms of arthritis and musculoskeletal injury or disease occasionally are interpreted as angina. Musculoskeletal dysfunction may be the main determinant of the patient's ability to rehabilitate postoperatively.
Any history of a bleeding abnormality or unusual susceptibility to infection should be recorded and evaluated by relevant blood screening tests. A history of easy bruising, joint hematoma, or excessive bleeding from prior dental work or surgical procedures in an indication for further hematologic evaluation and consultation. Anemia may unmask coronary artery disease by triggering angina. A history of a transfusion reaction and the patient's attitude or religious beliefs relevant to blood transfusion should be solicited. Immunosuppressed patients require full evaluation of their defenses against infection.
Diabetes is commonly associated with ischemic heart disease, and insulin-dependent diabetes over many years may be associated with moderate or severe renal and peripheral vascular disease. In addition, a severe diabetic may have retinopathy and peripheral neuropathy that will not be helped by cardiac surgery. Non-insulin-dependent diabetes does not add to operative risks.
Rare patients may present with hypothyroidism or hyperthyroidism. Hypothyroid patients recover from anesthesia slowly, and hyperthyroid patients may have angina or more frequent angina because of their hypermetabolic state. When suspected, blood triiodothroidine should be measured.
The family history of heart disease is usually recorded in the medical evaluation and is relevant primarily to the etiology of the heart disease and the risk of heart disease in individual family members but does not often influence the indications for or conduct of operation. However, the presence of an extensive family history of atherosclerotic disease, including coronary, cerebrovascular, and peripheral vascular disease, may affect the patient's motivation for surgical therapy.
History of tobacco, alcohol, or substance abuse should be recorded in terms of duration, frequency, and amount. The patient's history of work and activities may give an indication of the need for and ability to rehabilitate the patient postoperatively. The social history is often very relevant to patient care during the first few weeks after hospital discharge and the need for a rehabilitation or convalescent facility.
If the patient is admitted directly to the surgical service, the surgeon is responsible for a complete and thorough physical examination. This examination is often done by a general internist or cardiologist. However, the wise surgeon, who is most aware of abnormalities or conditions that adversely affect surgical outcome, selectively checks for specific findings relevant to the planned operation. The surgeon is responsible for preoperative orders
Before elective cardiac surgery, correctable abnormalities such as infection, rhythm disturbances, fluid overload, hypertension, electrolyte or sugar imbalances, and so on are resolved. The surgeon must be sure that the patient is indeed ready for operation and that the correctable but unresolved abnormalities that may lead to postoperative complications are addressed. An example is treating acute or chronic bronchitis before an elective operation.
These are checked for temperature elevation, arrhythmias, tachypnea, and hypo-or hypertension.
HEAD, EYES, NOSE, AND THROAT
Sunken eyes in an elderly patient who is sedentary and frail are a poor prognostic sign; these patients have often lost interest in life. Carious teeth should be removed or repaired before aortic or valve surgery and, if severe, before any cardiovascular surgery. Carotid bruits require noninvasive preoperative testing to estimate the severity of stenoses and risk of stroke ] ; in selected patients, further testing and the possibility a combined carotid/cardiac procedure may be indicated . Funduscopic observation of cholesterol or atherosclerotic emboli may be a contraindication to operation.
Cardiac rhythm and murmurs should be confirmed to be sure that the findings are consistent with other data from the cardiac workup. Physical evidence of pulmonary rales, pleural effusions, or areas of absent or poor breath sounds prompt careful examination of the chest x-ray. The site of the planned incision should be inspected for skin lesions. A murmur of mild aortic regurgitation may complicate administration of antegrade cardioplegia.
The abdomen is palpated for evidence of liver, spleen, other organ enlargement, abnormal masses, and abdominal aortic aneurysms. The presence of ascites and areas of point tenderness may prompt further testing. Bruits over the abdomen may be an indication of diffuse vascular disease.
PELVIS AND RECTUM
The pelvic and rectal examinations usually are not done in patients with cardiac disease, especially if coronary artery disease is suspected. These examinations are done by general internists or other specialists after the cardiac condition is corrected, unless performed previously within a few months.
Signs of motor and sensory deficit and evidence of peripheral neuropathy should be documented thoroughly. The patient should be examined for signs of stroke, dementia, Alzheimer's disease, and deterioration of mental function.The preoperative examination provides an extremely important baseline for postoperative evaluations of possible new central or peripheral neurologic lesions.
A chart or diagram showing the strength of brachial, radial, femoral, popliteal, dorsalis pedis, and posterior tibial pulses should be recorded in the hospital chart. Diminished pulses or bruits indicative of aortoiliac-femoral occlusive disease are specifically noted. Feet should be inspected for signs of ischemia that may impair postoperative lower leg healing. Patients with lower extremity occlusive disease may require balloon pump insertion into the ascending aorta to avoid ischemic leg complications.] Occlusive disease is also associated with a greater incidence of stroke and leg wound complications.
Superficial leg and arm veins should be examined to determine suitability for coronary artery bypass grafting. Venous conduit may be absent due to amputation or prior excision. Varicosities, venous stasis changes, palpable thrombosis of veins, and prior operations or injuries in the region of the superficial veins may render veins unsuitable for bypass grafting. Unavailability of the greater saphenous, lesser saphenous, cephalic, or basilic vein should be described and prompts further studies to locate a suitable conduit
Evidence of cholesterol or atheromatous embolization to the skin or the blue toe syndrome is indicative of generalized atheromata and greater risk of intra- and postoperative stroke, renal insufficiency, and extremity necrosis. ] Because cardiac surgery and cardiopulmonary bypass greatly increase the risk of embolization in these patients, and because preventive measures are not available, operation may be contraindicated.
The patient should be inspected for bruising, petechiae, ecchymoses, rashs, pimples, boils, factitial lesions, spider hemangiomas, liver palms, or any sign of systemic or skin disease. Skin lesions or infection, particularly if near the proposed incision, may require further diagnosis and therapy before operation.
COMPLETE BLOOD COUNT
Measurement of blood hemoglobin or hematocrit, white blood cell count, and platelet count is routine for every preoperative patient. Anemia (hematocrit < 35 percent) is associated with greater need for blood transfusion and postoperative morbidity.Leukocytosis (white cell count > 10,000 per cubic millimeter) requires further evaluation for sources of infection or inflammation. A platelet count below 100,000 per cubic microliter is a clue for heparin-induced thrombocytopenia and/or thrombosis and requires further evaluation of possible IgG antibodies against platelets in the presence of heparin.
Hypokalemia is the most common preoperative electrolyte abnormality and is found most often in hypertensive patients who are taking diuretics. Unsuspected hyperkalemia, hyponatremia, or hypernatremia necessitates explanation and further evaluation. High bicarbonate concentrations may be associated with respiratory acidosis (co 2 retention) due to chronic obstructive lung disease.
Elevated preoperative creatinine is a strong predictor of postoperative renal failure and other postoperative complications.] The normal creatinine level is less than 1.5 mg/dL (133 µmol/liter) and is in the upper range for more aged patients because of a reduced number of nephrons. Blood urea nitrogen ranges between 10 and 20 mg/dL (3.6 and 7.1 mmol/liter). Unexpected values above the normal range may require further evaluation.
OTHER BLOOD MEASUREMENTS
Other blood chemical studies, such as glucose and bilirubin, may be included in the hospital blood chemistry panel that is measured automatically with blood electrolytes, creatinine, and urea nitrogen at low cost. Values outside the normal range may or may not trigger concern. Before cardiac surgery, both the prothrombin time and partial thromboplastin time should be measured with a platelet count and careful history of bleeding problems to rule out the possibility of an occult bleeding disorder. Routine preoperative bleeding times are not recommended.
All patients should have blood typing with a sample available in the blood bank before operation.
Urinalysis is a cost-effective method to detect occult urinary tract and renal disease. Glucosuria, proteinuria, hematuria, and pyuria may require further preoperative evaluation and treatment. A Gram stain of urine bacteria may provide enough information for antibiotic prophylaxis to avoid delay of operation if the patient is not febrile, but the urine also should be cultured.
The basic examination includes posteroanterior and lateral views. Pulmonary mediastinal and spinal abnormalities unrelated to the patient's cardiac disease and not known before may require further evaluation before operation
Cardiac abnormalities observed on chest x-ray should be consistent with other information obtained by physical examination, electrocardiogram, and cardiac catheterization. The chest x-ray often provides additional information relevant to operation. In patients who require reoperation, the proximity of the aorta or right ventricle to the underside of the sternum on the lateral view may prompt a decision to cannulate groin vessels before sternotomy or to expose the heart through a right thoracotomy. An ascending aortic aneurysm abutting the sternum or a mycotic or pseudoaneurysm is often an indication for presternotomy groin cannulation. Evidence of calcification of the ascending aorta, aortic valve, or mitral valve should be noted and may alter operative decisions. If the right phrenic nerve is paretic or paralyzed, the surgeon may be deterred from using the left internal mammary artery and risking injury to the left phrenic nerve.
The electrocardiogram (ECG) is most helpful in determining abnormalities of heart rhythm, conduction, and rate, recent or remote myocardial infarction, and left or right ventricular hypertrophy. Preoperative control of heart rate is particularly important, and medications, with the exception of amiodarone, are continued until induction of anesthesia to prevent breakthrough of the arrhythmia for which the drug or drugs were prescribed. A series of ECGs is especially helpful for distinguishing recent changes from more remote disease. Tachycardia should be controlled preoperatively by medication or cardioversion. Bradyarrhythmias may require adjustment of medication or even pacing preoperatively. Evidence of ischemia or infarction requires enzyme testing to estimate the possibility and timing of a recent infarction.
Cardiac catheterization within at least 6 months in stable patients and preferably closer to the time of operation is required for the vast majority of adult patients who have open heart surgery. Currently, no other diagnostic test provides details of the anatomy and pathology of the coronary vasculature. Coronary arteriography provides the “roadmap” that guides all revascularization operations and is usually indicated in patients with acute life-threatening complications of myocardial infarction (e.g., postinfarction ventricular septal defect, postinfarction mitral regurgitation). Cardiac catheterization provides chamber pressures and estimates of cardiac output and pulmonary and systemic arterial resistances. In selected patients with congenital, valvular, or aortic disease who are under 40 years of age, cardiac catheterization may be omitted in favor of echocardiography; however, this practice is the exception and not the rule.
The surgeon's preoperative evaluation of cardiac catheterization data is critical. The pathologic anatomy of the coronary arteries must be memorized. The presence or absent of valve disease must be noted; significant mitral regurgitation from ischemia may need treatment; even mild aortic insufficiency may preclude or compromise antegrade cardioplegia. Chamber pressures and the causes of elevated chamber pressures must be well understood. If left ventricular end-diastolic pressures are very high in a patient with low cardiac output and severe aortic stenosis, relief of stenosis immediately improves ventricular function. If left ventricular end-diastolic pressures are elevated from severe myocardial disease that is not likely to be reversed by revascularization, little or no benefit can be expected. A decision to repair tricuspid regurgitation may rest on the expected immediate relief of pulmonary hypertension from left-sided valvular or ischemic disease.
The arterial-venous oxygen saturation difference is a more reliable index of cardiac function at the time of blood sampling than estimates made by the Fick equation or by thermodilution. Oxygen saturation is easily measured precisely, and catheters can be placed in the pulmonary and systemic arteries reliably. The Fick equation requires measurement or estimates of oxygen comsumption for a specified time period; this measurement is usually estimated from tables rather than measured.
Although other tests may raise the suspicion or make the diagnosis of coronary arterial disease, coronary angiography is essential to indicate the location and severity and anatomy of both obstructed and nonobstructed vessels. Coronary angiograms are evaluated for the presence of significant obstruction in both native and previous vein or arterial grafts, areas suitable for bypass grafting, and the existence of bypassable vessels in areas of jeopardized myocardium. Vulnerable myocardium without target vessels suggests the presence of bypassable vessels not visible on the angiogram due to total occlusion and poor collateral flow. In reoperative patients, coronary angiograms indicate the location of previous pedicled mammary arterial grafts, the degree of stenosis in partially occluded vein grafts at risk of perioperative embolization, and the approximate location of target vessels that may be difficult to find because of an intramyocardial location or pericardial adhesions and epicardial fibrosis.
If questions arise concerning the availability of internal mammary, gastroepiploic, or inferior epigastric arteries for myocardial revascularization, selective angiograms may be obtained during cardiac catheterization.] Alternatively, the mammary, radial, and inferior epigastric arteries can be evaluated by duplex scanning. A reduced brachial blood pressure may be indicative of subclavian artery stenosis.
A left ventriculogram is indicated in most patients who have cardiac catheterization but is often omitted in patients with severe left ventricular dysfunction or with moderately severe or severe renal disease. Contraction abnormalities on the ventriculogram may represent scar or infarcted, stunned, or hibernating myocardium. Low ejection fraction with a history of multiple myocardial infarctions, long-standing mitral insufficiency, or congestive cardiomyopathy is indicative of severe left ventricular function and possibly much greater operative risk. Low ejection fraction with aortic valve disease, particularly aortic stenosis, is not associated with increased operative risk in our experience. In patients with low ejection fraction and coronary artery disease, the outcome of bypass grafting may be excellent if sizable portions of the noncontracting myocardium are viable but stunned or hibernating. Operation carries a low risk in patients with angina and minimal or no heart failure and left ventricular end-diastolic pressures less than 20 mmHg. Patients with low ejection fraction who have a much greater risk and lesser benefit from coronary arterial bypass grafting are those with some or all of the following characteristics: long history of symptomatic heart failure; failure symptoms are predominant over anginal symptoms; significant cardiac chamber enlargement by ventriculogram, chest x-ray, or echocardiogram; and ECG evidence of old myocardial infarction.
RIGHT-SIDED HEART CATHETERIZATION
Right-sided heart catheterization is usually not performed in patients with coronary artery disease with good or excellent left ventricular function. The examination is important in patients with chronic mitral valve disease, congenital heart disease, tricuspid valve disease, pulmonary vascular disease, or severe left ventricular dysfunction.
The size of the ascending aorta should be observed carefully in whatever projections it is viewed, including coronary artery injections, left ventriculogram, or aortogram. If the ascending aorta appears to be greatly enlarged, a computed tomographic (CT) scan may be necessary to determine the need for aortic replacement. Mobile atheromata may be visible on the aortogram but are more likely found by echocardiography. Aortic, valvular, coronary artery, and other sites of cardiac calcification should be noted. Aortic atherosclerosis is a major risk factor for perioperative stroke.
] Extensive or near-total calcification of the ascending aorta may preclude aortic cross-clamping or proximal anastomoses of vein grafts and necessiate more complicated surgery or contraindicate operation entirely.
EMERGENCY AND URGENT OPERATION
The basic evaluation may be incomplete in unstable patients who require operation quickly. The most extreme example is a patient who is brought to the hospital by ambulance after an acute coronary event. If the patient is intubated and no family is present, very little history is available. Hemodynamic instability may preempt evaluation of organ systems other than the heart. Immediate operation before cardiac catheterization is rarely indicated in these patients. The cause and reversibility of the cardiovascular disease must be known with reasonable certainty before operation. The best approach is to stabilize the circulation by drugs and/or temporary mechanical circulatory assistance until sufficient information can be obtained.
Patients scheduled for interventional cardiologic procedures should have the basic evaluation, including blood group typing, before the procedure. Between 2 and 7 percent of patients undergoing percutaneous transluminal coronary angioplasty (PTCA) develop abrupt closure of a coronary artery. Although occasional patients with unstable angina or myocardial infarction undergo catheter thrombolytic therapy or angioplasty before the basic evaluation is completed, as much information as possible regarding function of other organ systems, prior operations, allergies, and medications should be obtained before and during the PTCA procedure.
If the circulation cannot be stabilized in the catheterization laboratory, and if rational indications for operation exist, the surgeon may be forced to obtain as much useful information as possible on the way to the operating room with an unstable patient. Aside from concerns regarding the reversibility of the cardiac dysfunction and ischemic damage to other organ systems, the surgeon must ascertain that venous or arterial conduit is available. In the absence of data from the basic evaluation, the risk of death and/or intra- and postoperative complications increases markedly.
Preoperative evaluation of a patient who is already hospitalized on the cardiac surgical service should not be overlooked when an early return to the operating room is needed. Updated hematocrit, white cell and platelet counts, coagulation tests, an ECG, and chest x-ray are desirable for operative management and postoperative comparisons. It also may be necessary to send another sample of blood to the blood bank for crossmatching.
FURTHER PREOPERATIVE EVALUATION
The results of the basic evaluation indicate areas that require further evaluation. To control costs and to protect the patient, further studies must be selected carefully for relevance to indications and timing of operation and for preventing and controlling intraoperative and postoperative complications. In this section we present additional studies that are often helpful in achieving these goals.
MYOCARDIAL ENZYME TESTING
Creatine phosphokinase and the MB isoenzyme should be measured to rule an acute myocardial infarction in or out in patients with a history of recent chest pain lasting over 15 minutes and/or ECG evidence of myocardial infarction. Creatine kinase is normally under 90 units/liter, and the MB fraction, which is specific for cardiac muscle, should be less than 6 percent. Absence of enzyme elevation does not completely rule out recent infarction because of clearance; therefore, serial ECGs should be obtained if suspicion of an acute infarction is high.
TRANSTHORACIC ECHOCARDIOGRAPHY (TTE)
Transthoracic two-dimensional echocardiography and color-flow Doppler mapping image ventricular dimensions and chamber sizes; segmental wall motion and thickness; presence of mural thrombus, pericardial constriction, or effusion; some segments of the aorta; septal defects; and valvular anatomy and function. The specific reason for obtaining a two-dimensional echocardiogram before operation varies with the patient. In adults with ischemic heart disease, ejection fraction, left ventricular chamber size, specific wall motion abnormalities (relevant to stenotic or obstructed coronary arteries), and the presence and degree of mitral regurgitation are common indications for a preoperative echocardiogram. After recent myocardial infarction, an echocardiogram may detect a ventricular mural thrombus . Because mural thrombus is a risk factor for perioperative stroke, we obtain an echocardiogram on patients with recent myocardial infarction whenever possible.
Transthoracic echocardiography may provide important information regarding left ventricular function in patients with valve disease or ischemic damage. Patients with severely impaired left ventricular function may not be improved by revascularization if large areas of scar are present and heart failure is the predominant ischemic symptom. Depressed left ventricular function is not a contraindication to operation in patients with aortic stenosis but may be in patients with moderate or severe mitral regurgitation. TTE is useful for detecting vegetations and abscesses in patients with infective endocarditis.
TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE)
Transesophageal echocardiography (TEE) is indicated preoperatively for patients in whom the TTE examination is incomplete or not satisfactory for a variety of reasons. TEE requires sedation or light general anesthesia, whereas TTE can be done in any cooperative patient.
TEE is now an essential intraoperative monitor for patients who have valvular and aortic surgery, for all patients with poor right or left ventricular function, for unexpected patients who develop poor cardiac function following cardiopulmonary bypass, and for locating positions of intraaortic devices. The method is also standard for evaluating repaired mitral and tricuspid valves (see Chap. 33). In unstable patients with suspected aortic dissection, traumatic rupture of the aorta, or massive pulmonary embolism, TEE may be used for preoperative diagnosis in the operating room. TEE requires a skilled operator to obtain and interpret images.
Intraoperative direct echocardiography, wherein the echo probe is encased in a sterile sleeve and manipulated by the surgeon, is used to detect the presence and severity of aortic atheroma in patients with suspicious aortograms or TEE images or in patients who develop aortic atheroemboli during cardiac catheterization.
Exercise testing is used to determine the severity and significance of coronary artery disease and to determine which patients will benefit from myocardial revascularization. Many patients have exercise testing before referral for operation. Thus the exercise test is important for determining the indication for operation but is not otherwise important in preoperative evaluation.
THALLIUM-201 AND SESTAMIBI MYOCARDIAL IMAGING
Radionuclide myocardial imaging is a sensitive and reliable means to visualize acute myocardial infarction. In patients with chronic myocardial ischemic disease, radionuclide imaging is combined with exercise, dipyridamole, or adenosine to demonstrate areas of myocardium that cannot increase coronary blood flow in response to demand or vasodilatation.] These studies are usually done before operation is prescribed to relate areas of viable myocardium to stenotic or obstructed vessels that can be revascularized. Radionuclide studies also may be done in patients with poor left ventricular function in an attempt to differentiate viable myocardium from scar.
Positron-emission tomographic (PET) scanning is advocated for predicting wall motion recovery after revascularization in patients with coronary disease and poor left ventricular function. The method differentiates stunned and hibernating myocardium from scarred myocardium in patients who have both anginal pain and symptoms of heart failure. The method may extend surgical revascularization to subgroups of patients who otherwise would not be considered candidates for surgery because of high risk. The method is helpful but not infallible because scans must be interpreted. PET scanning is expensive and not widely available; therefore, the utility of the method in most practices is low.
COMPUTED TOMOGRAPHIC SCANS
Computed tomographic (CT) scans are particularly useful for evaluation of the thoracic aorta if abnormalities, dissection, or enlargement is suggested by the basic evaluation, chest x-ray, cardiac catheterization, or echocardiogram. Saccular aneurysms and the relationship of abnormal aortic segments to surrounding structures are well delineated by CT scans. CT scans are also indicated for mass lesions, such as primary or secondary tumors, that involve the heart, pericardium, lungs, or pleura. An abdominal CT examination may be ordered to rule out an abdominal aortic aneurysm in an obese patient.
Rapid CT scans are rarely prescribed for preoperative patients but can provide high-resolution images of left ventricular masses, chamber size, abnormal masses, and wall thickness changes during the cardiac cycle. These scans are helpful in selected patients with repaired or unrepaired complex congenital heart lesions, in the location of abscesses, and in defining the anatomy of the great vessels. Rapid CT scans are also used to assess right ventricular volume and function.
MAGNETIC RESONANCE IMAGING
Magnetic resonance imaging (MRI) also is used selectively for the preoperative evaluation of cardiac surgical patients. MRI requires a cooperative patient, does not expose the patient to radiation, detects blood flow, and provides high-resolution images in coronal, sagittal, and transverse views. In general, MRI provides similar morphologic information as rapid CT but also can determine whether or not an aneurysm is leaking or a previous vein graft is patent. MRI also can provide sophisticated information about segmental wall motion and ventricular remodeling. The expense, availability, and additional information provided by MRI restrict its use to a few highly selected patients with atypical cardiovascular problems.
PERIPHERAL ARTERIAL STUDIES
Peripheral noninvasive arterial studies (Doppler pulses, segmental pressure measurements, etc.) should be performed in patients with severe arterial occlusive disease by history and physical examination to determine the preferred site for harvesting venous conduit. In patients with peripheral vascular disease, a vein is removed from the leg with the least occlusive desease, as determined by the ankle-brachial index. Thigh veins may be preferable in patients with bilateral peripheral vascular disease. Aortoiliac occlusive disease often prevents passage of an intraaortic ballon or perfusion catheter from the groin.
The combination of ultrasound and color-flow Doppler velocity mapping is commonly termed duplex scanning . Vein mapping by duplex scanning is useful to locate suitable conduit or to select the site for harvesting conduit. The study is particularly helpful in minimizing dissection in very obese patients, patients who have had multiple vascular procedures, and patients with a history of deep venous phlebitis. If greater saphenous veins have been stripped or removed previously or are varicose or phlebitic, we determine the size and location of the lesser saphenous vein by duplex scanning , although scans may underestimate vein size. Vein mapping is also recommended in patients who have arterial occlusive disease and an ankle-brachial index less than 0.6 to minimize dissection necessary to harvest the vein. In some patients, mapping arm veins by duplex scanning is helpful.
In patients needing elective operations, any new pulmonary symptom or abnormality on chest x-ray requires further investigation to determine etiology. This may require treatment of pneumonia, pleurocentesis, or a full workup for a mass lesion. A decision to treat the pulmonary disease before or after operation first requires thorough knowledge of both the cardiac and pulmonary diseases, the urgency of one or the other, and the impact of the first treatment on the deferred disease.
The most common reason for delaying operation for pulmonary reasons is the need to treat productive cough with or without wheezing. Usually this is due to acute or chronic bronchitis that may be exacerbated by smoking. If pneumonia is ruled out by physical examination and chest x-ray, broad-spectrum antibiotics will control productive cough in most patients. Sputum Gram stain and/or culture may guide prescription of more specific antibiotics in patients with poor pulmonary function. Bronchodilators may be necessary preoperatively to relieve bronchoconstriction and wheezing; steroids are needed occasionally. The hospital is a smoke-free environment, and smoking is prohibited during hospitalization.
Dyspnea during rest or moderate exercise may be due to heart disease, pulmonary disease, or both. Further evaluation to determine the severity of lung disease in usually indicated, but extensive tests in preoperative patients are rarely indicated. Bedside spirometry, pulse oximetry, and/or measurement of arterial blood gases may be all that is needed for even high-risk cardiac patients. The absence of dyspnea with moderate exercise and a normal basic evaluation is adequate evidence of satisfactory lung function for operation.
Bedside spirometry measures vital capacity (VC), inspiratory and expiratory volumes, total lung capacity, and simple dynamic measurements such as forced expiratory volumes (FEV) versus time The patient's measurements are compared with predicted meaurements based on the patient's age, sex, and size. Spirometry reliably detects severe restrictive lung disease and also chronic obstructive pulmonary disease (COPD)
. Normally, the FEV 1 (FEV in 1 second) is 80 percent of predicted; values below 50 percent usually require further evaluation that includes laboratory pulmonary function tests, ventilation-perfusion scans, and pulmonary consultation. Bedside testing may underestimate the patient's best FEV 1 or VC.
Pulse oximetry is a cost-effective method to determine arterial oxygen saturation at the bedside. Because of the prevalence of COPD in adult patients with coronary arterial or aortic disease, pulse oximetry is often used as a screening test for the need for further evaluation of advanced pulmonary disease.
ARTERIAL BLOOD GASES
Arterial blood gases are usually the next step if the basic evaluation and bedside spiromety indicate intrinsic lung disease. Chronic obstructive pulmonary disease (COPD) is common in adult patients who need cardiac surgery; blood gases are helpful in estimating the severity of COPD and/or the need for preoperative bronchodilator and nonsmoking therapy. Dyspneic patients with severe COPD may have nearly normal arterial blood oxygen saturations and low-normal arterial Pco 2 because of hyperventilation; laboratory pulmonary function tests are needed to help estimate the severity of the COPD. In other patients with severe bronchitis and COPD, the resting arterial Pco 2 is increased and the arterial Po 2 is reduced; a resting arterial Pco 2 above 50 mmHg or room air arterial Po 2 of less than 70 mmHg indicates very severe bronchitic COPD. Severe COPD is a risk factor for morbidity] and mortality and raises the question of whether the benefit of the operation justifies the risk.
Occasional patients may have hypoxia and increased intrapulmonary shunting from reversible causes such as atelectasis, bronchospasm, or pleural effusions.
Ventilation-perfusion scanning is useful in preoperative evaluation for cardiac surgery only if pulmonary emboli are suspected. Ventilation-perfusion scans and other special pulmonary tests may be part of an extensive pulmonary workup for intrinsic pulmonary disease.
In our experience, current smoking is not a risk factor for mortality or morbidity following coronary artery bypass grafting. Smokers have greater red cell volume and hematocrit and are less likely to require transfusion postoperatively. Others find that current smoking is a risk factor for stroke, sternal wound complications, and pulmonary complications. Stopping smoking for less than 6 weeks preoperatively does not diminish the incidence or severity of pulmonary complications. Educational materials that advocate cessation of smoking are part of our preoperative preparation, but patients are not required to stop smoking prior to operation. Coronary artery bypass grafting is a potent incentive to stop smoking; up to 80 percent of patients stop smoking long term after myocardial revascularization.
If the patient's serum creatinine is less than 1.5 mg/dL and urinalysis is normal, no further renal evaluation is needed. Patients with successful, functioning renal transplants are not at higher risk for cardiac surgery. Nonsteroidal anti-inflammatory drugs or angiotensin-converting enzyme (ACE) inhibitors should be stopped for 48 hours in diabetics and patients with serum creatinine levels greater than 1.5 mg/dL if the patient is stable. ACE inhibitors may predispose to hyperkalemic renal failure.
If creatinine is greater then 1.7 mg/dL, a creatinine clearance is helpful if the patient's stability permits. Normal values range between 90 and 130 mL/min. Below-normal creatinine clearance and serum creatinine levels greater than 1.7 mg/dL are relevant to medication doses and may prompt increased hydration, low-dose dopamine, and stopping nephrotoxic medications before operation. Renal ultrasound is a good method to determine the presence of solitary kidney, cystic renal disease, or urinary obstruction above the bladder.
Selected patients with chronic renal insufficiency and even dialysis dependency may undergo cardiac surgery but at higher risk of mortality and morbidity. During cardiopulmonary bypass, both fluids and solutes can be removed by dialysis to maintain normal electrolyte concentrations
A history of prostatism, nocturia, or pyuria prompts measurement of residual urine. If obstructive uropathy is present, urine culture, antibiotic therapy, and catheter drainage of the bladder for 48 to 72 hours preoperatively may be advisable.
CAROTID ARTERIAL DUPLEX SCAN
Patients with history of stroke or transient ischemic attacks and/or carotid bruits are at greater risk of stroke. If the urgency of the patient's cardiac conditions allows, we perform carotid artery duplex scanning preoperatively in such patients. Cerebrovascular disease or carotid stenosis of greater than 80 percent is correlated with postoperative stroke and may prompt consideration of a combined operation on both the carotid artery and heart . A cerebral angiogram may be required in selected patients to further evaluate the carotid lesion. Preoperative cerebrovascular disease increases postoperative morbidity and mortality. We do not recommend an electroencephalogram as part of the preoperative evaluation.
BRAIN CT OR MRI SCANS
Preoperative evaluation of the brain in patients with stroke, transient ischemic attack, or change in mental capacity or status may be important for comparison with postoperative studies if a neurologic event accompanies operation. MRI is useful when multiple small strokes or strokes in the posterior cerebral circulation are suspected. Preoperative MRI studies of patients having coronary artery bypass grafting show that 58 to 93 percent of patients have preoperative abnormalities.
Patients with anemia or a history of heartburn, epigastric pain, dysphagia, or ulcer disease may require further evaluation prior to operation. In anemic patients scheduled for elective surgery, stool is examined for occult blood. If stool contains blood, a bleeding source within the upper gastrointestinal (GI) tract is sought and controlled before exposing the patient to heparin and cardiopulmonary bypass, but it is usually not necessary to perform exhaustive studies of the lower GI tract before operation. Esophagogastroduodenoscopy (EGD) is recommended to locate and sometimes treat an upper GI bleeding source. If the EGD is normal and liver function tests are normal, proceeding with operation is usually safe.
The presence of liver disease may be suggested by the history or dark urine and acholic stools. If hepatosplenomegaly, ascites, jaundice, spider hemangiomas, or palmar erythema is present, liver function is evaluated by blood tests. Hyperbilirubinemia, hypertransaminasemia, high serum alkaline phosphatase, and hypoproteinemia are indications for further evaluation of liver function before operation.
Hyperbilirubinemia is indicative of hepatic disease, biliary disease, hemolysis, or a genetic defect in bilirubin metabolism. Further investigations including imaging studies are necessary to determine whether hepatobiliary disease is the cause. High alkaline phosphatase and glutamyl transpeptidase levels are also indications for imaging studies of the liver and biliary tree for evidence of mass and/or obstructive lesions. In the absence of anticoagulant therapy preoperatively, hypoprothrombinemia is usually indicative of hepatic dysfunction.
Significant liver disease greatly increases operative risk, and often the benefits of operation are meager. Nonoperative forms of therapy should be considered seriously if the hepatic dysfunction is independent of cardiac disease. Although the operative risk of valve surgery is greater in patients with associated congestive hepatomegaly, early relief of hepatic congestion usually reverses liver dysfunction and provides excellent long-term benefits.
Platelet count, prothrombin time, and partial thromboplastin time are recommended preoperatively as part of the basic evaluation. If the history, physical examination, or abnormal basic laboratory studies suggest possible coagulation deficiency, more specific analysis of soluble blood coagulation proteins is recommended to determine the cause and also treatment.
Temporary coagulation abnormalities are common in cardiac surgical patients who receive heparin, aspirin, or thrombolytic therapy preoperatively. We do not consider these abnormalities a contraindication to operation. Sustained prior heparin administration may produce heparin resistance (inability to adequately prolong the activated clotting time) at the time of operation. Heparin resistance is due to a relative deficiency of antithrombin, the essential cofactor of heparin, and is treated by infusion of fresh-frozen plasma. Aspirin inhibits all platelets at the time of administration but does not affect new platelets that are constantly being added to blood. Aprotinin is effective in patients who have received prior aspirin, and if postoperative bleeding occurs, platelet transfusions are given. Similarly, preoperative fibinolytic drugs may partially deplete plasma fibrinogen, but this can be replaced by fresh-frozen plasma.
Diabetes is common in adult patients requiring cardiac operations and is usually discovered from the patient's history. Occasionally, hyperglycemia is found by urinalysis or blood chemistry without a prior history, and control is necessary with insulin or oral hypoglycemics before operation.
Diabetics undergoing cardiopulmonary bypass usually require larger amounts of insulin than during other types of surgery. Blood sugars are monitored during and early after operation by finger stick and daily chemistry until the patient is eating normally. Insulin-dependent diabetics who have taken protamine insulin preparations are more prone to protamine reactions.
Internal mammary grafts in insulin-dependent diabetics are associated with an increased incidence of sternal wound complications and phrenic nerve dysfunction.Other morbidity associated with insulin-dependent diabetes includes longer hospital stay, mortality, renal failure, wound complications, infection, and stroke. Unfortunately, no preoperative intervention lowers the risk of complications in diabetics.
Treatment of myxedema may be delayed until after coronary artery bypass grafting in patients with coronary disease. Hyperthyroidism should be controlled before cardiac surgery.
Patients with unstable angina and hypercalcemia due to hyperparathyroidism may be managed medically until after coronary artery bypass grafting.
Routine nutritional assessment is of no value in guiding preoperative management. In very aged patients, cachexia (body weight below the tenth percentile) is a risk factor for mortality.
Extreme obesity is easily determined subjectively, but the degree can be quantitated by the body mass index. Various studies show that obesity is a risk factor for sternal and leg wound infection, postoperative arrhythmias, myocardial infarction, postoperative bleeding, and length of hospital stay but not mortality. Although weight loss is encouraged and recommended for all obese patients, extreme obesity is rarely a reason for delaying operation. Preoperative weight loss may improve symptoms of angina and heart failure as part of medical therapy but is not effective once surgery is indicated.
Although others recommend surveillance nasal cultures to reduce the risk of postoperative infection by prophylactic antibiotics, we do not recommend screening patients to determine their carrier state. Prophylactic antibiotics may enhance colonization of more pathogenic organisms and require costly repeated cultures and assessment. Prolonged preoperative stay is associated with an increased risk of infectious complications.
Latent infections that are asymptomatic or produce low-grade, chronic inflammation should be treated with specific antibiotics preoperatively to prevent bacteremia. Examples include chronic bronchitis with sputum production, prostatitis, pyelonephritis, pyuria, and skin infections, including cellulitis, boils, and eczema. Cultures and, if time is a factor, Gram stains should be obtained to identify specific organisms and guide antibiotic therapy. In the absence of pus, treating skin lesions rarely decreases the infectious risk of operation. Psoriasis and other noninfectious skin diseases do not require culture or antibiotics.
Carious, infected teeth should be treated or extracted prior to elective valve operations, but this is usually not necessary before coronary arterial surgery. Preoperative dental work is usually not possible or advisable in unstable patients; broad-spectrum antibiotics are used to reduce the possibility of septicemia in these individuals.
Occasionally, endocarditis is insidious and may present with nonspecific symptoms in afebrile patients. Valve dehiscence within the first year after operation is frequently due to infection with Staphylococcus epidermidis or low-grade nosocomial organisms. The surgeon should seek evidence of endocarditis by history and physical examination, including search for microembolic manifestations of endocarditis in nails, skin, eye grounds, and urinalysis. Suspicion of endocarditis is an indication for echocardiography and blood cultures.
Patients with low serum potassium levels are susceptible to premature ventricular contractions, ventricular fibrillation, and ventricular tachycardia. If a patient's preoperative serum potassium level is less than 3.5 meq/liter, parenteral potassium supplements are given preoperatively. Oral potassium supplements are used for serum potassium levels between 3.5 and 4.0 meq/liter. Our goal is a serum potassium level above 4.0 meq/liter before beginning operation.
Prophylactic digoxin is generally not indicated but may be started for heart failure or supraventricular arrhythmias or in patients with recent myocardial infarction or in those who require valve surgery.
Beta-blocking agents, calcium-channel blockers, and other antiarrhythmics, except amiodarone, are continued up to operation. Prophylactic digoxin, calcium-channel blockers, and amiodarone do not reduce the incidence of postoperative atrial fibrillation; however, in patients with adequate left ventricular function, some reports indicate that prophylactic beta blockade reduces postoperative atrial fibrillation.
STEROIDS AND VITAMIN A
Steroids are not discontinued before operation in patients who receive these drugs long-term. Indeed, these patients receive supplemental intravenous steroids during operation and for the first day or two afterwards. Chronic steroid therapy is a risk factor for wound complications. Vitamin A, 50,000 units per day, may be given prior to operation to block the effect of steroids on wound healing.
The most common approach for operations on the heart and aortic arch is the median sternotomy. The skin incision is made from the jugular notch to just below the xiphoid process. The subcutaneous tissues and presternal fascia are incised to expose the periostium of the sternum. The sternum is divided longitudinally in the midline. After placement of a sternal spreader, the thymic fat pad is divided up to the level of the brachiocephalic vein. An avascular midline plane is identified easily, but is crossed by a few thymic veins that are divided between fine silk ties or hemoclips. Either the left or right, or occasionally both, lobes of the thymus gland often are removed in infants and young children to improve exposure and to minimize compression on extracardiac conduits. If a portion of the thymus gland is removed, excessive traction may result in injury to the phrenic nerve. The pericardium is opened anteriorly to expose the heart. Through this incision, operations within any chamber of the heart or on the surface of the heart, and operations involving the proximal aorta, pulmonary trunk, and their primary branches can be performed. Extension of the superior extent of the incision into the neck along the anterior border of the right sternocleidomastoid muscle provides further exposure of the aortic arch and its branches for procedures involving these structures. Exposure of the proximal descending thoracic aorta is facilitated by a perpendicular extension of the incision through the third intercostal space.
Bilateral Transverse Thoracosternotomy (“Clam Shell” Incision)
The bilateral transverse thoracosternotomy (“clam shell” incision) is an alternative incision for exposure of the pleural spaces and heart. This incision may be made through either the fourth or fifth intercostal space, depending on the intended procedure. After identifying the appropriate interspace, a bilateral submammary incision is made. The incision is extended down through the pectoralis major muscles to enter the hemithoraces through the appropriate intercostal space. The right and left internal thoracic arteries are dissected and ligated proximally and distally prior to transverse division of the sternum. Electrocautery dissection of the pleural reflections behind the sternum allows full exposure to both hemithoraces and the entire mediastinum. Bilateral chest spreaders are placed to maintain exposure. Morse retractors are particularly suitable with this incision. The pericardium may be opened anteriorly to allow access to the heart for intracardiac procedures. When required, standard cannulation for cardiopulmonary bypass is achieved easily. This incision is popular for bilateral sequential double lung transplants because of enhanced exposure of the apical pleural spaces. When made in the fourth intercostal space, the incision is useful for access to the ascending, arch, and descending thoracic aorta.
The right side of the heart can be exposed through a right anterolateral thoracotomy. The patient is positioned supine, with the right chest elevated to approximately 30 degrees by a roll beneath the shoulder. An anterolateral thoracotomy incision can be made that can be extended across the midline by transversely dividing the sternum if necessary. With the lung retracted posteriorly, the pericardium can be opened just anterior to the right phrenic nerve and pulmonary hilum to expose the right and left atria. The incision provides access to both the tricuspid and mitral valves and the right coronary artery. Cannulation may be performed in the ascending aorta and the superior and inferior caval veins. Aortic cross-clamping, administration of cardioplegia, and deairing of the heart after cardiotomy are difficult through this approach. This incision is particularly useful, nonetheless, for performance of the Blalock-Hanlon atrial septectomy or for valvar replacement after a previous procedure through a median sternotomy. A left anterolateral thoracotomy performed in a similar fashion to that on the right side may be used for isolated bypass grafting of the circumflex coronary artery, or for left-sided exposure of the mitral valve.
A left posterolateral thoracotomy is used for procedures involving the distal aortic arch and descending thoracic aorta. With left thoracotomy, cannulation for cardiopulmonary bypass must be done through the femoral vessels.
Diltiazem induced a significant reduction of heart rate throughout the first 24 postoperative hrs.
Since postoperative AP was comparable in both groups, the PPR as an indicator of myocardial oxygen demand was also lower in the diltiazem group.
However, although HR was significantly lower, CI was comparable to nitroglycerin-treated patients, indicating that the negative inotropy of diltiazem did not depress perioperative myocardial function.
The HR lowering effect of diltiazem may have contributed to its antiischemic efficacy, since an increased heart rate is a primary factor in the pathogenesis of myocardial ischemia.
Effects of Diltiazem on Supraventricular and Ventricular Arrhythmias:
In accordance to various clinical findings, diltiazem significantly reduced the incidence of postoperative atrial fibrillation.
The importance of perioperative supraventicular arrhythmias and their contribution to the occurrence of postoperative ischemia and/or other complications appear to be significant.
They are frequently not well tolerated by patients and induce various symptoms such as temporary hemodynamic instability, shortness of breath or chest discomfort.
Consequently, the pharmacological prevention of perioperative arrhythmias should be mandatory during postoperative intensive care management and is effectively provided by diltiazem.
The applied standard infusion rate of diltiazem in this commented studies had no apparent influence on AV-node conduction.
The incidence of perioperative AV-block I was low and almost identical in both treatment groups.
No case of AV-block II or III was observed. In none of these patients the conduction abnormality was permanent or required temporary external pacing due to hemodynamic instability.
Diltiazem significantly lowered the average number of ventricular couplets and runs per patient.
Under normal conditions, diltiazem has only negligible effects on the effective refractory periods of the ventricle or HIS-Purkinje system.
However, it is known to suppress premature ventricular contractions under ischemic conditions.
This effect is due to an improvement of ischemia induced prolongation and dispersion of conduction time.
Consequently, it may be assumed, that the antiischemic efficacy of diltiazem may have induced and/or contributed to its antiarrythmic effect in this commented study.
Effects of Diltiazem on Incidence and Extent of Myocardial Ischemia:
The diagnosis of myocardial ischemia in the perioperative setting still provides significant problems.
Most studies rely on the occurrence of a new Q-wave in postoperative ECG´s as indicator for perioperative MI.
However, it was shown that this diagnostic approach is not only of limited sensitivity and specificity in cases of transmural infarction, but also misses the diagnosis of substantial myocardial ischemia and cell necrosis. In addition, due to its relatively low overall incidence in elective ACBP operations, the use of a new Q-wave as an endpoint diagnostic parameter for defining perioperative ischemia does not allow to differentiate between the antiischemic efficacy of therapeutic regimens in studies with relatively low number of patients.
In the presented studies, myocardial ischemia was independently diagnosed by the combined analysis of serial 12-lead ECG and continuous Holter monitoring and the analysis of highly ischemia-specific laboratory parameters. In addition to the occurrence of a new Q-wave following persistent ST-segment elevation, patients with persistent negative T-waves of >3mm were diagnosed as having new, perioperative MI.
Consequently, the incidence of perioperative MI was slightly higher in the present investigation (study II: 3.3 vs. 6.7%) as compared to studies that solely rely on the occurrence of a new Q-wave as a proof for MI. Nevertheless, in this study it was not possible to demonstrate a statistically significant reduction of the incidence of peri-operative MI by diltiazem, although the incidence of MI was only half of that observed in the nitroglycerin group.
In addition to the occurrence of new MI, diltiazem markedly decreased the overall number and the mean duration of TIE´s per patient, which certainly reflects the severity of the underlying ischemic process.
The clinical value of this finding seems important, since prevention of perioperative ischemic events may predict a lower incidence of MI or reappearance of angina during postoperative follow up, as has been shown for variant or unstable angina in patients with CAD.
The analysis of laboratory parameters in this commented studies clearly demonstrated the antiischemic efficacy of diltiazem: Peak values of CK-MB, MB-M and troponin-T were significantly lower in the diltiazem group.
Troponin-T levels in the diltiazem group were actually almost half of that observed in the nitroglycerin group. In the subgroups of patients with either TIE´s or MI, only the analysis of troponin-T and MB-M allowed to differentiate between the two treatment groups. Both parameters were markedly lower in diltiazem treated patients, indicating that the extent of cardiac cell necrosis was significantly lower.
In this respect, it may be concluded that the markedly lower numbers and shorter duration of transient ischemic events in the diltiazem group do reflect a clinically significant antiischemic effect.
Effects of Diltiazem on Myocardial Function:
TEE was primarily used to investigate, whether or not diltiazem significantly influences postoperative myocardial function.
Myocardial performance early after CBP highly depends on multiple factors such as pre- and afterload, variations in HR, level of anesthesia, etc., which may complicate the assessment of direct drug-related effects.
Therefore, study II compared changes in myocardial function between periods of relative hemodynamic stability such as immediately before surgery and at 4 hours after opening of the ACC.
Qualitative grading of segmental myocardial function is the most common method in perioperative monitoring by TEE.
However, this method is unable to detect small changes in regional wall motion and cannot be used to define global changes in the inotropic state of the myocardium.
In contrast, the computer assisted calculation of %FAC is a widely accepted quantitative method for assessing even small changes in global myocardial function.
In addition, the measurement of changes in systolic %WTh certainly provides the most precise method for quantitative analysis of changes in regional myocardial function.
In this commented study (II), quantitative assessment of peri-operative changes in myocardial function revealed a significant improvement of global myocardial function %FAC in the diltiazem, but not in the nitroglycerin group.
The diltiazem induced improvement in global function was probably caused by the observed augmentation of %WTh in the anterior wall of the left ventricle.
The data cannot explain the slight but significant reduction of regional function in the posterior wall of patients treated with nitroglycerin.
However, although there appears to be no rational explanation, it has been shown, that postoperative regional wall motion abnormalities are more often located in the posterior as compared to the anterior wall.
Since the Holter data do not allow the exact localization of ST-segment alterations, it remains open, whether the higher incidence and severity of perioperative TIE´s in the nitroglycerin group was mainly caused by ischemia in the posterior wall and may explain the significant reduction of %WTh in this area.
The results of qualitative segmental grading support the findings of these quantitative measurements.
Although there was a trend towards more postoperative normokinetic segments in both treatment groups, the amount of severe hypo-akinetic segments was lower in the diltiazem group at postoperative evaluation. In addition, the postoperative improvement in functional grading was more pronounced in the diltiazem group in segments that showed severe hypokinetic-akinetic function preoperatively.
Although the differences were not significant, these trends further substantiate the beneficial effect of diltiazem on post-operative function and confirm the reported protective efficacy of diltiazem in segments of most severe dysfunction.
The diastolic performance of the left ventricle is a complex sequence of various interrelated events and is affected by numerous factors such as age, HR, loading conditions, etc.
Nevertheless, impaired relaxation of the left ventricle during diastole has been consistently observed in patients with CAD and often reflects or even precedes a deterioration in systolic function. In this study, diastolic compliance was characterized by the ratio between early diastolic and late atrial filling as assessed by transmitral diastolic doppler flow velocitiy time integrals (E/A ratio).
This index has been shown to be a useful parameter in providing a non invasive and reliable estimate of diastolic performance especially in patients with CAD.
Preoperatively, the E/A ratio was comparable in both groups (1.66 vs. 1.68) and indicated a slightly decreased diastolic compliance when compared to values for patients with normal ventricular function.
No comparable data exist to confirm the findings that at 4 hrs after CABG, diastolic function is significantly depressed.
The observed postoperative decrease of the E/A ratio in both groups apparently reflects the effect of intraoperative ischemia on the diastolic compliance.
This assumption is substantiated by the fact that, except for HR, hemodynamic variables that may influence the assessment of diastolic function such as systemic arterial, central venous or pulmonary wedge pressure, were almost identical in both treatment groups. In this respect, the significantly lower reduction of the E/A ratio in the diltiazem group indicates a beneficial effect of diltiazem on peri-operative preservation of diastolic function.
Mechanisms of the Protective Effects of Diltiazem:
There are many possible explanations for the observed beneficial effects of diltiazem on perioperative ischemia and myocardial function.
Coronary bypass surgery can be interpreted as a model of transient, total ischemia (ACC time) followed by reperfusion.
Myocardial ischemia during ACC is total under any circumstances and cannot be influenced by drug-induced coronary vasodilatation. However, at reperfusion, cytosolic calcium overload becomes a critical determinant of postischemic myocardial ultrastructure and function. Several mechanisms such as increased influx through membrane calcium channels, increased sodium-calcium exchange, or inadequate intracellula compartmentalization of calcium contribute to abnormal calcium homeostasis, induce cell damage and adversely affect myocardial contractility.
Although under normal conditions, diltiazem dose dependently induces a negative inotropic effect, its application during ischemia and/or reperfusion has been reported to decrease ultrastructural cell damage and to increase post-ischemic myocardial function.
The significant lower postoperative peak values of ischemia-specific laboratory parameters in the diltiazem group clearly demonstrate a substantial lesser extent of perioperative ultrastructural damage.
Consequently, a diltiazem-induced protection from calcium overload together with other mechanisms of calcium blockade during reperfusion, such as preservations of ATP-levels and diminution of ATP- catabolism, may explain the beneficial effects of diltiazem on postoperative myocardial function and ischemia.
Finally, the well documented coronary vasodilative potency of diltiazem may have contributed to its antiischemic efficacy. A decrease in flow resistance increases blood flow in grafts and coronary arteries.
This mechanism conceivably reduces the incidence and severity of regional myocardial ischemia or flow disturbances which may otherwise induce significant ischemia during the early postoperative period.
Increase in pulse pressure, LV becomes dilated and hypertropied
Pulmonary congestion and edema are common
Cerebral insufficiency, dizziness, pulsating headaches, dyspnea, increased pulse pressure,
and pulmonary congestion and edema. Coronary insufficiency mat occur
Left heart failure followed by right heart failure
Surgical replacement with a prosthetic valve is treatment.
Increase in the systolic pressure within the left ventricle
Dizziness and fainting and angina pectoris are common. Easily fatigability exertional
dyspnea and palpitations may also occur.
Sudden death occurs in approximately 30% of cases
Valve replacement is the treatment of choice.
Supravalvular or Subvalvular or Idiopathic hypertrophic subaortic stenosis
Defect in which there is a opening between the aorta; near it's valve; and the pulmonary artery.
This window functions as a patent ductus arteriosus pathology and clinical features are the same.
Most cases shunt is large and increased pulmonary hypertension.
Operative closure early is indicated, Correction contraindicated if shunt is right to left.
Atrial Septal Defect
Most common defect in adults.
1) Ostium primum- occurs low in septum and frequently associated with partial or complete cleft in medial mitral valve
2) Ostium secundum- most common type usually located in the central portion of atrial septum.
3) Sinus venosus- located high on the atrial septum near opening of SVC, occasionally anomalous drainage associated
Some pulmonary hypertension may develop no cyanosis until right to left shunt occurs.
Common atrium a secundum defect involving almost all of septum is rare.
Compression of the heart due to the collection of fluid (blood) within the pericardium
Venous return to the right ventricle during diastole is restricted.
Increased right ventricular end diastolic pressure
Removal of blood from pericardium usually results in dramatic recovery.
Term used for myocardial disease of unknown etiology
1) Hypertrophic-subdivided into conditions with or without obstruction.
2) Congestive-characterized by congestive heart failure
3) Obliterative- conditions in which the cavity of ventricle obliterated by abnormal tissue
4) Restrictive- restricts ventricular filling extremely rare
Coarctation of the Aorta
Most commonly found in the thoracic aorta distal to subclavian artery but may be located anywhere in aorta.
Constriction can be pre or post ductal.
Constriction usually produces arterial hypertension and left ventricular hypertrophy in proximal artery.
Distal artery will show hypotension blood supply by collateral.
Exertional dyspnea, frank congestive heart failure, hypertension, claudication in the low extremities.
Defect repaired by resection of the coarctation and resuturing the aorta. Small tube graft may be used for large repair.
Relatively rare congenital defect in which the left atrium is divided by a septum. commonly
located transversely, divides the left atrium into two chambers.
Posterior chamber receives all of the flow from the pulmonary veins, a small opening or
openings connect the two left atrial chambers and offer high resistance to blood flow.
Pulmonary venous hypertension, pulmonary arterial hypertension, and right ventricular
hypertrophy. Difficulty in breathing; exertional dyspnea and orthopnea
Surgical correction involves excision of the septum between the left atrial chambers.
Defect of the great vessels are transposed but the ventricles are also transposed.
Blood circulates in normal fashion venous blood passes through a mitral valve.
Systemic blood passes through a tricuspid valve then out aorta.
most of time no problem unless associated defects VSD, pulmonary stenosis, MV
abnormalities and disturbance in the A-V conduction system.
Surgical Jatene or Le Compte
When ventricular septum so grossly deformed that it appears to be absent. ASD and transposition commonly found
Surgical correction is difficult and unsuccessful in most cases.
Double outlet right ventricle both aorta and pulmonary artery leave RV may appear to be Tetralogy of Fallot or VSD
Sometime referred to as partial transposition.
Part of the septal and posterior leaflets are attached directly to the right ventricular wall
Divides the RV into two parts; proximal RV (atrialized part) and distal or functional RV
Patent foramen ovale or ASD common finding.
Tricuspid insufficiency common and occasionally tricuspid stenosis is also present
Dyspnea, cyanosis and clubbing are common. Cardiac arrhythmias common.
70% pts untreated die before age 20 many suddenly.
Valvuloplasty indicated in only 30%
Endocardial Cushion Defects
Two ridges of embryonic tissue which fuse and close the atrioventricular canal and the septal cusps of the mitral and
1) Ostium primum defect
2) Ostium primum defect is present and clefts in both the mitral and tricuspid leaflets. Small bridge of tissue interrupts
this cleft and prevents it from becoming a common valve. A small VSD may be present.
3) Ostium primum defect and continuous cleft through both the mitral and tricuspid common valve to both sides.
This is called atrioventricular communis (A-V canal)
Dyspnea and fatigue common as are respiratory infections.
70% infants with defect die within the 1st yr of life.
ASD repaired by direct closure. Clefts are sutured closed.
Hypoplastic Left Heart Syndrome
Underdeveloped left side of the heart.
Aortic valve atresia, extreme hypoplasia of the aorta, mitral valve atresia or hypoplasia
Foramen ovale usually opened and a patent ductus arteriosus along with intact ventricular
Fourth most common defect accounts for 25% of cardiac deaths during the 1st month.
Staged Norwood procedure only treatment.
Left Ventricle-Right Atrial Communication
A high VSD connecting the left ventricle with the right atrium surgical correction by direct closure
Incomplete closure or absence of a mitral valve.
Increased filling in left ventricle which results in dilation and hypertrophy.
Peak pressure in atrium can reach 50-70 mmHg
Increased pulmonary artery and RV systolic pressures
Palpitations, fatigue, orthopnea, and pulmonary edema secondary to LV volume overload
Right heart failure may occur
Treatment is prosthetic valve replacement usually.
Most common valvular defect.
Rise in left atrial pressure due to slowed flow to ventricle during diastole
Palpitations, weakness, orthopnea, dyspnea, pulmonary edema, and hemolysis common
Edema and cyanosis may occur in advanced stages.
Usually valve replacement or mitral commissurotomy are repair.
Patent Ductus Arteriosus
Should form ligamentum arteriosum within 12 days of birth.
Left to right Shunt; dyspnea, fatigue, diminished growth, and cardiac failure if the shunt is large.
Subacute bacterial endocarditis may develop.
Could be right to left shunt if pulmonary resistance is higher than systemic; cyanosis and fatigue main complaints.
Ductus is closed by ligation and/or complete division, When shunt is right to left surgical correction contraindicated.
Defect which includes hypoplasia or absence of the main pulmonary artery. Pulmonary
circulation is dependent upon a patent ductus arteriosus and VSD
Resemble those of tricuspid atresia, dyspnea, fatigability, frequent respiratory infections,
cyanosis, hypoxia, and cardiac failure are all common findings.
Surgical correction involves closing the VSD and patent ductus arteriosus, Rastelli procedure.
Valvular pulmonary atresia is the failure of the development of the pulmonary valve and normal development of the right ventricular chamber.
Arterial pulmonary atresia is failure of embryologic development of the main pulmonary artery.
Circulation depends on the patent foramen ovale or the atrial septal defect and a patent ductus arteriosus.
Severe cyanosis, clubbing, dyspnea, and fatigue are common.
Complications include subacute bacterial endocarditis, brain abscess, embolism, and cerebral vascular accidents.
Surgical correction depends on the RV development
If right ventricle is normal a simple pulmonary valvulotomy may be performed.
Right ventricular chamber hypoplastic with a normal pulmonary artery ( Cooley, Blalock-Taussig, Potts, Glenn Shunts,
or the Rashkind procedure
Main Pulmonary artery hypoplastic Fontan procedure
Right ventricle normal pulmonary artery hypoplastic the Rastelli is effective
Compromises 10-15% of congenital defects.
Four types can occur
1) Valvular Stenosis
2) Infundibular stenosis (or combination of the two)
3) Stenosis of the pulmonary artery (Supravalvular stenosis or coarctation of the PA)
4) Peripheral pulmonary stenosis
Causes obstruction of blood from the RV increasing the work load of the right ventricle.
Pulmonary Stenosis may be described by RV pressure as the following:
1) mild 45mmHg or less
2) moderate 46-89 mmHg
3) severe 90 mmHg or more
Exertional dyspnea, and frank cardiac failure.
systolic pressure gradient of 60mmHg or more indication of operation.
If pure valvular fused commissures are incised by direct vision
If infundibular hypertrophy in the pulmonary outflow tract is resected.
Tetralogy of Fallot
Consists of four distinct features:
1) Pulmonary stenosis
3) Overriding aorta
4) Right ventricular hypertrophy
If ASD present Pentalogy of Fallot
Cyanosis and clubbing common, Clotting abnormalities; hypoxic episodes, cerebral thrombosis, brain abscess
and pulmonary hemorrhage are other occurrences
Surgical palliation has been recommended for small infants
1) Blalock-Taussig or 2) Potts
Total Anomalous Pulmonary Venous Return
When four pulmonary veins return blood to the right side of the heart. Intracardiac defect
must be present for left side circulation. Usually a ASD. Can also be partial left called
Partial anomalous pulmonary return.
Can fall into three categories.
1) Supracardiac- most common type 50% pulmonary vein empties into left SVC,
then innominate vein and finally into the SVC.
2) Cardiac- 30% return frequently empties into the coronary sinus, occasionally R. atrium
3) Infracardiac- 10% return into a common venous trunk that descends and enters the IVC
or portal vein below the diaphragm.
Cyanosis characteristic of all types. Cardiac failure and pulmonary hypertension are consequential.
Surgical treatment aimed at redirecting the venous return to the left side.
Transposition of the Great Vessels
Complete transposition the aorta arises from the right ventricle and is located anterior
to the pulmonary artery, pulmonary artery arises from the left ventricle and is posterior to
the aorta. When this is present, normal circulation is interrupted and blood circulates around
the systemic circulation without passing through the pulmonary circulation. A patent ductus
arteriosus, patent foramen ovale are present in 50% of the cases, most common VSD.
cyanosis, frequent respiratory infections, spells of hypoxia, or anoxia, myocardial infarction
pulmonary hypertension, and congestive failure.
Surgical correction Blalock-Hanlon
Total correction of this defect involves rearranging the atrial septum so that the atrial
chamber receiving blood from the superior and inferior vena cava will empty into the
ventricle from which the pulmonary artery leaves, same for the systemic system.
This rearranging procedure is the Mustard or Senning
Absence of tricuspid valve, prevents normal heart circulation. Blood must flow through a
ASD or patent foramen ovale
VSD or patent ductus arteriosus must be present for blood to get to pulmonary vessels.
high mortality rate, 50% die within six months.
Severe cyanosis, clubbing, dyspnea, and fatigue common, as is right heart failure.
Complications include subacute bacterial endocarditis, brain abscess, embolism,
and cerebrovascular accidents.
Surgical correction usually limited to increasing pulmonary blood flow
1) Cooley shunt
2) Blalock- Taussig
4) Glenn procedure
Extremely rare finding; congenital or rheumatic disease, trauma or endocarditis occasionally
cause tricuspid insufficiency.
Edema and ascites are usually present, also hepatomegaly, and splenomegaly.
Primary cardiac defect must be corrected. Repair is usually limited to valvuloplasty.
Rare instances is congenital. almost always due to rheumatic fever.
Tricuspid commissures fuse and fibrose.
right heart failure symptoms; edema, systemic venous hypertension, and ascites.
Usually corrected by valvuloplasty unless a valve leaflet has been destroyed, in this case
valve replacement is necessary
VSD with a single vessel, single ventricular valve. Pulmonary arteries may arise separately
or from a common stem.
PVR compared to SVR largely determines the clinical picture. If PVR low in comparison
then pulmonary flow is normal or increased. cardiac failure.
Dyspnea, fatigability, frequent respiratory infections, cyanosis, hypoxia, clubbing are all
Surgical correction involves the closing of VSD, removing the pulmonary arteries from the
wall of the truncus, and inserting a woven Dacron tube graft which incorporates a
prosthetic valve between RV and left pulmonary artery. Rastelli
Ventricular Septal Defect
Four types: top to bottom of septal wall
1) located between the crista supraventricularis and the pulmonary valve
2) just caudal to the crista supraventricularis
3) Beneath the septal leaflet of the tricuspid valve in an area where the A-V conduction bundle is susceptible to injury.
4) located in the muscular septum near the apex of the right ventricle
Size and pulmonary resistance determine the volume of blood shunted, increased pulmonary blood flow increased PVR
When PVR becomes more pronounced (PVR higher than SVR) right to left shunt occurs once this happens surgical
correction uniformly unsuccessful. Correction may be carried out by direct closure
Blalock-Hanlon- does not involve CPB involves excising a portion of the atrial septum
Blalock-Taussig- right subclavian to pulmonary artery
Cooley - aorta to right pulmonary artery
Fontan- right atrium to the pulmonary artery
Glenn- superior vena cava and right pulmonary artery.
Jatene- descending aorta and main pulmonary artery are transected into normal fashion.
Le Compte- vessels transected but the ascending aorta is behind the pulmonary bifurcation.
Mustard- switching of the atrium in transposition of the great vessels by inflow inversion
Norwood- right atrium to pulmonary (modified Fontan) intra atrial baffle
Potts- aortic to left pulmonary artery
Rashkind- pulling a balloon catheter through left atrium into right atrium Cath lab procedure (Atrial Septostomy)
Rastelli- tube graft right ventricle and pulmonary artery
Senning- switching of the atrium in transposition of the great vessels by inflow inversion.
This diagram depicts the surfaces and margins of the heart as viewed anteriorly with the patient supine on the operating table (left), and as viewed from the cardiac apex (right).
Cardiac hypertrophy is the compensatory response of the myocardium to increased work Myocardial hyperfunction induces an increase in the overall mass and size of the heart that reflects increased size of myocytes through addition of contractile elements (sarcomeres) and mitochondria.
Cardiac myocyte diameters, normally approximately 15 µm, can increase to 25 µm or more in hypertrophy.
Since cardiac myocytes are terminally differentiated cells that cannot divide, augmentation of myocyte number (hyperplasia) does not occur in the adult heart.
Since the vasculature does not proliferate commensurate with increased cardiac mass, hypertrophied myocardium is usually relatively deficient in blood vessels. Moreover, myocardial fibrous tissue may be increased.
Pressure overloaded ventricles (e.g., resulting from hypertension or aortic stenosis) develop concentric hypertrophy with an increased ventricular mass and ratio of wall thickness to cavity radius, without appreciable dilatation. In contrast, volume overloaded ventricles (e.g., resulting from chronic aortic or mitral regurgitation) develop hypertrophy with chamber dilatation in which both ventricular radius and wall mass are increased.
However, in vol
ume hypertrophy, dilation masks the degree of hypertrophy, and wall thickness frequently is near normal.
Concentric hypertrophy is accomplished predominantly by augmentation of cell width (parallel addition of sarcomeres); in contrast, dilatation stimulates augmentation of both cell width and length (parallel and series addition of sarcomeres).
However, hypertrophy (with or without chamber dilatation), decreases myocardial compliance, may hinder diastolic filling, and often is associated with depressed myocardial contractility.
Thus, the mechanical changes described previously initially enhance function and are thereby adaptive but may ultimately become deleterious. In situations where there is obvious death of myocytes (e.g., myocardial infarction), the remaining, non-infarcted regions of myocardium not only hypertrophy (called compensatory hypertrophy) but also may be overwhelmed by mechanical disadvantage. In contrast, the chamber wall is affected globally by the increased chamber pressure of hypertension, the increased pressure or volume work load of valvular heart disease, and in dilated cardiomyopathy.
In hypertrophied hearts molecular changes that initially mediate enhanced function may subsequently contribute to the development of heart failure.
Hemodynamic overload alters myocardial gene expression, leading to re-expression of a pattern of protein synthesis that has features that occur during both mitosis of other types of cells capable of normal proliferation and fetal cardiac development.
Proteins comprising contractile elements and those involved in excitation-contraction coupling and energy utilization are altered quantitatively or through production of different isoforms; such variant proteins may be less functional than the normal.
Hypertrophied and/or failing myocardium may have additional abnormalities that include reduced adrenergic drive, decreased calcium availability, impaired mitochondrial function, and microcirculatory spasm.
Nevertheless, neither the mechanisms by which mechanical load induces cardiac cellular hypertrophy nor those that mediate the progression from hypertrophy to cardiac failure are understood in detail.
In sum, cardiac hypertrophy comprises a tenuous balance between adaptive characteristics (including new sarco-meres) and potentially deleterious structural, functional, and biochemical/molecular alterations (including enlarged muscle mass with enhanced metabolic requirements,
synthesis of abnormal proteins,
decreased capillary/myocyte ratio,
and impaired contractile mechanisms).
Thus, cardiac hypertrophy can evolve to cardiac failure. In addition, left ventricular hypertrophy is an independent risk factor for cardiac mortality and morbidity, especially for sudden death.
Left ventricular hypertrophy induced by systemic hypertension is reversible in many cases
However, it is uncertain to what extent hypertrophy owing to other stimuli is capable of resolution. Indeed, the hemodynamic adjustment that occurs following cardiac valve surgery is not always accompanied by reversal of the myocardial changes secondary to the valvular disorder, and progressive cardiac failure may ensue despite valve replacement or repair
. Even in well-compensated ventricles postoperatively, regression of hypertrophy often is incomplete, and some degree of hypertrophy may persist for decades.
In addition, the increased cardiac muscle mass in many patients requiring cardiac surgery, with its attendant global ischemia, renders intraoperative myocardial preservation difficult to achieve and the heart thereby particularly susceptible to ischemic damage.
Atherosclerosis is a chronic, progressive, multifocal disease of the vessel wall intima whose characteristic lesion is the atheroma or plaque. The key processes, intimal thickening (mediated predominantly by smooth muscle cell proliferation), and lipid accumulation (mediated primarily by monocyte phagocytosis), primarily affect the large elastic arteries and large and medium-sized muscular arteries of the systemic circulation, particularly at points of branches, sharp curvatures, and bifurcations. Importantly, and not entirely understood, coronary atherosclerosis generally is limited to the epicardial vessels and does not involve their intramural branches. Moreover, venous bypass grafts interposed within branches of the arterial system also can develop intimal thickening and ultimately atherosclerotic obstructions, yet, for inexplicable reasons, some arteries are consistently spared (such as the internal thoracic [mammary] artery). Although isolated plaques in the aorta are virtually always eccentric in location (that is, involving only a portion of the arterial circumference), atheromas in the coronary arteries may be either concentric (25–30 percent) or eccentric (70–75 percent). The plaque-free segment may comprise a substantial fraction of the vessel wall. With early lesions, the arterial lumen remains circular in cross section and often is essentially the same size as originally, despite plaque formation, in a process often called vascular remodeling. High-grade but slowly developing occlusions probably stimulate collateral vessels over time that may protect against distal myocardial ischemia and infarction.
The contemporary understanding of the pathogenesis of atherosclerosis envisions an initial interaction of the cells of the blood vessel wall (especially smooth muscle cells and endothelial cells, circulating blood cells (platelets and monocytes) and plasma lipoproteins
] In the most recently modified response-to-injury hypothesis, the initiating event is a subtle, non-denuding injury to endothelial cells (owing to the effects of chronic hypercholesterolemia, homocystinemia, chemicals in cigarette smoke, viruses, localized hemodynamic forces, systemic hypertension, hyperglycemia or the local effects of cytokines)
The endothelial cell injury (termed endothelial dysfunction) is characterized by altered metabolism (e.g., depressed production of vasorelaxants such as nitric oxide [NO]), alteration or loss of the selective permeability barrier with entry of plasma lipoproteins into the vessel wall, induction of a thrombogenic surface on endothelial cells (largely by endothelial cell membrane expression of tissue factor), and/or adherence of inflammatory cells or platelets, mediated by injury-induced surface expression of molecules that increase endothelial cell-monocyte adhesion.
A complex series of events ensues, including
(1) adherence of blood monocytes to endothelial cells and their emigration into the subendothelial space;
(2) transformation of blood monocytes into tissue macrophages;
(3) smooth muscle cell migration from the media into the intima;
(4) smooth muscle cell proliferation within the intima
(5) secretion of large amounts of collagen and other extracellular matrix components by intimal smooth muscle cells;
(6) lipid accumulation, both intracellularly (primarily in macrophages, but also in smooth muscle cells [ultimately producing foam cells]) and extracellularly;
(7) oxidative modification of lipoproteins that generate potent biological stimuli (neoantigens, chemoattractants, cytotoxins) within the vessel wall;
(8) cell death with release of intracellular lipids (mostly cholesterol esters), and often;
(9) calcification; and
(10) a chronic inflammatory reaction (that includes lymphocyte/macrophage infiltration, and neovascularization).
In essence, atherosclerosis is an inflammatory-and-healing response of the arterial wall to various stimuli, an initially protective and adaptive response that in excess becomes a disease process.
Atherosclerotic plaques have three major components:
(1) cells, including vascular smooth muscle cells and blood-derived monocytes/macrophages;
(2) connective tissue fibers (e.g., collagen) and amorphous extracellular matrix, both predominantly synthesized by smooth muscle cells; and
(3) lipids imbibed from blood, largely low density lipoprotein (LDL) cholesterol and its esters. In the early stages, lesions remain covered by endothelial cells. Mature atheromatous plaque is composed of a core (containing lipid and cholesterol crystals, macrophages, foam cells, necrotic cell debris, and plasma proteins and degenerating blood elements), separated from the lumen by a layer of fibrous tissue (fibrous cap). To a great extent, the integrity of the fibrous cap determines plaque stability.
The composition of atheromas can vary considerably, among individuals, among arteries in the same individual, or among regions of one artery.
The clinical effects of advanced atherosclerotic plaques in most medium-sized arteries, including the coronary arteries, are either owing to their encroachment of the lumen, leading to progressive stenosis, or acute plaque disruption with thrombosis
In contrast, in larger vessels such as the aorta, ulcerated atheromatous plaques can
(1) release atheroemboli from soft plaques;
(2) become covered with mural thrombus that may dislodge to yield peripheral thromboemboli; or
(3) impinge on the media with resultant tissue atrophy or destruction that may cause vascular dilation, aneurysm formation, and potential rupture.
The natural history of atheromatous plaque and the efficacy and safety of interventional therapies likely depend on relative plaque composition and the spatial distribution of the constituents.
The distinction between soft atheromas, consisting primarily of necrotic debris and therefore potentially moldable, versus hard, fibrocalcific, rigid plaques may be important clinically, because plaque mechanical properties can determine the propensity to complications as well as influence the success rate of interventions such as balloon angioplasty
An individual plaque region can be characterized as soft or hard by intravascular ultrasound, and calcification, portending hard plaque, can be detected noninvasively by electron beam computed tomography.
However, despite group epidemiological correlations of outcome with luminal stenosis and plaque calcium, neither predict plaque rupture or subsequent thrombosis in an individual patient.
Ischemic Myocardial Injury
Cardiac ischemia is typified by an imbalance between the supply and demand of tissue for blood. It is caused most commonly either by decreased perfusion (e.g., vascular obstruction or narrowing caused by atherosclerosis, thrombosis, embolism, or spasm), global hypotension (such as occurs in shock or during cardiopulmonary bypass), or vascular compression; or by increased cardiac demand for blood (such as occurs in exercise, tachycardia, hyperthyroidism, or ventricular hypertrophy/or dilatation). Its consequences depend on severity and duration, and on the pre-existing adaptive and nutritional/metabolic state of the affected cells and tissues. Ischemic injury is potentiated by anemia, hypoxemia, or cardiac failure and protracted onset may permit development of collaterals and metabolic adjustments. Moreover, as discussed above, hypertrophy increases vulnerability to myocardial ischemic injury through the combined effects of increased numbers of cells requiring perfusion, coupled with relatively decreased vascularity.
PROGRESSION OF DAMAGE
Intracellular changes following the onset of myocardial ischemia are sequential, complex, and difficult to recognize early
Cardiac myocyte ischemia induces anaerobic glycolysis within seconds, leading to both inadequate production of high-energy phosphates (e.g., creatine phosphate and ATP) and the accumulation of potentially noxious breakdown products (e.g., lactic acid), thereby causing intracellular acidosis.
Myocardial function is exquisitely sensitive to these cellular biochemical consequences of severe ischemia and rapidly becomes deranged; a striking contractility defect is evident within 60 seconds.
Within a few minutes, characteristic ultrastructural changes develop, including glycogen depletion, and cell and mitochondrial swelling.
Nevertheless, these early changes are sublethal and cell death is not immediate. Ischemic changes in an individual cell are potentially reversible if the duration of ischemic injury is short and perfusion is restored prior to the onset of irreversible lesions. Irreversible (lethal) injury of cardiac myocytes (associated with structural defects in the sarcolemmal membrane) is evident at least focally only after 20–40 minutes of severe ischemia (when regional blood flow is 10 percent of normal or less). When ischemic injury is of sufficient severity and duration, groups of involved cells die, and myocardial infarction results.
Within the region made vulnerable by loss of perfusion (so-called area at risk), not all cells are equally injured
A gradient of ischemia exists across the myocardium; the most affected regions are the subendocardium and papillary muscles. Thus, following the abrupt occlusion of a coronary artery by thrombus, the most severely ischemic myocytes (and the first to become necrotic) are in the center of the perfusion defect, near the endocardium. However, the myocytes immediately beneath the endocardium (to a depth of approximately 100 µm) usually are effectively perfused by the well-oxygenated blood in the left ventricular chamber. As uninterrupted ischemia progresses, there is a wave-front of cell death (called coagulation necrosis) outward from the mid-subendocardial region toward and eventually encompassing the lateral borders and less ischemic subepicardial and peripheral regions.
The final transmural extent of an infarct is generally established within 6–12 hours. At autopsy, the presence of a necrotic region may be indicated as a staining defect with triphenyl tetrazolium chloride (TTC), a dye that turns myocardium a brick-red color on reaction with intact myocardial dehydrogenases (indicating viability), as early as 2–3 hours following onset of infarction.
During cardiopulmonary bypass or organ procurement for transplantation, susceptibility to ischemic injury is global.
Existing hypertrophy and coronary obstructions tend to enhance injury, whereas decreased tissue temperature and cardioplegic arrest slow chemical reactions and thereby protect myocytes from progressive ischemic damage. Moreover, when the heart's chambers are not filled with oxygenated blood (such as in donor heart transport for transplantation), the immediately subendocardial myocytes, normally perfused from the lumen and protected from acute ischemic injury, are also vulnerable to ischemic injury.
Myocardial ischemia also contributes to the induction of arrhythmias.]
Sudden death usually is caused by ventricular tachycardia/fibrillation caused by myocardial irritability induced by ischemia or infarction. This conclusion derives from autopsy studies of sudden death victims and clinical studies of resuscitated survivors that show that only a minority develops acute myocardial infarction.
Thus, ischemia caused by severe chronic coronary arterial stenosis, and in many cases, acute plaque change with less than occlusive thrombus, and possibly emboli, presumably leads directly to lethal arrhythmias.
The histologic changes of myocardial necrosis that occurred less than approximately 6 hours prior to death generally are not visible. Inflammatory exudation, initially with polymorphonuclear leukocytes, begins following approximately 6–12 hours and the stereotyped sequence of tissue changes ensues. The inflammatory reaction that eventuates in necrotic tissue removal by macrophages (in days) is followed by a fibroblastic reparative response accompanied by neovascularization (granulation tissue) beginning (1 week or more subsequent to tissue injury) at the margins of preserved tissue. Overall, the repair sequence following an infarct is similar to that which follows tissue injury of diverse causes and at various non-cardiac anatomic sites. Since cardiac muscle cells are incapable of regeneration, the infarcted tissue ultimately is replaced by scar; maturation usually is complete in approximately 6 weeks. Healing of myocardial ischemic injury may be slowed by anti-inflammatory agents administered following myocardial infarction or as a component of immunosuppressive therapy following transplantation.
Resolution may also be slowed in otherwise debilitated or malnourished patients. Sublethal but chronic ischemic injury may be revealed by myocyte vacuolization, usually most prevalent in the subendocardium.
The progression of myocardial ischemic injury can be modified by restoration of blood flow to jeopardized myocardium (reperfusion). Reperfusion salvages reversibly injured myocytes; reperfusion occurring early before the onset of irreversibility (less than 20 minutes in the most severely ischemic regions and less than a few hours overall), may substantially limit infarct size or prevent cell death altogether. In contrast, later reperfusion does not prevent infarction entirely, but myocytes that are only reversibly injured at the time of reflow may be salvaged. The potential for recovery decreases with increasing severity and duration of ischemia. Nevertheless, late reperfusion, following the interval at which myocyte salvage continues to be possible, may also lead to functional benefits, by mechanisms that are yet poorly understood.
. Hemorrhage may be seen grossly and microscopically
Moreover, reperfusion has structural and biochemical effects on cells that were already lethally injured at the time of reflow, including marked cell swelling, massive cellular Ca 2+ entry from the plasma, and myocyte contraction bands (representing coalescence of multiple hypercontracted sarcomeres, often with calcification visible by light microscopy or transmission electron microscopy) (see
Areas of necrosis with contraction bands (often called contraction band necrosis) frequently are seen in hearts of patients with infarcts treated early with thrombolytic therapy, and in those following cardiac surgery. In widespread and severe cases of such damage, the left ventricular myocardium may undergo a massive tetanic contraction to a small, hard mass that comprises the “stone heart syndrome.”
Restoration of systemic pressure to an artery supplying an intact and patent microvasculature generally will restore adequate blood flow. However, since microvascular damage accompanies severe, prolonged ischemia, achievement of arterial pressure to an artery supplying a damaged capillary bed may have additional effects that are deleterious:
(1) hemorrhage, owing to vascular wall incompetence; or
(2) impaired local return of myocardial blood flow (no-reflow), owing to occlusion of capillaries by extravascular compression, cardiac rigor, endothelial swelling, or platelet or inflammatory cell aggregates.
Moreover, there is evidence that the process of reperfusion may damage some of the myocytes that were not already dead at the time at which reflow occurred, often called reperfusion injury (a term that is frequently, and undesirably, used to describe the constellation of morphologic changes described in the preceding that occur on reperfusion of ischemic myocardium).Reperfusion injury is mediated primarily by toxic oxygen species (such as free radicals) that are overproduced by myocytes or polymorphonuclear leukocytes upon restoration of oxygen supply to the tissues. Complement activation also may contribute. Consequently, injury may be ameliorated by free radical scavengers such as superoxide dismutase and catalase, inhibitors of polymorphonuclear leukocyte endothelial cell adhesion, or drugs that regulate complement.
Although reperfusion of reversibly salvaged myocytes usually prevents their subsequent necrosis, metabolic and functional recovery are not instantaneous, and contractile dysfunction may continue for hours to several days following brief periods of ischemia.The prolonged biochemical and functional abnormalities of reversibly injured cells comprise a state of post-ischemic myocardial dysfunction, often called myocardial stunning, which may have important clinical implications.
For example, persistent but ultimately recoverable contractile abnormalities are encountered after thrombolysis or cardiopulmonary bypass. It is difficult to quantitate the impact of stunning on the function of reperfused hearts containing areas of necrosis. However, potentially recoverable but stunned myocardium may contribute to reversible cardiac failure in humans with acute infarction (with or without thrombolysis), postoperatively, or subsequent to cardiac arrest, thereby providing the pathophysiologic rationale for the use of cardiac assist devices in some instances.
Regrettably, histological markers for stunned myocardium are not available.
Hibernating is a term used to describe viable regions of myocardium with impaired function in the setting of chronically reduced coronary blood flow. Contractile function of hibernating myocardium should improve if blood flow returns toward normal or if oxygen demand is reduced.
Myocardial hibernation is characterized by:
(1) persistent wall motion abnormality (diagnosed by ventriculography or echocardiography);
(2) low myocardial blood flow (reflected by a defect in perfusion by thallium scanning or positron-emission tomography [PET]);
(3) evidence of viability of at least some of the affected areas (demonstrated by PET or stimulation of contraction by inotropic agents); and
(4) functional improvement following return of normal coronary blood flow. Indeed, correction of this abnormality is likely responsible for the reversal of long-standing defects in ventricular wall motion that may be observed following coronary bypass graft surgery or angioplasty.
Interestingly, adaptation to short-term transient ischemia may induce tolerance against subsequent, more severe ischemic insults (ischemic preconditioning).Typically, a short (5-min) period of cardiac ischemia followed by reperfusion is capable only a short time later of protecting the affected myocardium against injury from a much longer period of subsequent ischemia. The mechanism of this protection is uncertain, but stimulation of adenosine receptors when adenosine is released during ischemia and enhanced expression of heat-shock proteins, which makes the heart more resistant to prolonged ischemia, have been suggested.
VASCULAR GRAFT HEALING
The healing of fabric prostheses or components within the cardiovascular system can yield exuberant fibrous tissue at the anastomosis as an overactive but physiologic repair response Synthetic and biological vascular grafts often fail because of generalized or anastomotic narrowing mediated by connective tissue proliferation in the intima, and heart valve prostheses can have excessive pannus that occludes the orifice . Intimal hyperplasia results primarily from smooth muscle cell migration, proliferation, and extracellular matrix elaboration following and possibly mediated by acute or ongoing endothelial cell injury.
Contributing factors include
(1) surface thrombogenesis;
(2) delayed or incomplete endothelialization of the fabric;
(3) disturbed flow across the anastomosis; and
(4) mechanical factors at the junction of implant and host tissues.
Tissue lining a vascular graft or coating a heart valve sewing cuff has two major sources: overgrowth from the host vessel across anastomotic sites, and tissue ingrowth through fabric interstices.
A potential third mechanism, deposition of functional endothelial cell from the circulating blood, is non-existent or ineffective. In a graft with interstices large enough to permit ingrowth of fibrovascular elements, endothelial cells can arise from capillaries extending from outside to inside the graft and migrate to the luminal surface at a large distance from the anastomosis. However, since most clinical vascular grafts are impervious, in order to obviate hemorrhage, existing grafts (and other fabrics used as cardiovascular implants) heal primarily by ingrowth of endothelium and smooth muscle cells from the cut edges of the adjacent artery or other tissue.
Humans have a limited ability to spontaneously endothelialize cardiovascular prostheses, and full endothelialization of clinical grafts (yielding an intact neointima) usually does not occur.
Luminal coverage develops relatively slowly and incompletely. For uncertain reasons, endothelial cell coverage generally is restricted to a zone near an anastomosis, typically 10–15 mm, thereby allowing healing of intracardiac fabric patches and prosthetic valve sewing rings, but not long vascular grafts. Thus, except adjacent to an anastomosis, a compacted platelet-fibrin aggregate (pseudointima) comprises the inner lining of clinical fabric grafts, even after long-term implantation. Because firm adherence of such linings to the underlying graft may be impossible, dislodgement of the lining and formation of a flap-valve can occur and cause acute obstruction.] Since therapeutic endothelial seeding of vascular grafts has yielded only modest benefit, attempts to seed genetically modified endothelial cells and block smooth muscle cell proliferation are ongoing.
Infection, occurring in as many as 5–10 percent of patients with implanted prosthetic devices, is a frequent source of morbidity and mortality. Because medical devices usually are coated with platelet-fibrin thrombus and are remote from capillary vessels, associated infections often are difficult to treat with antibiotics and are resistant to host defenses. Consequently, such infections generally persist until the devices are removed.
Early implant infections (less than approximately 1–2 months postoperatively) most likely result from intraoperative contamination or early postoperative wound infection, whereas late infections generally occur by a hematogenous route, and can be initiated by bacteremia induced by therapeutic dental or genitourinary procedures.] Antibiotics given prophylactically at device implantation and shortly before subsequent diagnostic and therapeutic procedures may protect against implant infection. Infections associated with foreign bodies are characterized microbiologically by a high prevalence of coagulase-negative staphylococci, including Staphylococcus epidermidis , an organism with low virulence, and an infrequent cause of non-prosthesis-associated deep infections, as well as other more virulent staphylococci, especially S. aureus , and less virulent strains of streptococci.
The presence of a foreign body potentiates infection in several ways.
] Micro-organisms may inadvertently be introduced by device contamination, provided access to deeper tissue by damage to natural barriers against infection during implantation or subsequent device function, and permitted to survive adjacent to the implant. Moreover, through damaged vasculature, an implanted foreign body could limit phagocyte migration into infected tissue or interfere with inflammatory cell phagocytic mechanisms, by release of soluble implant components or surface-mediated interactions.
Despite the large numbers of implants used clinically over an extended duration, neoplasms occurring at the site of implanted cardiovascular and other medical devices are exceedingly rare.
ISCHEMIC HEART DISEASE
The dominant influence in the causation of the ischemic heart disease syndromes is diminished coronary perfusion relative to myocardial demand, owing largely to a complex dynamic interaction among fixed atherosclerotic narrowing of the epicardial coronary arteries, intraluminal thrombosis overlying a ruptured or fissured atherosclerotic plaque, platelet aggregation, and vasospasm.Increased myocardial demand or reduced oxygen carrying capacity of the blood may be contributory.
ROLE OF FIXED CORONARY OBSTRUCTIONS
Under normal conditions, coronary arterial flow provides adequate myocardial perfusion at rest, and compensatory vasodilation provides flow reserve that is generally more than sufficient to accommodate the increased myocardial metabolic demands during vigorous exertion. When the luminal cross-sectional area is decreased by 75 percent or more, coronary blood flow generally becomes limited with exertion. With 90 percent or greater reduction, coronary flow may be inadequate at rest. Over 90 percent of patients with ischemic heart disease have advanced stenosing coronary atherosclerosis (fixed obstructions). Among these, most have one or more lesions causing at least 75 percent reduction of the cross-sectional area in one or more of the major epicardial arteries. Thus, the clinical effects of advanced atherosclerotic plaques in most medium-sized arteries, including the coronary arteries, are in part owing to their encroachment on the lumen, leading to stenosis.
However, the onset and prognosis of ischemic heart disease and other complications of atherosclerosis are not well predicted by the arteriographically determined extent and severity of fixed anatomic disease. Considerable evidence exists that dynamic vascular changes are largely responsible for the conversion of chronic stable angina or an asymptomatic state to acute ischemic heart disease (unstable angina, myocardial infarction, or sudden coronary death). Acute coronary occlusion can be caused by vasospasm, intravascular plugging by blood constituents, disruption of or hemorrhage into plaque, platelet aggregation, thrombosis, embolization, or a combination of these events.
ROLE OF ACUTE PLAQUE CHANGE
The acute coronary syndromes—unstable angina, acute myocardial infarction, and sudden ischemic death—usually are precipitated by atherosclerotic plaque disruption with hemorrhage, fissuring, and/or ulceration.
Angiographically, disrupted plaque appears substantially different from that of chronic stable disease. Microscopically, injury spans a broad morphologic range, from minimal surface erosions, to lacerations that extend deep within the plaque. Regardless of the extent of injury, however, the result is flow disruption and exposure of the luminal blood to a thrombogenic surface (collagen or necrotic debris), thereby setting the stage for mural or total thrombosis
Pathologic and clinical studies also show that plaques that undergo abrupt disruption leading to acute ischemic heart disease often are those that previously produced only mild to moderate luminal stenosis.
Plaque fissures without substantial thrombosis also are found in occasional patients without acute coronary syndromes. In a group of patients who died of non-cardiac disease, plaque fissures without thrombosis were found in 9 percent of patients without hypertension or diabetes and 17 percent of those with these atheroma-related diseases.
Potential outcomes for unstable lesions include healing at the site of plaque erosion, atheroembolization, nonocclusive thrombosis, thromboembolization, organization of mural thrombus (plaque progression), acute thrombotic occlusion, and organization of the occlusive mass, with varying degrees of recanalization. Among these outcomes, the most common fate is plaque progression, owing either to resealing of the plaque fissure or to organization of a nonocclusive mural thrombus. Indeed, asymptomatic plaque rupture and its subsequent healing is likely an important mechanism of stenosis progression.
The events that trigger abrupt changes in plaque configuration and superimposed thrombosis are poorly understood.
Influences both extrinsic and intrinsic to the plaque likely are important. Surface erosions, fissures, and ruptures are more likely to involve soft and eccentric plaques than hard and concentric lesions, those that contain large areas of foam cells, and fibrous caps that are thin or contain clusters of inflammatory cells that can produce tissue metalloproteinases that degrade collagen. Fissures and ruptures most frequently occur at the junction of the fibrous cap with the adjacent normal arterial wall (plaque-free segment), a location associated with high circumferential stress.
Vasospasm, tachycardia, hypercholesterolemia, or intraplaque hemorrhage are likely contributors, as are stresses produced by abnormal blood flow and/or coronary intramural pressure or tone in areas of stenosis.
Interestingly, there is a pronounced circadian periodicity for the time of onset of acute myocardial infarction and other acute coronary syndromes, with a peak incidence between 9–11 a.m., concurrent with a surge in blood pressure and immediately following heightened platelet reactivity.
VALVULAR HEART DISEASE
Normal valve function requires integrity and coordinated interactions among all components in the system. For the mitral valve, these elements comprise the so-called mitral apparatus: including leaflets, annulus, chordae tendineae (tendinous cords), papillary muscles, and the atrial and ventricular myocardium. For the aortic valve, they comprise the cusps and their supporting structures in the aortic root.
Structure-Function Correlations in Normal Valves
Of the two leaflets of the mitral valve, the anterior (also called septal, or aortic) leaflet is roughly triangular and deep, with the base inserting on one-third of the annulus. The posterior (also called mural, or ventricular) leaflet, although less deep, is attached to about two-thirds of the annulus, and typically has a scalloped appearance. The mitral leaflets have a combined area approximately twice that of the annulus; they meet during systole with apposition to approximately 50 percent of the depth of the posterior leaflet and 30 percent that of the anterior leaflet. Each leaflet receives chordae tendineae from both the anterior and posterior papillary muscles.
The mitral valve orifice is D-shaped, with the flat anteromedial portion comprising the attachment of the anterior mitral leaflet in the subaortic region. This part of the annulus is fibrous and non-contractile; the remainder is muscular, and contracts during systole, thereby reducing the area of the orifice, but asymmetrically. The edges of the mitral leaflets are held in or below the plane of the orifice by the submitral components of the mitral apparatus. The orifice of the tricuspid valve is larger and less distinct than that of the mitral; its three leaflets (anterior, posterior, and septal) are larger and thinner than those of the mitral valve. The mitral and tricuspid valves comprise the atrioventricular valves.
The functional elements of the aortic valve are cusps, annular fibrous tissue, and aortic root, including the dilated pockets of aortic root behind the valve cusps called the sinuses of Valsalva, from which the right and left coronary arteries arise from individual orifices. At the midpoint of the free edge of each cusp is a fibrous nodule (nodule of Arantius). A thin, crescent-shaped portion of the cusp on either side of the nodule, termed the lunula, defines the surface of apposition of the cusps when the valve is closed (approximately 40 percent of the cuspal area). Fenestrations (holes) near the free edges and within the lunula commonly occur as a developmental or degenerative abnormality. They generally are small (less than 2 mm diameter) and have no functional significance, since the lunular tissue does not contribute to separating aortic from ventricular blood during diastole. In contrast, fenestrations below the lunula are not only associated with functional incompetence but also suggest previous or active infection. The pulmonic valve cusps and surrounding tissues have architectural similarity to but are lighter than that of the corresponding aortic components, and lack coronary arterial origins. The aortic and pulmonic valves are called the semilunar or arterial valves.
All cardiac valves essentially have the same microscopically inhomogeneous architecture. The prototypical aortic valve cusps have four well-defined tissue layers, observable histologicall
(1) the thin ventricular layer (or ventricularis), facing the left ventricular chamber, is comprised predominantly of collagenous fibers with radially aligned elastic fibers;
(2) the centrally located spongy layer (or spongiosa), is composed of loosely arranged collagen and abundant proteoglycans;
(3) the thick fibrous layer (or fibrosa), is composed predominantly of circumferentially aligned, densely packed collagen fibers, largely arranged parallel to the cuspal free edge; and
(4) the thin aortic layer (or aorticus) consists of a few collagen fibers along the aortic surface of the cusps.
The fibrosa provides structural integrity and mechanical stability. The spongiosa, in contrast, has negligible structural strength, but appears to lubricate relative movement between the two fibrous layers and absorb shock during closure. The rich elastin of the ventricularis enables the cusps to have minimal surface area when the valve is open but stretch during diastolic back pressure to form a large coaptation area. Endothelial cells line the surfaces of the valves, and the predominant deep cells are fibroblasts. Normal human aortic and pulmonary valve cusps are nearly avascular; they are sufficiently thin to be perfused from the surrounding blood. In contrast, the mitral and tricuspid leaflets contain a few capillaries in their most basal thirds.
The orientation of architectural elements is nonrandom in the plane of the cusp, yielding unequal mechanical properties of the valve cusps in different directions (anisotropic behavior). Consequently, although the pressure differential across the closed aortic valve during the diastolic phase induces a large load on the cusps, the geometry of the whole valve and the fibrous network within the cusps effectively transfers the resultant stresses to the annulus and aortic wall. With specializations that include crimp of collagen fibers along their length and bundles of collagen in the fibrous layer, oriented largely toward commissures and that produce grossly visible corrugations, cusps are extremely soft and pliable when unloaded, but taut and stiff during the closed phase. This minimizes sagging of the cusp centers, preserving maximum coaptation, and prevents regurgitation. For the mitral valve, the subvalvular apparatus (including tendinous cords and papillary muscles) serves a similar function.
During valve closure, cusps and leaflets do not touch along only their free edges like closing double doors. Rather, adjacent cusps coapt with relatively large areas of surface-to-surface contact. This involves the lunular surfaces of semilunar valve cusps and roughly the apical third of atrioventricular valve leaflets. Thus, normal cusp and leaflet areas are substantially greater than that needed to close the valve orifice.
Etiology and Pathologic Anatomy
Cardiac valve operations usually are undertaken for dysfunction caused by calcification, fibrosis, fusion retraction, perforation, dilatation, or congenital malformations.] Valvular stenosis almost always both is caused by a primary cuspal abnormality and is a chronic process (except for massive vegetations). Valvular insufficiency may result from either intrinsic disease of the valve cusps or damage to or distortion of the supporting structures (e.g., the aorta, mitral annulus, chordae tendineae, papillary muscles, and ventricular free wall) without primary cuspal pathology. Both stenosis and insufficiency can coexist in a single valve, usually with one process predominating. Regurgitation may appear either acutely, as with rupture of cords, or chronically, as with leaflet scarring and retraction.
DEGENERATIVE CALCIFIC AORTIC VALVE STENOSIS
The most frequent valvular abnormality requiring surgery, acquired aortic stenosis (AS) usually is the consequence of calcification of aortic valves with previously normal anatomy in aged individuals or calcification induced by “wear and tear” of congenitally bicuspid valves ] Stenotic, previously normal valves (with three cusps) come to clinical attention primarily in the eighth to ninth decades of life. Pre-existing bicuspid valves with superimposed age-related degenerative calcification generally become symptomatic earlier (usually sixth to seventh decades).
Nonrheumatic, calcific aortic stenosis (involving valves with either two or three cusps) is characterized by heaped-up, calcified masses initiated in the cuspal fibrosa at the points of maximal cusp flexion (the margins of attachment); they ultimately ulcerate and protrude distally into the sinuses of Valsalva, inhibiting cuspal opening. Distinct from the cellular proliferation and lipid deposition that typify atherosclerosis, the dystrophic calcification process does not involve the free cuspal edges and largely preserves the microscopic layered architecture. Aortic valve sclerosis comprises an earlier, hemodynamically less significant, stage of the calcification process. In contrast to rheumatic aortic stenosis, appreciable commissural fusion is absent and the mitral valve generally is free of rheumatic changes.
Aortic valves are congenitally bicuspid in approximately 1–2 percent of the population. Most frequently, the two cusps are of unequal size, with the larger (conjoined) cusp having a midline raphe, representing an incomplete separation or congenital fusion of two cusps. Less frequently, the cusps are of equal size, and a raphal ridge may or may not be identifiable. When a raphe is present, the most commonly fused cusps are the right and left, accounting for about 75 percent of cases. Neither stenotic nor symptomatic at birth or throughout early life, bicuspid valves are predisposed to accelerated calcification, especially along the raphe. Less often, they may become incompetent, be complicated by infective endocarditis, or be associated with acute aortic dissection.
Aortic stenosis leads to a gradually increasing pressure gradient across the valve, which may reach 75–100 mg Hg in severe cases, with a left ventricular pressure of 200 mg Hg or more; cardiac output is maintained by the development of concentric (pressure overload) left ventricular hypertrophy. The onset of symptoms (particularly angina, syncope, or heart failure) in aortic stenosis heralds the exhaustion of compensatory cardiac hyperfunction, and therefore carries a poor prognosis if not treated by aortic valve replacement (>50 percent mortality within 3 years). If cardiac output is low, as may occur in heart failure or in the elderly, then neither the gradient nor the resultant murmur may appear significant. In this setting, critical aortic stenosis can be overlooked clinically.
MITRAL ANNULAR CALCIFICATION
Degenerative calcific deposits also can develop in the ring (annulus) of the mitral valve of elderly individuals, especially women, and may accompany mitral valve myxomatous degeneration (see the following). Although generally asymptomatic, the calcific nodules may lead to regurgitation by interference with systolic contraction of the mitral valve ring or, very rarely, stenosis by impairing opening of the mitral leaflets. Occasionally, the calcium deposits may penetrate sufficiently deeply to impinge on the atrioventricular conduction system and produce arrhythmias (and rarely sudden death). Patients with mitral annular calcification have an increased risk of stroke, and the calcific nodules can be the nidus for thrombotic deposits or infective endocarditis
When valvular calcific deposits extend as nodules below the leaflets, leaflets can become immobilized, producing either stenosis or regurgitation. As a general rule, for both aortic and mitral valves, the more heavily calcified a valve becomes, the less likely it is to become infected.
MYXOMATOUS DEGENERATION OF THE MITRAL VALVE (MITRAL VALVE PROLAPSE)
Myxomatous mitral valve disease is the most frequent cause of chronic, pure, isolated mitral regurgitation. Usually, one or both mitral leaflets are enlarged, redundant or “floppy” and prolapse, or balloon back into the left atrium, during ventricular systole
The three essential anatomic changes in mitral valve prolapse are
(1) interchordal ballooning (hooding) of the mitral leaflets or portions thereof (most frequently the posterior half of both leaflets), with or without elongated, thinned, or ruptured cords;
(2) rubbery diffuse leaflet thickening that hinders adequate coaptation and interdigitation of leaflet tissue during valve closure; and
(3) substantial annular dilation, with diameters and circumferences usually exceeding 3.5 and 11.0 cm, respectively
Pathological mitral annular enlargement is usually confined to the posterior leaflet, since the anterior leaflet is firmly anchored by the fibrous tissue at the aortic valve end and is far less distensible. Histologically, the essential change is attenuation or focal disruption of the fibrous layer of the valve, on which the structural integrity of the leaflet depends. This is accompanied by focal or diffuse thickening of the spongy layer. Deposited amorphous extracellular matrix gives the tissue an edematous, blue appearance on routine hematoxylin and eosin staining, an appearance called “myxomatous” by pathologists. Concomitant involvement of the tricuspid valve is present in 20–40 percent of cases, and the aortic and pulmonic valves also may be affected. Myxomatous tricuspid valve may be associated with pulmonary disease.
Secondary changes may occur, including:
(1) focal pad-like fibrous thickening along both surfaces of the valve leaflets;
(2) linear thickening of the subjacent mural endocardium of the left ventricle as a consequence of friction-induced injury by cordal “hamstringing” of the prolapsing leaflets;
(3) thrombi on the atrial surfaces of the leaflets, particularly in the recesses behind the ballooned leaflet segments;
(4) calcification along the base of the posterior mitral leaflet; and
(5) chordal thickening and fusion (resembling post-rheumatic disease). In a presently largely unidentifiable subgroup of affected individuals, mitral valve prolapse is associated with infective endocarditis, stroke or other manifestation of thromboembolism, progressive congestive heart failure, or sudden death.
The pathogenesis is uncertain, but this valvular abnormality is one common feature of Marfan's syndrome and occasionally occurs with other hereditary disorders of connective tissues, suggesting an analogous but localized connective tissue defect.
Distinction should be made between the clinical diagnosis of mitral valve prolapse in young people and the pathologic diagnosis of a myxomatous (or floppy) mitral valve in mature individuals. The former generally is associated with a competent and minimally distorted valve and occurs in women about 1.5 times as frequently as in men. The latter, in contrast, usually is severely regurgitant and structurally deformed and affects men more often than women. More important, probably 95 percent of young people with clinically detected mitral valve prolapse will never develop severely distorted and incompetent mitral valves as they grow older.
RHEUMATIC HEART DISEASE
Rheumatic fever is an acute, often recurrent, inflammatory disease that generally follows a pharyngeal (but not skin) infection with group A beta-hemolytic streptococci, principally in children. In the past several decades, rheumatic fever and rheumatic heart disease have declined markedly but not disappeared in the United States and other developed countries. Evidence strongly suggests that rheumatic fever is the result of an immune response to streptococcal antigens, inciting either a cross reaction to tissue antigens, or a streptococcal-induced autoimmune reaction to normal tissue antigens. The cardiac surgical implications of rheumatic fever primarily relate to chronic rheumatic heart disease, characterized principally by chronic, progressive, deforming valvular disease (particularly mitral stenosis), that produces permanent dysfunction and severe, sometimes fatal, cardiac failure decades later.
Chronic rheumatic heart disease most frequently affects the mitral and to a lesser extent the aortic and/or the tricuspid valves. Chronic rheumatic valve disease is characterized by fibrous or fibrocalcific distortion of leaflets or cusps, valve commissures, and chordae tendineae, with or without annular or papillary muscle deformities
. Stenosis results from leaflet and chordal fibrous thickening and from commissural and chordal fusion, with or without secondary calcification. Regurgitation entails other mechanisms, including scarring-induced retraction of chordae and leaflets and, less commonly, fusion of a commissure in an opened position. Only very rarely does chordal rupture involve a rheumatic valve. Combinations of lesions may yield valves that are both stenotic and regurgitant. Although considered the pathognomonic inflammatory myocardial lesions in acute rheumatic fever, Aschoff nodules are found infrequently in myocardium sampled very late at autopsy or at valve replacement surgery, most likely reflecting the extended interval from acute disease to critical functional impairment.
Infective endocarditis is characterized by colonization or invasion of the heart valves, mural endocardium, aorta, aneurysmal sacs, or other blood vessels by a microbiologic agent, leading to the formation of friable vegetations laden with organisms. Virtually any type of microbiologic agent can cause infective endocarditis, but most cases are bacterial (i.e., bacterial endocarditis).
The clinical classification into acute and subacute forms is based on the range of severity of the disease and its tempo, on the virulence of the infecting microorganism, and on the presence of underlying cardiac disease. Acute endocarditis is a destructive infection, often involving a previously normal heart valve, with a highly virulent organism, that leads to death within days to weeks in over 50 percent of patients. In contrast, in subacute endocarditis, organisms of low virulence cause infection on previously deformed valves; the infection pursues a protracted course of weeks to months and may be undetected and untreated.
Vegetations in both clinical variants are composed of fibrin, inflammatory cells, and organisms. Staphylococcus aureus is the leading cause of acute endocarditis and produces necrotizing, ulcerative, invasive, and highly destructive valvular infections. Cardiac abnormalities, such as rheumatic heart disease, congenital heart disease (particularly anomalies that have small shunts or tight stenoses creating high-velocity jet streams), myxomatous mitral valve, only mildly calcified bicuspid aortic valve, and artificial valves and their sewing rings predispose to the subacute form, usually caused by Streptococcus viridans . In intravenous drug abusers, left-sided lesions predominate, but right-sided valves are commonly affected; the usual organism is S. aureus .
In about 5–20 percent of all cases of endocarditis, no organism can be isolated from the blood (“culture-negative” endocarditis), often because of prior antibiotic therapy.
The complications of endocarditis include valvular insufficiency (or rarely stenosis), ring (annular) abscess, suppurative pericarditis, and embolization. With appropriate antibiotic therapy, vegetations may undergo progressive sterilization, organization, fibrosis, and occasionally calcification. Regurgitation generally occurs on the basis of cusp or leaflet perforation, chordal rupture, or fistula formation (from a ring abscess into an adjacent cardiac chamber or great vessel). Ring abscesses tend to be associated with virulent organisms, are technically difficult to deal with surgically, and are associated with a relatively high mortality rate.
Reconstructive procedures to eliminate mitral insufficiency of various etiologies and to minimize the severity of rheumatic mitral stenosis are now highly effective and commonplace, accounting presently for over 70 percent of mitral valve operations.Reconstructive therapy of selected patients with aortic insufficiency and aortic dilatation may also be donebut repair of aortic stenosis has been notably less successful. The major advantages of repair over replacement relate to the elimination of both prosthesis-related complications and the need for chronic anticoagulation. Other reported advantages include a lower hospital mortality, better long-term function and a lower rate of postoperative endocarditis. illustrates the pathologic anatomy of various mitral valve reconstruction procedures.
MITRAL VALVE REPAIR
The hemodynamic disturbances in most forms of mitral valve disease are the result of multiple structural deformities at different levels within the complex mitral apparatus. Identification of each component of the anatomic lesion and an underlying understanding of normal valve anatomy and function is essential to adequate valve reconstruction.
In general, reconstructive techniques are more easily applied to mitral valves with nonrheumatic disease than those affected by rheumatic disease. The fibrosis and shortening of both chordae and leaflets that causes mitral stenosis and is the result of an advanced rheumatic process that makes gaining adequate mobility and adequate leaflet area difficult. Commissurotomy commonly is employed in the operative repair of a stenotic mitral valve. In mitral stenosis, leaflet calcification, subvalvar (predominantly chordal) fibrotic changes, and significant regurgitation owing to scar retraction are major factors that inhibit reconstructive surgical repair, and thereby necessitate valve replacement. Since the annular portions of the leaflet are normally devoid of chordal support, splitting to 2–3 mm from the annulus may avoid the potential complication of a new or residual regurgitant jet. Anterior leaflet mobility often is sufficient to allow an acceptable mitral opening despite posterior leaflet immobility, and pliable leaflets can partially compensate for a rigid subvalvar apparatus.
Five factors compromise the late functional results of mitral commissurotomy:
(1) left ventricular dysfunction;
(2) pulmonary venous hypertension and right-sided cardiac factors, including right ventricular failure, tricuspid regurgitation, or a combination of these;
(3) systemic embolization;
(4) other co-existent cardiac disorders, such as coronary artery or aortic valve diseases;
(5) residual or progressive mitral valve disease. Late deterioration following mitral commissurotomy may be owing to restenosis of the valve, residual (unrelieved) stenosis, or regurgitation induced at operation.
The structural defects in mitral regurgitation include:
(1) dilatation of the mitral annulus;
(2) elongation or rupture of chordae tendineae, permitting leaflet prolapse into the atrium;
(3) redundancy and deformity of leaflets;
(4) leaflet perforations or defects;
(5) restricted leaflet motion as a result of commissural fusion in an opened position, and leaflet retraction, chordal shortening or thickening or both.
Necrosis solely of a papillary muscle following an acute myocardial infarction generally does not induce insufficiency. More frequently, mitral regurgitation results from the underlying necrotic and nonfunctional free wall segment or distortion of the papillary muscle geometry by ventricular dilatation, where lateral movement of the papillary muscles alters the axis of their tension on the cords.
Leaflet abnormalities in mitral regurgitation include retraction, redundancy or perforation. The posterior leaflet is more delicate and has a shorter annulus-to-free-edge dimension than the anterior. It is therefore more prone to postinflammatory fibrous retraction. Following resection of excess anterior or posterior leaflet tissue, as in floppy valves, annuloplasty with or without a prosthetic ring generally is used to reduce the annulus dimension to correspond to the amount of leaflet tissue available. Tissue substitutes such as glutaraldehyde-pretreated xenograft or autologous pericardium can be used to repair or enlarge leaflets. A smooth white leaflet perforation with raised borders suggests prior healed infection, whereas irregular pink-tan borders or vegetations signal an active infection. Retracted or elongated chordae, respectively, reduce or enhance leaflet mobility. Ruptured or elongated chordae may be treated by shortening procedures or replacement with pericardial tissue or thick suture.
CATHETER BALLOON VALVULOPLASTY
Percutaneous transluminal balloon dilatation of stenotic valves has been used successfully to relieve congenital and acquired stenoses of native pulmonary, aortic, and mitral valves, and stenotic right-sided porcine bioprosthetic valves.
Mitral valvuloplasty yields favorable results in elderly patients with mitral stenosis complicated by pulmonary hypertension, a difficult group of patients to manage surgically. For acquired calcific aortic stenosis, individual functional responses to balloon dilatation vary considerably and data suggest a modest incremental benefit, high early mortality, and high restenosis rate Some patients have dramatic improvement in valvular and ventricular function, whereas others show little change. The major reported complications of balloon valvuloplasty include cerebrovascular accident secondary to embolism or massive regurgitation owing to valve trauma, cardiac perforation with tamponade, and with mitral valvuloplasty, creation of an atrial septal defect owing to septal dilatation.
Improvement following catheter balloon valvuloplasty of aortic stenosis derives from commissural separation, fracture of calcific deposits, and displacing and stretching of the valve cusps. Fractured calcific nodules can themselves prove dangerous In pediatric cases in which the cusps are generally pliable, cuspal stretching, tearing, or avulsion may also occur. In the relief of mitral stenosis, balloon valvuloplasty largely involves commissural separation; thus, this procedure is unlikely to provide significant alteration in the subvalvular pathology of the chordae and papillary muscles of patients with rheumatic mitral stenosis. Commissural splitting generally is successful only in valves with little or no commissural calcification. Thus, balloon valvuloplasty has been far more applicable in third world countries in which rheumatic mitral stenosis is commonly severe but noncalcific at a young age, rather than in the United States, in which the disease is usually only severe and calcific in middle-aged or elderly adults.
SURGICAL AND LASER DEBRIDEMENT
Since valvular aortic stenosis in most patients over 60 years of age is characterized by calcific deposits superimposed upon a valve largely free of either congenital or rheumatic deformities, such valves are stenotic simply because the leaflets are immobilized by extensive deposits of calcium. However, because the calcific deposits arise deep in the valve fibrous layertheir removal by sharp dissection or ultrasonic debridement generally requires dissection that removes this layer and may cause damage to the spongiosa layer, resulting in severe compromise of cuspal mechanical integrity. In some cases, the vegetations of infective endocarditis may be surgically debrided.
Severe symptomatic valvular heart disease other than pure mitral stenosis of incompetence is most frequently treated by excision of the diseased valve(s) and replacement by a functional substitute.
] Five factors principally determine the results of valve replacement in an individual patient:
(1) technical aspects of the procedure;
(2) intraoperative myocardial ischemic injury;
(3) irreversible and chronic structural alterations in the heart and lungs secondary to the valvular abnormality;
(4) coexistent obstructive coronary artery disease; and
(5) valve prosthesis reliability and host-tissue interactions.
VALVE TYPES AND PROGNOSTIC CONSIDERATIONS
Cardiac valvular substitutes are of two generic types, mechanical and biological tissue Prostheses function passively, responding to pressure and flow changes within the heart. Mechanical valves are usually composed of non-physiologic biomaterials that employ a rigid, mobile occluder (pyrolytic carbon disk) in a metallic cage (cobalt-chrome or titanium alloy [Bjork-Shiley, Hall-Medtronic, or OmniScience valves]) or two carbon hemidisks in a carbon housing (St. Jude Medical, Edwards-Duromedics, or CarboMedics CPHV prostheses). Pyrolytic carbon has high strength and fatigue and wear resistance, with exceptional biocompatibility, including thromboresistence. In contrast, tissue valves are, to a large extent, anatomically similar to natural valves. The major advantages of tissue valves compared to mechanical prostheses are their pseudo-anatomic central flow and relative nonthrombogenicity, usually not requiring anticoagulant therapy. Approximately two-thirds of all valves implanted in the present era are mechanical (mostly bileaflet tilting disk); nearly one-third are bioprosthetic (mostly xenografts fabricated from porcine aortic valve, which have been preserved in a dilute glutaraldehyde solution), and a small percentage are cryopreserved allografts
It is well accepted (but not proven) that in both animals and patients, valve replacement that preserves chordae and papillary muscles is associated with better postoperative left ventricular function when compared with replacement surgery that destroys the subvalvular apparatus, especially in patients with mitral regurgitation and impaired left ventricular performance. Analogously, this may be the reason why ventricular function is better preserved after mitral valve repair than after valve replacement. With modern substitute valves, especially bileaflet tilting disk valves that offer protection of the poppets from interference, a major drawback to prosthetic leaflet retention has been obviated.
Early mortality after cardiac valve replacement now is generally in the range of 3–5 percent, with the majority of deaths owing to hemorrhage, pulmonary failure, low cardiac output, and sudden death (with or without myocardial necrosis or documented arrhythmias). Early prosthetic valve-associated complications are unusual. Potential complications related to valve insertion include hemorrhagic disruption and dissection of the atrioventricular groove, perforation, or entrapment of the left circumflex coronary artery by a suture, and pseudoaneurysm or rupture of the left ventricular free wall. An additional advantage of resecting only the anterior leaflet and leaving the posterior leaflet intact is that postoperative rupture of the left ventricular free wall has nearly disappeared as a complication of mitral valve replacement.
Improvement in late outcome derives from earlier referral of patients for valve replacement, decreased intraoperative myocardial damage, and improved cardiac valve prostheses. Following valve replacement with currently used devices, the probability of 5-year survival is about 80 percent and of 10-year survival about 70 percent, dependent on overall functional state, preoperative left ventricular function, left ventricular and left atrial size, and extent and severity of coronary artery disease.
Prosthetic valve-associated pathology is common beyond the early postoperative period. The few randomized studies available show that with contemporary mechanical prosthetic and bioprosthetic valves, approximately 60 percent or more patients have an important device-related complication within 10 years postoperatively. However, as discussed in the following, thrombotic and thromboembolic problems that frequently complicate mechanical valves tend to occur earlier than the structural failures that complicate tissue valve prostheses. Valve-related complications frequently necessitate reoperation, now accounting for approximately 5–15 percent of all valve procedures, and they may cause death. Late death following valve replacement results predominantly from either cardiovascular pathology not related to the substitute valve or prosthesis-associated complications. Moreover, late death is caused by a device-related complication in 25–61 percent of patients. As might be expected, autopsy studies generally reveal a higher rate of valve-related pathology than clinical investigations. One-fifth or more of valve recipients will ultimately die suddenly; in a recent autopsy study of a highly selected referral population, 40 percent of valve recipients who died suddenly had a valve-related cause.
Four categories of valve-related complications are most important: thromboembolism and related problems, infection, structural dysfunction (i.e., failure or degeneration of the biomaterials comprising a prosthesis), and nonstructural dysfunction (i.e., miscellaneous complications and modes of failure not encompassed in the previous groups) The clinicomorphologic features of these problems have been widely described in the literature.The relative performance and risk of complications of various types of widely used substitute heart valve types is summarized in The risk of some valve-related complications (particularly thromboembolism) is potentiated by preoperative functional impairment.
Thromboembolic complications are the major cause of mortality and morbidity after cardiac valve replacement with mechanical valves, and patients with them require chronic therapeutic anticoagulation with warfarin derivatives. Thrombotic deposits can immobilize the occluder or shed emboli Tissue valves are less thrombogenic than mechanical valves. Most patients with bioprostheses and other tissue valves are not maintained on long-term anticoagulation, unless they have atrial fibrillation or another specific indication. Nevertheless, the rate of thromboembolism in patients with mechanical valves on anticoagulation is not widely different from that in patients with bioprosthetic valves without anticoagulation (2–4 percent per year). [ Chronic oral anticoagulation also induces a risk of hemorrhage.A recent study suggested that the optimal intensity of anticoagulation in patients with mechanical heart valves (balancing both thromboembolism and bleeding) both at approximately 2 percent per year was best achieved with a target INR (international normalized ratio) of 3.0–4.0.
As in the cardiovascular system in general, Virchow's triad of factors promoting thrombosis (surface thrombogenicity, hypercoagulability, and locally static blood flow) largely predicts the relative propensity toward and locations of thrombotic deposits. ] For example, with caged-ball prostheses, thrombi form distal to the poppet at the cage apex. Moreover, tilting disk prostheses are particularly susceptible to total thrombotic occlusion or emboli from small thrombi, both generally initiated in a stagnation zone in the minor orifice of the outflow region of the prosthesis. In contrast, late thrombosis of a bioprosthetic valve is unusual and, in most such cases, large thrombotic deposits are usually present in one or more of the prosthetic sinuses of Valsalva.] Usually, no causal underlying cuspal pathology can be demonstrated by routine microscopic studies. Noninvasive visualization of prosthetic valve thrombi is aided by transesophageal endocardiography.
As with other devices in which nonphysiologic artificial surfaces are exposed to blood at high fluid shear stresses, platelet deposition dominates initial blood-surface interaction and prosthetic valve thromboembolism correlates strongly with altered platelet function. ] , Nevertheless, although platelet-suppressive drugs largely normalize indices of platelet formation and partially reduce the frequency of thromboembolic complications in patients with mechanical prosthetic valves, antiplatelet therapy alone does not adequately prevent thromboembolism. The friability and thus susceptibility to embolization of thrombi that form on bioprosthetic or mechanical valves is prolonged, because lack of adjacent vascular tissue retards their histologic organization. For similar reasons, the age of such thrombi is difficult to determine microscopically. Moreover, in selected circumstances, thrombolytic therapy may be a practical nonsurgical option.Some valve thromboemboli, especially early postoperatively, are thought to be initiated at the valve sewing cuff.
High-intensity transcranial Doppler signals are reported to occur in many patients with heart valve prostheses. Although presumed by several authors to represent subclinical emboli, the origin and clinical significance of these signals is uncertain.
, prosthetic valve infective endocarditis occurs in 3–6 percent of recipients of substitute valves. Infection is generally categorized into early (less than 60 days postoperative) and late.the microbial etiology of early prosthetic valve endocarditisis dominated by staphylococcal species, S. epidermidis and S. aureus , even though prophylactic regimens used today are targeted against these microorganisms. The clinical course of early prosthetic valve endocarditis tends to be frequently fulminant, with rapid deterioration of the hemodynamic status due to valvular or annular destruction or persistent bacteremia.
In late endocarditis, a probable source of infection can be found in 25–80 percent of patients, the most frequent causes being dental procedures, urological infections and interventions, and indwelling catheters.
The most common organisms are S. epidermidis, S. aureus, Streptococcus viridans , and enterococci. Surgical reintervention usually is indicated by large highly mobile vegetations or if there are cerebral thromboembolic episodes. Transesophageal echocardiography enhances diagnosis of prosthetic valve endocarditis and its intracardiac complications.The rates of infection of bioprostheses and mechanical valves are similar, but previous endocarditis markedly increases the risk.
Virtually all infections associated with mechanical prosthetic valves and some with bioprosthetic valves are localized to the prosthesis-tissue junction at the sewing ring, and accompanied tissue destruction around the prosthesis ] This comprises a ring abscess, with potential valve dehiscence, paraprosthetic leaks, fistula formation, or heart block caused by conduction system damage. In addition, bioprosthetic valve infections may involve, and indeed are occasionally limited to, the cuspal tissue, sometimes causing secondary cuspal tearing or perforation with valve incompetence or obstruction , Cases without annular involvement have a better prognosis than those associated with infected annular margins of resection. Additional complications of prosthetic valve endocarditis include embolization of vegetations and congestive heart failure secondary to obstruction or regurgitation.
Prosthetic valve dysfunction owing to materials degradation can necessitate reoperation or cause prosthesis-associated death Durability considerations vary widely for mechanical valves and bioprostheses, for specific types of each, for different models of a particular prosthesis (utilizing different materials or having different design features), and even for the same model prosthesis placed in the aortic rather than the mitral site.
Fractures of metallic or carbon valve components occur rarely. Of approximately 86,000 Bjork-Shiley 60- and 70-degree Convexo-Concave heart valves implanted, a cluster of over 500 cases has been reported in which the welded outlet strut fractured because of metal fatigue, leading to disk escape Although complete strut fracture is usually fatal, elective removal of structurally intact prostheses is not recommended. However, a new cineangiographic imaging technique may facilitate detection of single leg strut fractures at a presymptomatic stage, thereby allowing consideration of elective valve removal. In contrast, fractures of carbon components (disks or housing) are unusual in single bileaflet tilting disk valves. However, a group of 37 fractures of an estimated 20,000 Edwards-Duramedics bileaflet-tilting valves has occurred, possibly a combined result of carbon coating defects and cavitation bubbles impacting on the carbon surfaces during function.
Structural dysfunction of tissue valves is the major cause of failure of the most widely used bioprostheses (flexible-stent-mounted, glutaraldehyde-preserved porcine aortic valves [Hancock and Carpentier-Edwards types])Within 15 years following implantation, 30–50 percent of porcine aortic valves implanted as either mitral or aortic valve replacements require replacement because of primary tissue failure.Cuspal mineralization is the major responsible pathologic process.Regurgitation through secondary tears is the most frequent failure mode. Pure stenosis owing to calcific cuspal stiffening and noncalcific cuspal tears or perforations (reflecting direct mechanical destruction of collagen) occur less frequently.Calcific deposits are usually localized to cuspal tissue (intrinsic calcification), but calcific deposits extrinsic to the cusps may occur in thrombi or endocarditic vegetations.
Calcification is markedly accelerated in younger patients with children and adolescents having an especially accelerated course. ,
Bovine pericardial valves suffer primarily design-related tearing, with calcification frequent but less limiting
Abrasion of the pericardial tissue is an important contributing factor. Bioprosthetic valve failure generally causes slowly progressive symptomatic deterioration, permitting reoperation. In contrast, mechanical valve failure is often catastrophic and may be life-threatening.
The morphology and determinants of calcification of bioprosthetic valve tissue have been widely studied in experimental models., The process is initiated primarily within residual membranes and organelles of connective tissue cells that are devitalized by glutaraldehyde pretreatment procedures.
The dystrophic calcification mechanism involves reaction of calcium-containing extracellular fluid with membrane-associated phosphorus. Subsequently, calcification of collagen occurs. The determinants of calcification include recipient metabolic factors (young age potentiates), valve factors (glutaraldehyde fixation enhances), and mechanical stress (accelerates). Since the endothelium of contemporary tissue heart valves is lost and their cells are nonviable, valve function resides in the integrity of the collagenous “skeleton.” However, without viable intravalvular fibroblasts, there is no way to repair or replenish collagen fibers that are damaged by normal wear-and-tear. An additional problem is that valve preservation causes the collagen to be mechanically “locked” so that normal cyclical cuspal deformation is inhibited, inducing abnormal stresses. Moreover, residual nonviable connective tissue cells serve no apparent beneficial role and, indeed, can be deleterious (e.g., causing calcification and potentially an immune response).
Commissural region dehiscence of the aortic wall tissue from the inside of the stent of porcine bioprosthetic valve in the mitral position causing mitral insufficiency has recently been described. Primarily reported for Carpentier-Edwards bioprostheses, this complication has also been noted in Hancock porcine valves of several models
Paravalvular defects may be clinically inconsequential or they may aggravate hemolysis or cause heart failure through regurgitation. Early paravalvular leak usually is the result of either suture knot failure, inadequate suture placement, or separation of sutures from a pathologic annulus in endocarditis with ring abscess, myxomatous valvular degeneration (floppy mitral valve), or calcified valvular annulus (calcific aortic stenosis or mitral annular calcification). Small and difficult to locate by surgical or pathological examination, late small paravalvular leaks usually are caused by anomalous tissue retraction from the sewing ring between sutures during healing
Hemolysis owing to turbulent flow and blood-material surface interactions is an ever-present risk. It was more common with earlier-model heart valve prostheses and resulted in renal tubular hemosiderosis or cholelithiasis in many patients. Although severe hemolytic anemia is unusual with contemporary valves, paravalvular leaks or dysfunction owing to materials degeneration may induce clinically important hemolysis.
Extrinsic factors can mediate late prosthetic valve stenosis or regurgitation, including a large mitral annular calcific nodule, septal hypertrophy, exuberant overgrowth of fibrous tissue, interference by retained valve remnants (such as a retained posterior mitral leaflet or components of submitral apparatus) or unraveled, long or looped sutures or knots
. For bioprosthetic valves, cuspal motion can be restricted by sutures looped around stents, and suture ends cut too long may erode into or perforate a bioprosthetic valve cusp.
Aortic or pulmonic valves (with or without associated vascular conduits) transplanted from one individual to another have exceptionally good hemodynamic profiles, a low incidence of thromboembolic complications without chronic anticoagulation, and a low reinfection rate following valve replacement for endocarditis.Early valvular allografts sterilized and/or preserved with chemicals (using propriolactone or ethylene oxide) or irradiation suffered a high rate of leaflet calcification and rupture yielding failure rates of near 50 percent at 10–12 years and 50–90 percent at 15–20 years. Pathologic examination of such valves revealed variable host fibrous tissue overgrowth, and marked structural changes, including loss of architectural elements and cellularity, fibrosis, calcification, and often cuspal ruptures.
Subsequent technical developments have led to cryopreserved allografts, in which freezing is performed with protection from crystallization by dimethyl-sulfoxide; storage until valve use is carried out at -196°C in liquid nitrogen. Contemporary allograft valves yield freedom from degeneration and/or replacement times equal to or better than those of conventional porcine bioprosthetic valves (approximately 50–90 percent valve survival at 10–15 years compared with 40–60 percent for bioprostheses).
Some studies suggest that a fraction of viable cells may remain at the time of implantation of grafts cryopreserved using current technology. However, unknown are the extent of residual cells and their functional activity on the one hand, and whether allograft cell viability at implantation is an important determinant of long-term durability on the other. While cellular preservation can be postulated to enhance both thromboresistance and durability, the presence of viable cells could have deleterious consequences, through potentiating immunological reactivity.
We recently studied 33 explanted left- and right-sided cryopreserved human allograft heart valves/conduits in place several hours to 9 years.Cryopreserved human allograft heart valves/conduits implanted >1 day had progressively severe loss of normal structural demarcations. Long-term explants were generally devoid of both surface endothelium and deep connective tissue cells and had hyalinized collagen, laminated elastin, and minimal inflammatory cellularity. Our studies and others demonstrate that cryopreserved allograft heart valves/conduits are morphologically non-viable, their structural basis for function seems primarily related to the largely preserved collagen. They are unlikely to have the capacity to grow, remodel, or exhibit active metabolic functions and their degeneration generally is not secondary to immunologic responses.
PULMONARY VALVULAR AUTOGRAFTS
Often called the Ross operation in recognition of its originator, pulmonary autograft replacement of the aortic valve is technically difficult but avoids anticoagulation, carries a low risk of thromboembolism, is purported to permit growth of the autograft proportional to the somatic growth of a child or young adult, and has excellent hemodynamic performance. The risk of late valve failure requiring reoperation for either the autograft valve or the homograft right ventricular outflow tract reconstruction is low. Ross and associates have reported freedom from autograft replacement of 85 percent at 20 years and a freedom from all valve-related events of 70 percent at 20 years. With the more recently used implantation of the autograft as a root replacement and the cryopreserved pulmonary homograft for right ventricular outflow tract reconstruction, actuarial freedom from reoperation (autograft or homograft) was 89 percent ± 3 percent at 5 years, and 92 percent ± 3 percent for the autograft alone.] Late autograft valve failure was most frequently due to aortic annulus dilatation and less frequently to degeneration. Autograft dysfunction can be corrected by autograft repair in patients with central insufficiency and aortic annular dilatation. The long-term structure of valvular autografts has not yet been reported.
Methods are being actively sought and studied to prevent calcification in bioprosthetic valves. Other approaches to provide improved valves include modifications of bioprosthetic valve stent design and tissue mounting techniques to reduce cuspal stresses, tissue treatments alternative to glutaraldehyde to enhance durability and post-implantation biocompatibility, non-stented porcine valves, minimally cross-linked autologous pericardial valves, flexible trileaflet polymeric (polyurethane) prostheses, and mechanical and tissue valves with novel design features to improve hemodynamics, enhance durability, and reduce thromboembolism.
Structure of the normal mitral and aortic valves. In (A), an opened left ventricle of the normal heart, various components of the mitral apparatus are demonstrated. al = anterior leaflet; pl = posterior leaflet; a = annulus; c = chordae tendineae; ap = anterior papillary muscle; pp = posterior papillary muscle; la = left atrium; lv = left ventricle. (B) Aortic valve, opened anteriorly to reveal the relationships of the anteromitral leaflet (al) to the aortic valve cusps (lrn = left/right non-coronary, respectively) and coronary arterial orifices (wide arrows). Note the small functionally insignificant fenestration in the lunula of the non-coronary cusp (narrow arrow). (C) Normal aortic valve histology, demonstrating layered structure, including the fibrosa (f) and spongiosa (s), the predominant layers. The inflow surface is indicated by the open arrow. Verhoeff van Giesen elastic tissue stain, 150×. Reproduced by permission from Schoen FJ: Interventional and Surgical Cardiovascular Pathology: Clinical Correlations and Basic Principles. Philadelphia, WB Saunders, 1989.
Two broad categories of myocardial disease are distinguished: cardiomyopathy (CM), defined as “heart muscle disease of unknown cause,” generally referred to as primary or idiopathic cardiomyopathy; and specific cardiomyopathy, formerly called specific heart muscle disease, defined as “heart muscle disease of known cause or associated with disorders of other systems.”Myocardial dysfunction also frequently occurs as a complication of ischemic, valvular, hypertensive (systemic and pulmonary), and congenital heart disease and some pericardial disease, through hypertrophy and subsequent degenerative changes and/or ischemic damage. Impairment of ventricular performance in the setting of coronary atherosclerosis often is called ischemic cardiomyopathy.
There are three functional/pathophysiologic/anatomic patterns–dilated, hypertrophic or restrictive. For each, the cause may be known or unknown. The cause of a specific cardiomyopathy is usually revealed by light and/or electron microscopic examination, whereas the morphology is non-specifically abnormal in idiopathic cardiomyopathy. Moreover, in idiopathic dilated cardiomyopathy, the severity of the morphologic changes does not necessarily correlate with the severity of dysfunction or the patient's prognosis.
Endomyocardial biopsy has been used widely in the diagnosis and management of patients with myocardial disease and in the ongoing surveillance of cardiac transplant recipients.The bioptome, inserted into the right internal jugular or femoral vein and advanced under fluoroscopic or echocardiographic guidance through the tricuspid valve, obtains 1- to 3-mm fragments of endomyocardium, most frequently derived from the apical half of the right side of the ventricular septum. Interpretation of right-sided biopsy specimens assumes that this location produces representative pathology. Since most myocardial diseases affect both ventricles, correlation between right- and left-sided findings generally is good.
Idiopathic dilated cardiomyopathy is characterized by biventricular hypertrophy and four-chamber dilatation of unknown cause and by subsequent cardiac failure.
Genetic influences have been documented increasingly, and dilated cardiomyopathy has a familial occurrence in approximately 25 percent of cases, with autosomal dominant, autosomal recessive, and X-linked inheritance variably proposed for particular kindreds.
A history of chronic alcoholism can be elicited in 20 percent of patients, and biopsy-proved myocarditis precedes the development of cardiomyopathy in 5–10 percent.
Pregnancy-associated nutritional deficiency or immunological reaction is another possible contributory factor.
The primary functional abnormality in dilated cardiomyopathy is impairment of left ventricular systolic function, as measured by the ejection fraction (<25 percent in end-stage, normal approximately 50–65 percent). Pathologic findings include cardiomegaly with heart weight two to three times normal and four-chamber dilatation. Cardiac mural thrombi, a potential source of thromboemboli, are sometimes present and may occur in any chamber. The histologic changes comprise myocyte hypertrophy and interstitial and endocardial fibrosis of variable degree, but they do not reflect an etiologic agent.
A recently described variant is arrhythmogenic right ventricular cardiomyopathy or arrhythmogenic right ventricular dysplasia, characterized by a focally to generally, but severely, thinned right ventricular wall, with extensive fatty infiltration, loss of myocytes, myocyte hypertrophy and interstitial fibrosis, with or without inflammation.
Sometimes familial, this disorder is most commonly associated with right-sided and sometimes left-sided heart failure and various rhythm disturbances, particularly ventricular tachycardia and sudden death.
Hypertrophic cardiomyopathy is characterized by a heavy muscular hypercontracting heart, in striking contrast to the flabby, hypocontracting heart of dilated cardiomyopathy. It represents a diastolic, rather than systolic, disorder.
The essential anatomic feature of hypertrophic cardiomyopathy is massive myocardial hypertrophy without dilatation.
The classic pattern is characterized by disproportionate thickening of the ventricular septum relative to the free wall of the left ventricle (ratio >1.5), frequently termed asymmetric septal hypertrophy, and usually localized to the subaortic region. When the basal septum is markedly thickened at the level of the mitral valve, the outflow of the left ventricle may be narrowed during systole.
Endocardial thickening in the left ventricular outflow tract and thickening of the anterior mitral leaflet result from contact between the two during ventricular systole (observed by echocardiography as systolic anterior motion of the mitral valve), correlating with systolic left ventricular outflow tract obstruction. Nonclassic cases also exist. In about 10 percent of cases, left ventricular hypertrophy is symmetric, and in other cases disproportionate hypertrophy involves the midventricular or apical septum, extends onto the left ventricular free wall anteriorly or inferiorly, or causes right ventricular outflow tract obstruction.
The most important microscopic features in hypertrophic cardiomyopathy include:
(1) haphazard disarray of myocytes and contractile elements within cells (myofiber disarray) typically involving 10–50 percent of the septum;
(2) extreme myocyte hypertrophy, with transverse myocyte diameters frequently more than 40 µm (normal approximately 15–20 µm); and
(3) interstitial and replacement fibrosis.
Nevertheless, despite these distinctive structural abnormalities, the diagnosis of hypertrophic cardiomyopathy cannot be made on endomyocardial biopsy.
Hypertensive heart disease coupled with age-related sub-aortic septal hypertrophy, amyloidosis, and occasionally, valvular or congenital sub-valvular aortic stenosis, various storage diseases, and mitochondrial cardiomyopathy can also mimic hypertrophic cardiomyopathy.
Hypertrophic cardiomyopathy has an extremely variable course, with potential complications including atrial fibrillation with mural thrombus formation, embolization from the mural thrombi, infective endocarditis of the mitral valve, intractable cardiac failure, and sudden death. Sudden death occurs in approximately 2–3 percent of adults and 4–6 percent of children per year and is the most common cause of death. It is particularly likely in young males with familial hypertrophic cardiomyopathy or with a family history of sudden death. In hypertrophic cardiomyopathy, cardiac failure is owing to reduced stroke volume that results from decreased diastolic filling of the massively hypertrophied left ventricle. Although symptoms are not owing solely to thickening of the ventricular septum, some patients benefit from thinning of the septum by surgical myotomy/myectomy. End-stage heart failure can be accompanied by dilatation, for which cardiac transplantation may be recommended.
Hypertrophic cardiomyopathy has a genetic basis in many cases.
In approximately half or more of patients the disease is familial, and the pattern of transmission is autosomal dominant with variable expression; remaining cases appear to be sporadic. In several kindreds with hypertrophic cardiomyopathy, various missense mutations have been identified in the genes for either isoforms of the heavy chain of cardiac myosin (the principal contractile protein in the thick filaments of muscle sarcomeres, located on chromosome 14), or other contractile proteins.
The mechanism by which defective sarcomeric proteins produce the phenotype of hypertrophic cardiomyopathy is uncertain. Interestingly, the different responsible gene mutations carry vastly differing prognoses and certain genetic defects indicate a relatively high likelihood of sudden death.
Restrictive cardiomyopathy is characterized by impeded diastolic relaxation and left ventricular filling. Left ventricular contractile (systolic) function is often unaffected. Morphologically, the ventricles are of approximately normal size or slightly enlarged, but the cavities are not dilated (unless valvular regurgitation coexists), and the myocardium is firm. Biatrial dilatation commonly is observed. Any disorder that interferes with ventricular filling can cause restrictive cardiomyopathy (including eosinophilic endomyocardial disease, amyloidosis, or postirradiation fibrosis), or mimic it (constrictive pericarditis or hypertrophic cardiomyopathy). Distinct morphologic patterns indicative of specific heart muscle disease may be revealed by light or electron microscopy of endomyocardial biopsy specimens, including amyloid deposition, or products of an inborn error of metabolism.
Cardiac transplantation provides long-term survival and rehabilitation to many individuals with end-stage cardiac failure.
Overall predicted 1-year survival is presently approximately 80 percent and 5-year survival is about 60 percent.
The most common indications for cardiac transplantation, accounting for 90 percent of the patients, are idiopathic cardiomyopathy and end-stage ischemic heart disease; other recipients have congenital, other myocardial, or valvular heart disease.
Explanted hearts typically have the expected pathologic features of the underlying diseases. However, previously undiagnosed conditions and unexpected findings may be encountered. Most frequent is eosinophilic or hypersensitivity myocarditis, seen in approximately 20 percent of explants and characterized by a focal or diffuse mixed inflammatory infiltrate, rich in eosinophils, and generally associated with minimal associated myocyte necrosis. [
In virtually all cases, the myocarditis represents hypersensitivity to one or more of the many drugs taken by transplant candidates, including dobutamine, and is unrelated to but superimposed on the original disease necessitating transplantation.
It is important to recognize that several diseases responsible for the original cardiac failure can recur in and cause dysfunction of the allograft. These include amyloidosis, sarcoidosis, giant-cell myocarditis, acute rheumatic carditis, and Chagas' disease.
Recipients of heart transplants undergo surveillance endomyocardial biopsies according to an institution-specific schedule, that typically evolves from weekly during the early postoperative period, to twice weekly until 3–6 months, and then approximately two to four times annually following 1 year, or at any time when there is a change in clinical state.
Histologic findings of rejection frequently precede clinical signs and symptoms of acute rejection. Optimal biopsy interpretation requires at least four pieces of myocardial tissue; reviews of technical details and artifacts are available.
The major sources of mortality and morbidity following cardiac transplantation are perioperative ischemic injury, infection, allograft rejection, lymphoproliferative disease, and obstructive graft vasculopathy.
Cardiac pathologists play an important role in the management of cardiac transplant recipients through the evaluation of endomyocardial biopsies for rejection and other pathological findings, and the effective communication of results to the clinical team.
EARLY ISCHEMIC INJURY
Ischemic injury can originate in the obligatory ischemia that accompanies procurement and implantation of the donor heart. Several time intervals are potentially important: (1) the donor interval between brain death and heart removal, perhaps partially related to terminal administration of pressor agents; (2) the interval of warm ischemia between donor cardiectomy to cold storage during transportation from donor to recipient; (3) the interval during cold transport; and (4) during warming, trimming, and reimplantation, or some combination of these. As in other situations of transient myocardial ischemia, either frank necrosis or prolonged ischemic dysfunction of viable myocardium or both may be present. Massive myocardial injury can cause potentially fatal low cardiac output in the perioperative period.
Donor cardiac hypertrophy and/or pre-existing coronary obstructions may contribute to inadequate preservation.
Perioperative myocardial ischemic injury as diagnosed by conventional histologic criteria is prevalent in endomyocardial biopsies early after heart transplantation at some institutions.
The histologic progression of healing of myocardial necroses in transplanted hearts, as noted on subsequent endomyocardial biopsies, is prolonged and the cellular infiltrate may be distorted owing to the anti-inflammatory effects of immunosuppressive therapy
. Therefore, the repair phase of perioperative myocardial necrosis frequently confounds the diagnosis of rejection in the first postoperative month, and in some cases, for as long as 6 weeks.
In contrast, ischemic necrosis noted following 3–6 months postoperatively is usually secondary to occlusive graft vasculopathy (see the following). It remains to be determined whether and to what degree early ischemic injury has a late impact on allograft dysfunction, possibly through loss of myocytes, accumulation of fibrosis, potentiation of rejection, or stimulation or graft vasculopathy (through associated vascular ischemic damage).
Improved current clinical immunosuppressive regimens in heart transplant patients have substantially decreased the incidence of serious rejection episodes.
Nonetheless, rejection phenomena still cause cardiac failure or serious arrhythmias in some patients. Hyperacute rejection occurs rarely, most often when a major blood group incompatibility exists between donor and recipient, and acute rejection is unusual earlier than 2–4 weeks postoperatively.
Acute rejection episodes occur largely but not exclusively in the first several months after transplantation. However, since rejection can occur years postoperatively, many transplant centers continue late surveillance biopsies at widely spaced intervals.
The histological features of acute rejection are an inflammatory cell infiltrate, with or without damage to cardiac myocytes; in late stages, vascular injury may become prominent ,
In general increasing numerical grades of rejection represent escalating severity of the rejection response, as manifested by the number and intensity of inflammatory cells, inflammatory foci, and amount of myocyte and ultimately vascular damage. The histologic diagnosis and grading of acute rejection on serial endomyocardial biopsies, based on the morphologic features originally described by Billingham, is used to guide the immunosuppressive therapy of heart transplant recipients.
Effective communication of results is facilitated through consistent reporting of histologic results by the pathologist to the clinical team, which itself has calibrated usual clinical responses to the specific morphology. Grading schemes facilitate communication between pathologists and clinicians;
The International Society for Heart and Lung Transplantation working formulation,
, is most widely accepted and used.
In this grading system, Grade O represents no evidence of rejection or healed rejection. Mild rejection (ISHLT grades 1A and 1B) is characterized by a focal or diffuse, respectively, mild perivascular (or interstitial) lymphocytic infiltrate without myocyte damage. Lymphocytic inflammatory infiltrates with associated myocyte encroachment or damage, generally called moderate rejection, either can be limited to a single focus (ISHLT grade 2), present in a multifocal pattern (ISHLT grade 3A), or distributed diffusely (ISHLT grade 3B). In severe rejection (ISHLT grade 4), myocyte necrosis is more evident, and there is often patchy interstitial hemorrhage owing to vascular damage, and vasculitis (usually arteriolitis) may be prominent. The increased inflammatory infiltrate often also includes neutrophils or eosinophils (presumably in response to myocyte necrosis or vascular damage).
Immunosuppressive protocols and the threshold for treatment of histological rejection vary greatly among heart transplant centers; in particular, the clinical significance of mild to low moderate rejection is controversial. ISHLT grades 1A, 1B, and 2 have been shown to resolve without specific change in management in over 80 percent of cases and, therefore, these levels of rejection remain untreated in many (but not all) heart transplant centers.
Progression of lower rejection grades to advanced rejection on subsequent biopsies becomes less likely with increasing postoperative interval, and is especially unusual beyond 2 years
To what extent lower grades of untreated rejection may contribute to long-term functional deterioration or chronic graft vasculopathy remains an important unanswered question.
Other important findings in surveillance endomyocardial biopsies that must be distinguished from rejection, but probably have no independent clinical significance, include lymphoid infiltrates either confined to the endocardium or extending into the underlying myocardium and often accompanied by myocyte damage (Quilty A or B lesions, respectively), and healing previous biopsy sites.
Lymphoproliferative disorders (see the following) may also be seen in biopsies.
The immunosuppressive therapy required in all heart transplant recipients confers an increased risk of infection with bacterial, fungal, viral, and protozoan pathogens. Such infections occasionally involve the heart. In particular, the cellular infiltrate associated with postoperative viral or parasitic infections (e.g., CMV [cytomegalic virus] or toxoplasmosis), occasionally can be difficult to distinguish from that of rejection. Both can produce multifocal lymphocytic infiltrates with occasional myocyte necrosis.
GRAFT VASCULOPATHY (GRAFT CORONARY DISEASE OR GRAFT CORONARY ARTERIOSCLEROSIS)
Graft vasculopathy is the major limitation to long-term graft and recipient survival following heart transplantation.
It represents a diffuse, concentric, or eccentric, proliferative intimal lesion in the coronary arteries of cardiac allografts that can cause distal ischemic injury
. Its pathogenesis remains uncertain. By 5 years following transplantation, up to 50 percent of recipients have angiographically evident disease.
Graft vasculopathy may become significant at any time during the posttransplant course and can progress at variable rates. Nearly half of our posttransplant deaths owing to graft coronary disease at the Brigham and Women's Hospital have occurred within 6–12 months postoperatively.
Coronary arterial occlusive disease in allografts can lead to myocardial infarction, arrhythmias, congestive heart failure, or sudden death.
The myocardial pathology resulting from the perfusion defects, and which may be noted on endomyocardial biopsy, includes subendocardial myocyte vacuolization, indicative of sublethal ischemic injury, and myocardial coagulation necrosis, indicative of infarction
Early diagnosis of graft vasculopathy is limited by the lack of clinical symptoms of ischemia in the denervated allograft, by the insensitivity of coronary angiography which frequently underestimates the extent and severity of this diffuse disease, and by the exclusive or predominant involvement of small intramyocardial vessels in some cases (which does not occur in typical atherosclerosis). Since the denervated transplanted heart has no afferent sensory nerves, myocardial ischemia usually does not elicit chest pain, and ischemic damage can be clinically silent until far advanced.
Intravascular ultrasound is becoming an important, albeit invasive, means of diagnosis, and correlates between anatomy and prognosis are under evaluation.
Paradoxical vasoconstriction induced by acetylcholine, suggesting defective endothelium-mediated vasodilation, may reveal early graft vasculopathy in some cases and also predict which patients eventually will develop occlusions.
Although graft vasculopathy has been called “accelerated atherosclerosis,” the morphology of the obstructive lesion of graft vasculopathy is distinctive in comparison to typical atherosclerosis (unless patients are hyperlipidemic or hypertensive)
Histologically, the vessels involved have occlusions characterized by marked cellular intimal proliferation with deposition of collagen, ground substance, and lipid. Lymphocytic cellular infiltration varies from almost none to quite prominent, yet lymphocytes often are noted in a subendothelial location in close approximation to the overlying endothelial cells.
The internal elastic lamina often is almost completely intact, with only focal fragmentation. Diffuse obliteration of intramyocardial vessels often is present.
The recipient's vasculature elsewhere is spared. Although the precise mechanisms of graft vasculopathy are not definitely established, proliferative vascular changes are probably the result of repetitive or continuous immunological damage to the intima followed by intimal proliferation of smooth muscle cells. As previously discussed, whether and to what extent either perioperative graft ischemia or low grades of rejection, cyclosporine, or CMV play a role in the the evolution of graft vasculopathy is uncertain.,
There is no apparent difference in the frequency with which graft vasculopathy develops in patients who were transplanted for end-stage coronary artery disease and those operated for idiopathic cardiomyopathy. Although not usually amenable to angioplasty, endarterectomy, or coronary artery bypass grafting because of their diffuse distribution, stenoses may be alleviated by these procedures in occasional cases. For most cases, however, retransplantation is the only effective therapy.
POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDERS
Lymphoproliferative disorders are a well-recognized complication of high-intensity long-term immunosuppressive therapy. Solid organ transplant recipients, including those with cardiac allografts, are at particular risk. Approximately 2 percent develop lymphoproliferative disorders.
Posttransplant lymphoproliferative disorders present as either an infectious mononucleosis-like illness or with localized solid tumor masses, especially in extranodal sites (e.g., heart, lungs, gastrointestinal tract). Most posttransplant lymphoproliferative disorders derive from the B-lymphocyte lineage.
There is strong evidence that the lesions progress from benign polyclonal B-cell hyperplasia to malignant lymphoma in a short period of time, in association with the appearance of cytogenetic abnormalities.
Epstein-Barr virus has been implicated as the causal agent. Interestingly, early lesions may respond to reduction in immunosuppression. However, although feasible in recipients of renal allografts, modification of therapy is difficult in heart, heart-lung, or liver recipients in which inadequately treated graft rejection is fatal. The mortality of posttransplant lymphoproliferative disorders exceeds 80 percent.
CARDIAC ASSIST AND MECHANICAL REPLACEMENT
Continuing and increasing discrepancy between the number of available donor hearts and the number of patients who might benefit from cardiac transplantation has prompted efforts in the development of mechanical assist devices, and cardiomyoplasty techniques.
These areas are briefly reviewed in the following, from the perspective of cardiac pathology.
Cardiac Assist Devices and Total Artificial Heart
Mechanical cardiac assist devices and artificial hearts have been used primarily in two settings: for ventricular augmentation sufficient to permit a patient to survive postcardiotomy or postinfarction cardiogenic shock while ventricular recovery is occurring; and as a bridge to transplantation, when ventricular recovery is not expected and the goal is hemodynamic support until a suitable donor organ is located.
In a small number of cases, ventricular assist devices and artificial hearts have also been used clinically with the intent of providing long-term cardiac support.
With either a left or right ventricular assist device, the inflow to the device is connected by means of a cannula to the atrium or ventricle of the natural heart, and the outflow is connected via a cannula to the appropriate great artery
Bilateral support can be provided by two separate pumps. In contrast, an artificial heart is composed of two chambers that replace both excised ventricles of the natural heart, analogous to an orthotopic cardiac transplant.
Current pumps have valves (mechanical or bioprosthetic), fabric (primarily Dacron) conduits, and a flexible, polyurethane, blood-containing chamber positioned within a rigid housing.
Most available pulsatile assist and replacement pumps are activated by rapidly delivered air pulses transmitted through tubes from an external pneumatic unit that result in high-velocity ejection of blood from the chamber. Heart rate, percent systole, dp/dt, and driving pressures are regulated by the pneumatic activator.
Temporary pumps may be positioned internally or externally, the latter adjacent to the patient, with the blood conduits passing percutaneously through the body wall. Internally placed pumps would have pneumatic tubes passing through the chest wall. Electrically powered, nonpulsatile centrifugal pumps, which move blood by means of rotating impellers, also are used as externally situated temporary assist pumps. Although some of these pumps can be used with peripheral access to the circulation (for example, femoral artery and vein), the present discussion primarily relates to implanted pumps with intrathoracic access to the cardiovascular system.
First used successfully by DeBakey in 1963, pneumatic ventricular assist pumps have provided temporary (days) circulatory support for patients with profound ventricular failure after open-heart operations.
When used as a left ventricular pump, the unit fills from the left atrium or left ventricle and ejects into the aorta; when used for right ventricular support, the pump fills from the right atrium or ventricle and discharges into the pulmonary artery.
The heart can be replaced by two pneumatically powered polyurethane sac-type blood pumps, implanted intrathoracically, that provide both systemic and pulmonary circulations.
Tilting-disk-type prosthetic inflow and outflow valves provide unidirectional blood flow in the two ventricles. The Jarvik-7 heart has served as a long-term mechanical cardiac replacement in several individuals since 1982; this and several other types of replacement devices have also been used as a bridge to transplantation.
Compact, totally implantable electrical motor-driven ventricular assist pumps and artificial hearts are being developed for long-term support of the systemic circulation in patients with irreparably damaged ventricles. A recent report describes 217 patients in which a total artificial heart was used clinically; survival was 56 percent with average duration of support 26 days (maximum 795 days).
The major observed complications of both cardiac assist and replacement with mechanical devices have been thrombus, thromboembolism, and infection
Thrombi form primarily in association with crevices and voids, especially in areas of disturbed blood flow such as near connections of conduits and other components to each other and to the natural heart. Although emboli have been less frequent with short-term devices (7–11 percent of the 217 patients mentioned previously), thromboembolism has occurred in most patients having long-term implantation of the Jarvik-7 artificial heart for temporary or permanent support.
Infectious complications have been a major limiting factor in the prolonged use of mechanical hearts, affecting many of the long-term recipients of the Jarvik-7 artificial heart and those with long-term ventricular assist devices.
Infection usually is within the device but may also be associated with percutaneous pneumatic drive lines, sometimes spreading to the mediastinum. Susceptibility to infection is not only potentiated by the usual prosthesis-associated factors, but also by the multisystem organ damage from the underlying disease, the periprosthetic culture medium provided by postoperative hemorrhage, and by prolonged percutaneous cannulas.
Device failure can also occur because of fracture of a mechanical prosthetic valve (this application provides a particularly severe test of prosthetic valve durability) or rupture of the synthetic diaphragm. Hemolysis generally is associated with an excessive pump pressure pulse rate (high dp/dt). Pannus formation can occlude conduits, especially at anastomoses.
Complications of the various forms of cardiac assist devices in potential transplant recipients do not differ widely from those encountered in the use of permanent artificial hearts or in the use of temporary assist devices in other patients. However, contraindications to transplantation such as infection or critical thromboembolism can develop during mechanical assist in candidates.
Nonthrombogenic blood-contacting surfaces are essential for a clinically useful temporary or permanent cardiac assist device or artificial heart.
The most fruitful approaches to design of the blood-material interface of the moving blood pump bladder have included smooth or textured (fibrillar) elastomeric polyurethane surfaces. Smooth surfaces are designed to repel thrombosis, whereas the textured surfaces accumulate a limited platelet/fibrin pseudointimal membrane. Although each type of surface has been associated with heavy mineralization in long-term investigational devices implanted into calves or sheep, macroscopic mineralization has not been noted following cardiac assist device or artificial heart implantation in humans.
Skeletal Muscle Augmentation of Cardiac Function
Autologous skeletal muscle has been used to provide active cardiac assist in the form of both cardiomyoplasty and skeletal muscle ventricles.
Chronic low-frequency electrical stimulation of skeletal muscle results in the acquisition by that muscle of fatigue-resistant properties and in accompanying structural and biochemical changes, including increases in capillary density, activity of oxidative enzymes, and mitochondrial volume.
Another approach is to use skeletal muscle to power a mechanical circulatory assist device. Relevant pathology in these applications has not yet been reported in detail.
NEOPLASTIC HEART DISEASE
Although metastatic tumors to the heart occur in about 5 percent of patients dying of cancer, primary tumors of the heart are unusual.
Those most common, in descending order of frequency, are: myxomas, fibromas, lipomas, papillary fibroelastomas, and rhabdomyomas, all benign and accounting collectively for 80–90 percent of primary tumors of the heart. The remaining 10–20 percent are usually malignant tumors, including angiosarcomas and other sarcomas.
Myxomas are the most common primary tumor of the heart in adults.
They may arise in any of the four chambers or, rarely, on the heart valves.
About 90 percent are atrial myxomas, with a left-to-right ratio of approximately 4:1.
Those in the left atrium usually arise along the septum in the region of the fossa ovalis.
The tumors almost always are single, although multiple tumors occur simultaneously in rare instances.
A familial syndrome (Carney's syndrome or syndrome myxoma) includes cardiac myxomas, cutaneous myxomas, and pigmented adrenal cortical lesions.
Myxomas range from small (<1 cm) to large (up to 10 cm) and form sessile or pedunculated masses that vary from globular and hard lesions mottled with hemorrhage to soft, translucent, papillary, or villous lesions having a myxoid and friable appearance
The pedunculated form frequently is sufficiently mobile to move into or sometimes through the ipsilateral atrioventricular valve annulus during ventricular diastole, thereby causing intermittent and often position-dependent obstruction. Sometimes, such mobility exerts a “wrecking ball” effect, causing damage and secondary fibrotic thickening to the valve leaflets.
Histologically, myxomas are composed of stellate or globular cells, often in formed structures that variably resemble poorly formed glands or vessels, endothelial cells, macrophages, mature or immature smooth muscle cells, and a variety of intermediate forms embedded within an abundant acid mucopolysaccharide matrix and covered by endothelium.
Although it has long been questioned whether cardiac myxomas are hamartomas or organized thrombi, the weight of evidence is on the side of benign neoplasia. All the cell types present are thought to derive from differentiation of primitive multipotential mesenchymal cells.
The major clinical manifestations are owing to either valvular obstruction, embolization, or a syndrome of constitutional symptoms, such as fever and malaise, likely owing to the elaboration by some myxomas of the cytokine interleukin-6, a major mediator of the acute phase response of the systemic inflammatory reaction. Sometimes, fragmentation with systemic embolization calls attention to these lesions.
Echocardiography provides a means to identify the masses noninvasively. Surgical removal usually is curative. Rarely, the neoplasm recurs months to years later, usually only if the stalk is incompletely removed at the time of surgical resection.
Other Cardiac Tumors and Tumor-Like Conditions
Lipomas are localized, poorly encapsulated, not necessarily neoplastic, masses, that may occur in the subendocardium, subpericardium, or within the myocardium.
Many are asymptomatic. They can create ball-valve obstructions as with myxomas, or produce arrhythmias, most often with lesions in the left ventricle, right atrium, or atrial septum.
Adipose depositions in the atrial septum are called “lipomatous hypertrophy.”
Papillary fibroelastomas are usually solitary incidental masses, and are generally located on the valves, particularly the ventricular surfaces of semilunar valves and the atrial surfaces of atrioventricular valves. They constitute a distinctive pompom-like cluster of hairlike projections up to 1 cm or more in length, and covering up to several centimeters in diameter of the endocardial surface
] Histologically, they are composed of a dense core of irregular elastic fibers, coated with myxoid connective tissue, and lined by endothelium.
They may contain focal platelet-fibrin thrombus and serve as a source for embolization. Although classified with neoplasms, fibroelastomas may represent organized thrombi, similar to the much smaller, usually trivial, whisker-like Lambl's excrescences that are frequently found on the aortic valves of older individuals.
Rhabdomyomas, included for completeness, comprise the most frequent primary tumor of the heart in infants and children. They consist of gray-white myocardial masses up to several centimeters in diameter that are located on either the left or right side of the heart, and may protrude into the ventricular or atrial chambers. Histologically, they consist of a mixed population of cells, the most characteristic of which are large, myofibril-containing rounded or polygonal cells containing numerous glycogen-laden vacuoles. These, in turn, are separated by strands of cytoplasm running from the plasma membrane to the more or less centrally located nucleus, forming so-called spider cells. Many cardiac rhabdomyomas occur in patients with tuberous sclerosis.
Cardiac angiosarcomas and other sarcomas are not distinctive from their counterparts in other locations. They tend to involve the right side of the heart, especially the right atrioventricular groove (or sulcus)
Recently described, and of importance only insofar as they need to be distinguished from primary cardiac tumors or metastatic carcinoma, are peculiar microscopic-sized cellular cardiac lesions that have been noted incidentally as part of endomyocardial biopsy or surgically removed tissue specimens or at cardiac surgery, free-floating or loosely attached to a valvular or endocardial mass.
Termed mesothelial/monocytic incidental cardiac excrescences (“MICE”), they appear histologically largely as clusters and ribbons of mesothelial cells and entrapped erythrocytes and leukocytes, embedded within a fibrin mesh. Some represent reactive mesothelial and/or monocytic (histiocytic) hyperplasia, whereas others are now considered to be artefacts formed by compaction of mesothelial strips (likely from the pericardium) or other tissue debris and fibrin, which are transported via catheters or around an operative site on a cardiotomy suction tip.
complication in cardiac surgery
Potential complications of thoracostomy tubes placed after or during operation include intercostal arterial bleeding, bleeding from the superior epigastric artery from a deep skin incision, disturbance of epicardial pacemaker leads, and rarely, intra-abdominal injury.
Thoracostomy tubes may also cause postoperative pain that disappears with removal of the tube. Intercostal or superior epigastric arterial bleeding is controlled by cautery or occasionally a deep suture, and the absence of bleeding at chest tube sites should be confirmed before the chest is closed.
Rarely persistent bleeding from the site of a thoracostomy tube may be found owing to an intra-abdominal injury.
Removing chest tubes may allow air to enter the chest if not done properly. A previously placed “U” stitch, an occlusive dressing, and removal during exhalation prevent air entry.
Fracture of a chest tube is very rare; if a segment remains in the chest, it should be removed by thoracoscopy.
Temporary Epicardial Pacemaker Leads
Temporary epicardial pacemaker leads are routinely left to facilitate control of postoperative arrhythmias after nearly every cardiac operation.
The most common problem is failure to function when needed owing to poor sensing or capture and dislodgement.
Occasionally metabolic and acid/base abnormalities impede capture, but mechanical causes are most common.
Placement of the leads approximately 2 cm apart and into a superficial layer of myocardium assures proper sensing and capture if the leads remain intact.
Separation by large distances sometimes interferes with sensing because the leads act as an antenna.
Failure to capture postoperatively initially is treated by reversing polarity; if this fails, extension cables and the pacemaker generator are replaced.
If failure to capture persists and the patient's circulation is unstable, a transvenous or transcutaneous lead is needed promptly.
The reported incidence of major complications of epicardial pacemaker leads is approximately 0.4 percent.
Bleeding can occur during insertion or at the time of removal.
Deep bites into the myocardium enhance bleeding, particularly at the time of removal.
Ventricular leads preferably are placed superficially in the longitudinal axis of the ventricle.
At least one atrial lead is placed within the ligature closing an atriotomy to reduce the chance of bleeding.
Placement of leads prior to administration of protamine is recommended to reduce the likelihood of overlooking myocardial bleeding before chest closure.
Bleeding may also occur from spearing an upper abdominal wall vessel during exteriorization of the leads.
Removal of temporary pacing wires may cause lacerations of the atrium or ventricle, injury to nearby coronary bypass grafts, and even strangulation of the heart by a surrounding loop of wire.
Bleeding significant enough to cause pericardial tamponade and require emergency thoracotomy may occur at the time of wire removal, particularly in anticoagulated patients.
Pacemaker wires are removed with the patient supine by gentle traction after cutaneous securing sutures are cut.
Patients remain at bedrest for a least 30 minutes afterwards, and vital signs are monitored.
Whenever possible, leads are removed before the patient is fully anticoagulated and are not removed until coagulation times above the therapeutic range are returned to the targeted range.
Excessive pull on lead wires is painful, may cause serious damage, and should be avoided. Preferably wires which are difficult to remove should be sterilized with betadine or alcohol at the skin, gently pulled and cut off at the skin with sterile scissors.
The retained wire rarely causes subsequent problems.
Great Vessel and Thoracic Duct Injuries
VENA CAVA AND LEFT INNOMINATE VEIN
Either the left innominate vein or the junction of the innominate vein with the subclavian and jugular to form the superior vena cava can be injured during median sternotomy, particularly in patients who have had previous operation through this incision.
The injury most often occurs when the sternal retractor is opened without first freeing the innominate vein from the overlying chest wall.
The incidence of the injury is not known since this complication rarely is reported.
The injury may produce dramatic bleeding that may require accelerated administration of heparin and institution of cardiopulmonary bypass by femoral cannulation.
If the injury to the left innominate vein is distant from the superior vena cava, the vessel can be ligated with little concern since collateral channels usually are sufficient to relieve elevated venous pressures.
If, however, left jugular and subclavian venous pressures are elevated above 25 mmHg, reconstruction of the injured left innominate vein should be considered and undertaken if possible.
If the innominate vein is separated from the superior cava at its junction, usually repair is needed to prevent upper body venous hypertension. If measured pressures in the left jugular and subclavian veins are below 25 mmHg, ligation and permanent separation are an option. If repair is needed, a patch of saphenous vein or pericardium is used to avoid tension on the suture line even after the vessels are freed from the chest wall and surrounding tissues.
Direct injuries to the superior or inferior vena cava occasionally occur during dissection of the heart for cannulation or from insertion of a cannula. Usually tears in the superior vena cava are easily repaired because exposure is good.
Tears at the diaphragmatic inferior vena cava are more difficult, particularly if the posterior or medial cava is torn. In such cases a cannula should be passed into the inferior cava beyond the tear if possible to reduce bleeding and sustain life. Insertion of a femoral venous catheter is done to permit temporary occlusion of the diaphragmatic cava while a repair using saphenous vein or pericardium is made.
Direct injuries to the proximal pulmonary arteries or veins during repeat cardiac operations are not common but do occur. In most instances these can be sutured closed easily by occluding bleeding by forceps,
Allyce clamps, or finger and suturing. If the site of injury is not exposed easily, cardiopulmonary bypass is started to reduce bleeding.
The artery is repaired either directly or, occasionally, with a pericardial patch during bypass using 5-0 prolene suture. Veins are repaired directly.
AORTIC FALSE AND MYCOTIC ANEURYSMS
Although endocarditis involving the aortic valve may produce a mycotic aneurysm of the aortic root, surgical incisions into the ascending aorta that for any reason leak or become infected produce a sterile false or mycotic aortic aneurysm.
The incidence of this serious complication is less than 0.8 percent, but the problem may account for up to 3 percent of late deaths after cardiac surgery.
The wall of the false or mycotic aneurysm is formed by fibrous tissue and does not contain tissue from the aorta.
Although thrombus may be present within the lumen of the aneurysm, unclotted blood also is present and communicates with the true aortic lumen through an opening that may be narrow but often is quite large. Typically the false or mycotic aneurysm extends to the anterior chest wall by the time it is recognized.
Pseudo or mycotic aortic aneurysms usually present late, but the interval after the original operation in which the aorta was incised ranges from 1 month to 9 years.
Chest pain; venous obstruction; dysphagia; hoarseness; stridor; an enlarging, palpable, pulsatile mass in the sternal notch, high interspace, or the root of the neck; or myocardial ischemia from compression of bypass grafts direct attention to the problem. Occasionally aortic false aneurysms are asymptomatic and are detected by discovering a widened mediastinum or mediastinal mass on chest X-ray.
If infection is present, the patient may have fever, lethargy, anorexia, anemia, and leukocytosis in addition to other symptoms and signs.
Infection may develop from a mediastinal infection or from septicemia. The most-common infecting organisms are Staphylococcus aureus and S. epidermidis and various streptococci. Sustained bacteremia over several weeks after cardiac surgery warrants further investigation for possible mycotic false aneurysm.
The aneurysm may be imaged by transthoracic echocardiography (TTE), computerized axial tomography (CT scan), magnetic resonance imaging (MRI), and aortography.
The mass must be differentiated from mediastinal abscess, postoperative hematoma, or an unrelated neoplasm. The initial examination is usually with TTE and color flow Doppler velocity mapping to establish the presence of an aneurysm.
MRI has the advantage over CT scan in that fluid and clotted blood are distinguished easily and good images of the neck of the aneurysm usually are obtained.
Both CT scans and MRI identify the size, anatomic location, and structures adjacent to the aneurysm satisfactorily and generally provide more information than aortography.
The presence of pseudo or mycotic aortic aneurysms is an indication for prompt operation because of the possibility of rupture. Often these aneurysms abut against the anterior chest wall beneath the sternotomy incision; therefore, femoral vessels are cannulated for partial cardiopulmonary bypass before the sternum is opened. If the femoral venous catheter reaches the right atrium, nearly the entire venous inflow can be diverted into the extracorporeal perfusion system.
Most commonly the patient also is cooled to 20°C or less so that a short period of circulatory arrest can be used to open the aneurysm, locate the true and false lumens, and differentiate the edges of the neck.
Alternatively in uninfected patients with small diameter communications a balloon catheter can be inserted into the distal aorta to control back bleeding while the aneurysm is repaired.
A patch of bovine pericardium or synthetic material is used to close the opening into the false aneurysm so that the true aortic lumen is not compromised.
If the aneurysm is infected, all infected prosthetic material and necrotic, inflamed host tissue must be excised, and all abscesses must be discovered and completely drained.
After debridement the surgical field is thoroughly irrigated with antiseptic solution.
The aorta is reconstructed using synthetic material or bovine pericardium.
Sometimes the new patch is covered with transposed omentum to further reduce the risk of continuing infection.
Intravenous antibiotics, started before operation, are continued afterwards but may be changed according to organisms cultured from the surgical field.
Approximately 70–80 percent of patients treated for mycotic false aneurysms of the ascending aorta survive.
Without infection, mortality is approximately 10 percent.
Mechanical injury to the aortic intima from incision, cannulation, clamp compression, or torsion may produce an aortic dissection
Femoral or iliac artery cannulation without a wire guide or incomplete incision of the intima during aortic cannulation may create an intimal flap that initiates a dissection when cardiopulmonary bypass starts.
For this reason it is important to test for pulsatile backflow after every arterial cannulation using large bore cannulas.
Dissections also begin at intimal tears produced by the aortic cross-clamp or the heel of a side-biting clamp, at the sites of a proximal aortic vein graft, or at a poorly closed aortotomy site.
Patients who are predisposed to dissection include those with congenital syndromes associated with an abnormal wall, severe atherosclerosis or calcification, or post-stenotic aneurysmal dilatation and thinning. The complication may also involve a normal aorta.
The incidence of acute aortic dissection during or shortly after cardiac surgery ranges from 0.03 to 0.35 percent.
The majority are identified in the operating room, and prompt recognition is fundamental to successful management.
Occasionally a dissection is first identified by transesophageal echocardiography during femoral cannulation or intra-aortic balloon insertion.
Rarely, an intraoperative aortic dissection may present several days after operation.
Development of bluish discoloration beneath the adventitia of an aortic segment is often the first sign of dissection.
The tense adventitia usually is not pulsatile because of cardiopulmonary bypass and is distinguished from an intramural hematoma by the extent and location of the involved aorta. If cardiopulmonary bypass is not satisfactorily established, it may be possible to stop bypass and resume the native circulation to permit transesophageal echocardiographic examination of the extent of the dissection. If the native circulation cannot be resumed rapidly, the inflow cannula should be relocated rapidly to another undissected site to establish an adequate circulation.
The damage then is assessed by direct inspection and echocardiography, and an operative plan to rectify the complication and to complete the planned operation is formulated.
A localized dissection that involves a small segment of the aortic wall or less than 15 percent of the aortic circumference often may be treated by plication.
Larger localized dissections that involve less than 50 percent of the aortic circumference may be excised with reconstitution of the aortic edges and closure using a Dacron or pericardial patch.
The dissected layers are reunited as a sandwich between two stripes of Teflon felt. More-extensive dissections are best treated by resection and graft replacement of the proximal aorta.
Usually iatrogenic dissections do not involve the aortic root, coronary ostia, or aortic valve; therefore, composite grafts are rarely necessary.
The arch, however, may be involved and require partial or complete replacement during deep hypothermia and circulatory arrest with or without retrograde cerebral perfusion
. If the dissection is recognized after proximal coronary bypass graft anastomoses are made, the segment of aorta containing the anastomoses can be patched onto the ascending aortic graft.
Early descriptions of this complication of cardiac surgery reported a mortality between 33 and 62 percent. More-recent experience reports a mortality of approximately 15 percent.
Measures to prevent iatrogenic acute aortic dissection include cannulation over a guide wire, complete incision of the intimal layer for aortic cannulation, application and removal of clamps during brief periods of reduced flow, careful inclusion of all aortic layers in suture lines, and avoidance of multiple aortic clamp applications.
ATHEROSCLEROTIC AORTIC EMBOLI
Moderate or severe atheromatous disease of the ascending aorta may be present in 5–13 percent of patients who have open heart surgery.
The extent of the disease is variable.
Normal aorta or minimal atherosclerotic disease involves less than 3 mm of intimal thickening; moderate disease includes focal areas of intimal thickening that exceed 3 mm; severe disease includes multiple or circumferential areas of significant intimal thickening with pedunculated or mobile atheromatous plaqu
The consistency of the atheromatous material varies among severe, “porcelain” calcification; ragged, diffuse solid atheromatous material; and yellow semiliquid “toothpaste” material within the aortic wall.
Unfortunately, gross inspection of the outside of the aorta does not provide clues to the degree of atheromatous involvement. However, the disease is most common in patients with symptomatic disease of other major arteries, smoking, hypertension, and increasing age.
Moderate or severe atheromatous disease of the ascending aorta may be a marker of generalized atherosclerosis, and these patients are at increased risk of morbidity and mortality.
Moderate and severe disease may be suggested by calcification of the ascending aorta in the perioperative chest X-ray.
The disease also is identified by intraoperative epiaortic echocardiography using a hand-held probe within a sterile sleeve.
These images can provide excellent maps of the areas of severe involvement of the ascending aorta but do not image the aortic arch well.
Transesophageal echocardiography produces satisfactory images of the ascending aorta and part of the arch but has a blind spot owing to the left main bronchus; nevertheless, this method is convenient and does not delay operation.
Aortic atheromata may be demonstrated by CT scanning and MRI, but these studies are seldom ordered because echocardiography can be used during operation.
Aortic atheromata may cause stroke, coronary arterial emboli, or emboli to the kidneys, gastrointestinal tract, or extremities.
Once the problem is identified, operation is modified
The aorta should not be manipulated until dislodgement of atheromatous material can be controlled. Cannulation and aortic cross-clamping are maneuvers that are associated with embolization.
The incidence of emboli in patients with severe disease is reported as high as 58 percent.
Proper management of the problem substantially reduces the morbidity and mortality of these emboli.
If the ascending aorta cannot be cannulated safely, sometimes the medial surface of the arch can be used with introduction of a long soft-tipped cannula that is advanced beyond the left subclavian artery.
Femoral cannulation may be necessary, but retrograde perfusion may dislodge atheromata in the descending thoracic aorta into cerebral and coronary vessels. If the aorta must be clamped because of severe aortic insufficiency, the most-proximal aorta that is usually least diseased is used. In patients with moderate disease, areas relatively free of disease may be selected for placement of the aortic cross-clamp. If the distal aorta can be clamped, the ascending aorta can be opened for removal of the atheromatous material, for excision of the most diseased areas with patch closure, or for replacement with a tube graft.] ,
If the ascending aorta cannot be safely cross-clamped, deep hypothermia with a period of circulatory arrest is advised.
This is used with retrograde cerebroplegia, which washes out embolic material from the cerebral vessels, and an open anastomosis of a Dacron graft to the distal ascending aorta or proximal arch. An 8-mm Dacron graft sewn to the side of the ascending aortic graft permits antegrade flow when perfusion is restarted after the period of circulatory arrest.
This prevents emboli from retrograde perfusion via the femoral artery.
In patients with generalized vascular disease or poor or absent peripheral pulses, no attempt is made to introduce catheters into the descending thoracic aorta because of the likely presence of atherotoma.
Transesophageal echocardiography reliably identifies descending thoracic aortic atherotoma, and inspection prior to femoral insertion of the intraaortic balloon pump is recommended to avoid “trash emboli” to the lower extremities, gastrointestinal tract, and kidneys.
Thoracic duct injuries during cardiac surgery are extremely rare in adults but are uncommon but not rare in children.
Branches of the thoracic duct infiltrate thymic tissue that may be transected during exposure of the aorta. The complication is recognized postoperatively by persistent, milky chest tube drainage that contains fat globules, chylomicrons, triglyceride concentrations greater than 110 mg/dL, and a high lymphocyte cell count. Initial management is dietary; oral fats are limited to medium-chain triglycerides supplemented by intravenous feedings.
The majority of leaks close without surgery. Should surgery be necessary, injection of heavy cream into a nasogastric tube may facilitate location of the leaks.
Complications associated with cardiopulmonary bypass
The incidence of pulmonary embolism after open heart surgery ranges between 0.56 and approximately 2 percent.
Nearly half the patients develop deep vein thrombosis of calf veins after myocardial revascularization, but nearly all are asymptomatic, are equally distributed between the donor leg and the opposite, and are only visible by duplex scanning.
The incidence of pulmonary embolism after coronary arterial bypass operations is 3.2 percent; risk factors include prolonged postoperative recovery, previous venous thromboembolism, obesity, and hyperlipidemia.
Interestingly, valve surgery is not associated with as high an incidence of pulmonary embolism.
Hospital mortality in patients with pulmonary emboli ranges between 19 and 34 percent.
Occasional patients, usually but not always thin individuals, complain of chronic pain in the region of palpable sternal wires in the absence of inflammation or infection. Rare patients present with a visible sternal wire protruding through the skin. In both instances removal of the wire or all wires during brief general anesthesia using small skin incisions over each wire relieves the problem. If pus is encountered, it is cultured, and a search for a deep sternal wound infection is begun after the procedure. It is unwise to extend the exploration without first obtaining a complete evaluation for deep infection.
STERILE WOUND DEHISCENCE
Sterile dehiscence of a median sternotomy may be owing to technical factors or to inability of sternal wires to maintain edge approximation because the sternum is soft and osteoporetic. ] If soft sternum is recognized at the time of operation or after dehiscence, closure may be reinforced using the Robicsek technique. This method weaves a heavy wire vertically around the costal sternal junction of each rib by passing the wire anterior to posterior to anterior up and down each side of the sternal plate
. Horizontal wires are placed around the vertical wires to approximate the divided sternal edges.
Sterile sternal dehiscence usually develops within the first week or 10 days after operation. Patients complain of pain and the sensation of movement, and sterile wound drainage may exit the wound. Often instability can be palpated when the patient coughs or moves. Drainage should be cultured and antibiotics given. The patient is returned to the operating room promptly for exploration, irrigation, and reclosure of the entire wound. These patients are at increased risk of a deep sternal infection or mediastinitis, but the vast majority heal without infection.
SUPERFICIAL WOUND INFECTION
Superficial wound infections are defined as those that do not penetrate the subcutaneous tissue layer. Approximately 1 percent of patients who have median sternotomy develop a superficial wound infection, usually 7–9 days after operation.
The wound may exhibit erythema and a small amount of drainage that contains bacteria. The skin and subcutaneous layer are opened promptly and packed to allow secondary wound closure. Antibiotics are not indicated, and extension to deeper layers is uncommon unless treatment is delayed.
DEEP WOUND INFECTION
Deep sternal wound infections include acute mediastinitis with sternal dehiscence and osteomyelitis of the sternum. The incidence of deep wound infections ranges 0.4–5 percent.
Immunosuppressed patients who receive a heart or lung transplant have a reported incidence of 3.4 percent.
Reexploration for bleeding and insulin diabetes with simultaneous harvest of both mammary arteries also increase the incidence of deep wound infection, but other putative risks factors including obesity, transfusion, prolonged ventilatory support, emergency surgery, prolonged operation, and renal insufficiency are no longer considered contributory.
The costs of deep wound infections are high, and every effort to reduce the incidence is worthwhile.
These include strict observance of sterile technique, careful hemostasis, operating room air filtration, reduced traffic in the operating room, and periodic surveillance cultures.
Deep sternal wound infections arise from direct contamination of the wound, from the bloodstream, or from direct extension of an adjacent infection.
Staphylococcal organisms are the most common agents, but other organisms including pseudomonas, enterobacter, serratia, acinetobacter, klebsiella, legionella, apergillus, and fungi have been isolated from infected wounds.
Presenting symptoms and findings include wound drainage, fever, sternal instability, excessive wound pain, leukocytosis, and dehiscence. Usually a deep wound infection becomes apparent 2–4 weeks after operation, but a few may present months or years later.
Any drainage from the wound should be cultured and the sensitivity of the organism or organisms to antibiotics determined. Usually the plain chest X-ray is not diagnostic and often does not suggest a deep infection.
A CT scan may show fluid or gas collections or inflammatory changes in part of the sternum and rules in or out involvement of the aortic wall, cardiac chamber, or bypass grafts.
Sternal wires somewhat impair interpretation of signs of sternal inflammation and additional tests such as radionuclide scanning using Indium-labeled
white cells may be needed. This test has a specificity of 95 percent.
The clinical signs, CT scan, and location of wound drainage usually suffice for both the diagnosis and localization of the infected tissues.
Appropriate antibiotics are given intravenously before and up to 4 or 6 weeks after the wound is opened. Past therapy prescribed opening the wound, debriding necrotic tissue, and allowing the open wound to granulate in with multiple daily packing. This method was associated with a 25 percent rate of recurrence, prolonged hospital stays, considerable patient discomfort, and significant mortality.
Rarely aortic or coronary arterial bypass graft pseudoaneurysm or right ventricular rupture may develop during or after open wound management.
If osteomyelitis is absent or is totally excised, exploration and debridement followed by continuous irrigation and drainage of the reclosed wound may be an option. Both supra- and infrasternal drains are used and the wound is irrigated with dilute povidine-iodine or Dakin's solution at 20–110 mL/hr for 5–7 days or until the effluent drainage is sterile. The mediastinal drains are removed over a 48- to 72-hour period. This method is associated with recurrence rates up to 2 percent but is less traumatic than the use of muscle flaps or omentum and nearly as efficacious. Additional advantages include a single operative procedure and early extubation and ambulation.
An alternative method uses mobilized muscle flaps or omentum to sterilize and close the infected wound . The wound is opened, debrided of necrotic tissue and bone, and thoroughly irrigated. It then may be packed for 4 or 5 days to permit granulation tissue to form. After that interval, the sternal edges are reapproximated, and the sternum is covered by mobilizing both pectoralis muscles as flaps sewn over the wound. If the wound is prepared for irrigation prior to closing the sternum, the muscle flap procedure may be done immediately. Occasionally a rectus muscle flap or omentum is needed to cover the caudad portion of the wound.
Omentum is useful for filling dead space beneath the sternum or for policing inflamed mediastinal tissues but is associated with significant discomfort and temporary ileus.
The recurrence rate of muscle flap procedures is approximately 10 percent. The most-common complication is bleeding beneath the flaps or dehiscence of the flap suture line. Postoperative functional testing indicates minimal disruption of chest wall mechanics and no significant impairment in breathing or activity.
The mortality associated with deep wound infections ranges from 10 to 15 percent.
COMPLICATIONS SPECIFIC TO ORGAN SYSTEMS
Heart and Pericardium
Postoperative complications involving the heart and pericardium are common after cardiac surgery primarily because of arrhythmias, conduction disturbances, and manifestations of ischemia. Prevention and control of these complications have had a major role in the evolution of cardiac surgery and in the successful outcome of most operations.
Atrial arrhythymias, primarily atrial fibrillation or, less commonly, atrial fluttter, occur in 10–40percent of patients after open cardiac surgery.
The usual onset is 1–3 days after operation, with a peak incidence at 48 hours; however, the arrythymia may occur at any time, including shortly after discharge.
Increasing age is the most consistent predisposing factor; less-constant antecedent conditions include valve surgery, history of rheumatic fever, duration of aortic cross-clamp time and cardiopulmonary bypass, method of cardioplegia, and abrupt stoppage of ß-blocking agents. Acidosis, hypokalemia, or hypoxemia may contribute to the onset of the arrhythmia and should be corrected prior to initiating definitive therapy.
In postoperative patients the diagnosis of atrial fibrillation or flutter is usually made from the electrocardiographic monitor or occasionally from a postoperative electrocardiogram.
A few patients experience symptoms of lightheadedness or palpitations, and inferequently a patient develops hypotension and reduced cardiac output from very rapid atrial fibrillation or flutter and requires prompt resuscitation. The diagnosis is made by electrocardiogram; in equivocal cases the atrial electrogram obtained from temporary atrial wires is helpful. Immediate electrical cardioversion is recommended for unstable, symptomatic patients. Stable patients with atrial flutter usually are converted to lower ventricular rates by overdrive pacing followed by anti-arrhythmic drugs.
In all patients antiarrhythmic drugs are given first to control ventricular rate by slowing intranodal conduction and second to achieve conversion to sinus rhythm. Class Ia drugs (e.g., Procainamide), and calcium-channel blockers frequently are prescribed, but all depress myocardial contractility to some degree. Digoxin is effective for chronic control. Amiodarone may be needed for refractory patients.
Attempts to prevent atrial fibrillation and flutter by prophylactic therapy are only partially successful. Large studies suggest that ß-blockers, such as propanalol, atenolol, and metoprolol, reduce the incidence of postoperative arrhythmias to some degree, but digoxin, calcium-channel blockers, and amiodarone are ineffective.
Treated postoperative atrial arrhythmias are usually well tolerated, and many patients revert to sinus rhythm during the first month after hospital discharge and no longer need drugs prescribed for rate control.
Patients who remain in atrial fibrillation have a two- or threefold increase in the risk of stroke, and long-term anticoagulation is recommended in the absence of contraindications.
Despite the morbidity of atrial fibrillation, early and late mortality rates do not appear increased by the dysrhythmia.
Postoperative ventricular arrhythmias range from occasional premature beats, bigeminy, trigeminy, and nonsustained ventricular tachycardia to sustained ventricular tachycardia and ventricular fibrillation. The benign arrhythmias occur in 20–60 percent of patients and infrequently produce symptoms or require treatment.
The incidence of sustained tachycardia or ventricular fibrillation after cardiac surgery ranges 0.4–1.4 percent.
These potentially lethal arrhythmias often are unexpected and may occur at any time during hospitalization and soon after discharge.
Predisposing factors include myocardial ischemia, low cardiac output, metabolic derangements, drug interactions, and severe left ventricular dysfunction (ejection fraction less than 40 percent).
Prophylactic correction of hypoxemia, acidosis, hypokalemia, and hypomagnesemia is particularly important in the immediate postoperative period. Development of ventricular arrhythmias should prompt evaluation for ongoing myocardial ischemia.
Immediate cardioversion followed by resuscitation and antiarrhythmic therapy is essential for sustained ventricular tachycardia and ventricular fibrillation. Once the patient is resuscitated, a cause for the event should be sought and corrected if possible (e.g., hypoxemia, hypercarbic, etc.). Because these arrhythmias are lethal, electrophysiologic testing is necessary to determine effectiveness of specific drugs in individual patients. This should be done before hospital discharge, and occasional patients may require an implanted automatic internal cardiac defibrillator prior to hospital discharge.
Sustained ventricular tachycardia and fibrillation have an associated mortality up to 44 percent that can be substantially reduced by aggressive therapy.
Transient conduction disturbances after open cardiac surgery are very common, and most do not require treatment other than transient pacing via temporary pacing wires.
The incidence of permanent disturbances varies widely but is as high as 34–55 percent in subsets of patients with coronary arterial disease
Hemiblock and bundle branch blocks are rarely symptomatic, but atrioventricular block and sinus node dysfunction that occur in 0.5–4 percent of patients usually require a pacemaker.
Possible contributing factors to the development of postoperative conduction disturbances include the severity of coronary arterial disease, particularly of septal vessels, duration of aortic cross-clamping and cardiopulmonary bypass, method of cardioplegia, depth of myocardial hypothermia, patient age, and specific operation.
Persistence of sinus node dysfunction or atrioventricular block beyond 4 or 5 days is an indication for a permanent pacemaker.
PERIOPERATIVE MYOCARDIAL INFARCTION
The reported incidence of perioperative myocardial infarction varies widely (2–30 percent) because of differing definitions and criteria for infarction but in most series is 3–7 percent.
Possible causes of infarction include incomplete myocardial protection during aortic cross-clamping, incomplete revascularization, vasospasm, atheromatous emboli from previous bypass grafts or the aorta, air embolism, and thrombosis of either a native vessel or a new graft.
Myocardial revascularization patients are at higher risk of perioperative infarction than patients having other cardiac procedures. With revascularized patients risk factors for infarction include extensive coronary arterial disease, prolonged aortic cross-clamp and cardiopulmonary bypass times, older age, and preoperative depressed left ventricular function.
Studies suggest that up to 80 percent of newly infarcted areas are supplied by patent bypass grafts.Improvements in cardioplegia have reduced the number of infarcts in areas supplied by bypass grafts, however, many infarcts are associated with reduced flow in the bypass conduit.
The reasons for reduced flow may be mechanical obstruction, limited runoff within the supplied vascular bed, emboli, or vasospasm of downstream native coronary vessels.
Perioperative infarction traditionally is diagnosed by the electrocardiogram and elevated serum levels of creatine kinase isoenzyme (CK-MB).
ST depression, T wave inversion, and particularly new Q waves with a significant increase in CK-MB are suggestive of perioperative myocardial damage, but often patients do not have evidence of compromised cardiac function.
In patients with ECG and enzyme evidence of infarction and hemodynamic instability, bedside echocardiography may be helpful in localizing areas of reduced wall motion that may indicate ongoing myocardial ischemia that is potentially reversible.
Emergency coronary angiography may show coronary vasospasm that may be responsive to calcium-channel blockers or nitrates or conduit complications that may require interventional cardiology or surgical exploration.
The risk of additional morbidity and mortality in patients who suffer perioperative infarction may be 2.5 times greater than with comparable patients who do not have infarction.
Patients with low cardiac output following perioperative infarction should have aggressive diagnostic evaluation and also mechanical circulatory support with an intra-aortic balloon pump.
Past experience with more advanced methods of circulatory support, such as left ventricular assist devices, generally has not been very successful, but more-recent experience is considerably better
Patients below age 65 who suffer massive myocardial infarction may be candidates for mechanical circulatory bridging to transplantation
bridging patients with recent myocardial infarction without explanting the native heart and providing total mechanical support is associated with significant morbidity and mortality.
EARLY AND LATE PERICARDIAL TAMPONADE
Although the majority of patients develop small, posterior pericardial effusions after open cardiac surgery, 3–6 percent develop early tamponade that requires reoperation.
Early pericardial tamponade is directly related to persistent mediastinal bleeding and may progressively reduce cardiac output despite adequate filling pressures. Typically, right atrial, pulmonary arterial, and wedge pressures trend toward equality.
However, loculated clot or fluid compressing the heart may prevent equalization of filling pressures but still compromise cardiac output.
Patients usually have excessive blood loss from chest tubes or a sudden decrease in previously brisk chest tube drainage.
Chest X-rays may not show a widened mediastinum in the AP view, and chest tube suction may fail to relieve the tamponade. The condition must be distinguished from perioperative infarction, right ventricular infarction, or severe left ventricular dysfunction from other causes. Although these conditions may be differentiated from tamponade by careful evaluation of pulmonary arterial catheter tracings, transthoracic or preferably transesophageal echocardiography reliably makes the diagnosis but may not be quickly available if the circulation deteriorates rapidly.
If tamponade is even a remote possibility, transfer to the operating room and emergency exploration of hemodynamically deteriorating patients with or without a definitive diagnosis may be lifesaving and is unlikely to harm patients with other causes of low cardiac output that may need mechanical circulatory assistance.
Symptoms of tamponade that develop more than 1 week after operation usually are categorized as delayed or late tamponade.
The reported incidence of late tamponade varies 0.5–2.0 percent.
The classical symptoms of constrictive pericarditis usually are absent; typically patients present with low cardiac output and refractory heart failure and complain of progressive dyspnea, orthopnea, and fatigue.
Neck veins may be distended; heart sounds are rarely attenuated, and heart size is not enlarged by chest X-ray. The electrocardiogram is not diagnostic. The diagnosis is made by echocardiograms that demonstrate the effusion.
The mechanism of late tamponade is incompletely understood but may be related to anticoagulation, the postpericardiotomy syndrome, excessive perioperative mediastinal drainage, chyle leak, and infectious pericarditis. Although effusions causing late tamponade usually present within 1 month of operation, delays as long as 6 months have been reported.
Late effusions may be aspirated by needle with ultrasound guidance to reverse the impaired hemodynamics. The rate of recurrence is low.
Patients on anticoagulants or with loculated effusions may require subxiphoid exploration and finger dissection of loculations.
Reexploration and pericardial stripping are rarely needed.
Constrictive pericarditis following cardiac surgery was first reported in 1975 and now complicates 0.2–0.3 percent of all operations without predilection to the type of procedure. The disease progresses from pericardial hemorrhage and inflammation to eventual organization into a fibrotic, pericardial shell that may contain calcium. The etiology of the process is unclear; postoperative wound infection, irrigation with povidine-iodine or antibiotics, dry pericardium, and bleeding plus pericardial trauma have been blamed. Nearly half of the patients have a history of post-cardiotomy syndrome.
Patients complain of dyspnea with minimal exertion, fatigue, and peripheral edema and present 2 weeks to 17 years after operation.
Symptoms and signs are non-specific, and the ECG often shows nonspecific ST segment changes. The chest X-ray may show cardiomegaly, however. Echocardiography, MRI, and CT scan all demonstrate pericardial thickening, effusions, and occasional pericardial calcium.
The most-common echocardiographic findings show biatrial dilatation, small to normal ventricular size, and an unyielding shell of pericardium.
Corticosteroids and nonsteroid anti-inflammatory agents generally are ineffective in preventing constrictive pericarditis in patients with the post-pericardiotomy syndrome, but a tapered dose of corticosteroids is recommended in patients with evidence of constrictive pericarditis within 2 months of operation if they are clinically stable
Persistent symptoms after 2 weeks of steroids, presentation after 2 months, or a compromised circulation are indications for surgery. Ideally the fibrotic pericardium is stripped from the epicardium without injury to either the heart or any bypass grafts.
The heart is decorticated as completely as possible and usually responds with immediate improvement in performance. Sometimes hemodynamic recovery is delayed, possibly because of myocardial atrophy beneath the fibrotic peel. Any threats of recurrence may respond to corticosteroids.
The mortality associated with late stripping ranges 5–15 percent.
The postcardiotomy syndrome or postpericardiotomy syndrome was first described after closed heart operations in 1953 and recognized to be similar in presentation to the syndrome described by Dressler after myocardial infarction.
In adults the incidence after open heart surgery is approximately 18 percent and decreases with advancing age.
The etiology is not totally clear, but the disease appears to be an autoimmune phenomenon associated with high titers of heart-reactive antibodies that develop in all patients who have open heart surgery.
Two-thirds of patients with the syndrome also have antibodies that react with a panel of eight common viruses.
The disease may progress to pericardial effusion and infrequently constrictive pericarditis.
The most-common presentation includes fever, pleuritic pain, malaise, and a pericardial friction rub. Occasional patients develop pleural or pericardial effusions or have pain with swallowing. Symptoms usually develop within the first month after operation and usually after the first week.
Late presentations up to 190 days after operation are described.
The disease must be differentiated from other postoperative fevers including atelectasis, pneumonia, endocarditis, and wound and urinary tract infection. A mild leukocytosis may be present, and the ECG may show nonspecific ST changes
The disease is self-limited with a mean duration of symptoms lasting 1 month. Patients are encouraged to limit activity, and analgesics (oxycodone, codeine) may be needed for pain relief. Nonsteroidal anti-inflammatory agents usually are prescribed; patients with severe or persistent symptoms may require a tapered dose of corticosteroids.
Up to 20 percent of patients develop a recurrence.
The syndrome is not associated with increased mortality.
Chest, Lung, and Airway
Although many advances have been made in anesthetic management, cardiopulmonary bypass, chest physiotherapy, assessment of pulmonary function, intrathoracic imaging, and infection control, pulmonary complications are common after open heart surgery and are reported in as many as 30 percent of patients.
The incidence is higher in older, sicker patients and those with compromised pulmonary function. Prevention of pulmonary complications and prompt effective therapy impact directly on length of hospital stay and mortality after cardiac surgery.
One to two percent of patients may develop pneumothorax after cardiac surgery.
The cause may be direct lung injury during division of the sternum, insertion of venous catheters, internal mammary artery harvest, insertion of a chest tube for effusion or hemothorax or from sternal wires during closing. Patients with apical blebs, emphysema, or bullae may develop pneumothorax during mechanical ventilation. Air may enter the hemithorax from chest tube removal or enter the opposite hemithorax across the anterior mediastinum from a pneumothorax of one lung.
All except very small pneumothoraces are identified readily by plain chest X-ray.
The clinical presentation varies. Pneumothorax may be discovered as an incidental finding on chest X-ray or cause cardiovascular collapse owing to tension pneumothorax in patients who are mechanically ventilated. Between these two extremes patients may develop dyspnea, pleuritic chest pain, hypoxia, arrhythmias, increased airway pressures, or hypotension. In stable patients the diagnosis is suspected by absent breath sounds and confirmed by chest X-ray.
With tension pneumothorax respiratory distress is present, and the trachea is deviated away from the affected lung.
Tension pneumothorax requires immediate relief by insertion of a sterile thoracostomy tube in the second anterior interspace in the midclavicular line. Closed suction is maintained until the patient is able to breath spontaneously. Lung leaks nearly always close spontaneously with reexpansion and adhesion to the chest wall. Very rare patients may require multiple chest tubes, thorascopic surgery with bleb or bulla removal, or pleurodesis.
Accumulation of blood or irrigation fluid in one pleural cavity, usually the left, is not unusual after open heart surgery. If the hemithorax is opened during operation, a chest tube is placed prior to closure. However, small unnoticed holes and tears may allow entry of mediastinal blood or irrigation fluid that is discovered on the postoperative chest X-ray. These collections should be treated by thoracostomy tube to allow the lung to completely expand and to remove the fluid.
Bleeding into the hemithorax occurs most often from the harvest site of the internal mammary artery.
These collections usually are not substantial and do not often affect hemodynamics, but occasionally an insidious, persistent bleeding vessel produces a large hemothorax over time. These patients may develop hypovolemia from the unrecognized bleeding and require several transfusions in addition to chest tube drainage and often reexploration. More-localized, undrained blood accumulations in the chest reduce pulmonary function by direct compression of the lung, increase the risk of infection in the compressed lung, and over 2 or 3 weeks' time produce a fibrinous peel that must be removed eventually.
Decortication is most easily done by thorascopic surgery early before the fibrinous peel is completely organized; fibrous peels discovered 3 to 4 weeks after hemothorax may require decortication.
LATE AIRWAY INJURIES
The endotracheal tube is involved in most postoperative airway injuries, and complications associated with its insertion are presented above. Late laryngeal complications are uncommon and may be produced by abrasion of the vocal cords or cuff injuries to the recurrent laryngeal nerve.
The mobility of the larynx increases the likelihood of abrasive irritation of the cords and temporary swelling and hoarseness.
A nasogastric tube combined with an endotracheal may cause posterior ulceration of the arytenoid cartilage.Recurrent laryngeal nerve injuries are related to endotracheal cuff pressure and rarely, cannulation of the jugular vein or harvesting an internal mammary artery.
The recommended position of the endotracheal tube cuff is at least 1.5 cm below the true vocal cords; the tip should be 2 cm above the tracheal carina.
Last, prolonged intubation may produce swallowing difficulties and laryngeal aspiration following extubation, particularly in older patients. Most laryngeal and swallowing problems resolve with time, but many increase length of stay and costs.
Injuries produced by prolonged overdistention of the endotracheal cuff are uncommon because of improved cuff designs that prevent ischemic injury to the tracheal wall and eventual stricture formation. Rarely, inflation of the cuff may cause posterior wall rupture that can be extended toward the carina by mechanical ventilation.
This injury may produce subcutaneous emphysema immediately and prompt immediate bronchoscopic examination to evaluate the injury; if possible, the operation should be delayed. Lacerations greater than one-third the circumference of the trachea should be closed at operation; small lacerations may be treated conservatively with antibiotics.
The trachea rarely is injured during cardiac operations but may be injured during aortic surgery near the isthmus and aortic arch. If injured, the trachea should be repaired primarily and covered with a muscle flap or adjacent tissue for reinforcement.
Up to 4 percent of patients undergoing cardiac surgery develop postoperative pneumonia. The incidence is increased in patients with underlying pulmonary disease, smokers, and aged patients with the potential for aspiration and is highest in patients who require prolonged ventilatory support.
Cardiopulmonary bypass activates and weakens the whole body defense system, and chronic obstructive lung disease and smoking weaken the intrinsic pulmonary defense system to increase the risk of lower airway infection.
Fever, productive sputum, pathogenic organisms identified by gram stain or culture in airway secretions or blood, together with chest X-ray signs of a new or progressive infiltrate, an area of consolidation, or a cavity establish the diagnosis. Immediate treatment with one or more broad spectra or preferably organism-specific antibiotics is indicated. In addition chest physiotherapy, encouragement of cough, and effective tracheal-bronchial suctioning are initiated to help remove secretions. Occasionally bedside bronchoscopy may be done to obtain a specimen for culture or to clear an airway of obstructing mucus. Concomitant pleural effusions are drained dry by needle aspiration or chest tube and cultured to prevent empyema. [,
If empyema develops, thorascopic surgery to completely drain the infection and reexpand the underlying and adjacent lung is mandatory.
Preventive measures to reduce the incidence of postoperative pneumonia include chest physiotherapy, incentive spirometry, preoperative antibiotic prophylaxis, and bronchodilators in patients with chronic bronchitis. Unfortunately, smoking must be stopped at least 2 months prior to operation to significantly reduce postoperative pulmonary complications, but cessation for this length of time is effective.
] Treatment of chronic bronchitis and surveillance cultures before operation is prudent, and only emergency procedures proceed without this preparation. The value of chest physiotherapy and incentive spirometry has been questioned on a cost basis, but both activities help to mobilize patients, increase tidal volume, and overcome fear of breathing-induced wound pain.
Use of antacids and H2-blockade for stress ulcer prophylaxis does not appear to predispose cardiac patients to aspiration pneumonitis, although other patients may be at risk.
PHRENIC NERVE INJURY
The exact incidence of unilateral phrenic nerve injuries during cardiac surgery is not clear but appears greater than 2 percent of patients.
Likewise the causes of the injury are not clearly understood. Direct injury during harvest of the internal mammary artery, cold injury owing to pericardial ice slush, and inadvertent stretch injuries during intrapericardial manipulations of the heart are documented causes, but the injury also occurs in some patients without apparent reason.
Cold reduces nerve conduction and causes direct injury to the nerve in animals, and intrapericardial ice slush increases the incidence of phrenic nerve, particularly left phrenic nerve, paralysis in patients.
The effectiveness of insulating partitions and cooling jackets recommended to prevent cold injury is not clearly established.
Bilateral phrenic nerve palsy occurs much less frequently, but the consequences of the complication are more serious.
The diagnosis usually is suspected by noting a high diaphragmatic shadow or lower lobe atelectasis on chest X-ray.
Nerve conduction and fluoroscopic and ultrasonic studies, each with limitations, are used to confirm the diagnosis in patients with persistent abnormal chest X-rays or pulmonary dysfunction. Although often benign, unilateral phrenic nerve paralysis increases the likelihood of atelectasis, pneumonia, and prolonged respiratory dependence, particularly in patients at risk for postoperative pulmonary complications. ,
Bilateral phrenic nerve injuries may be devastating and necessitate tracheostomy and prolonged mechanical ventilation.
These patients have a high incidence of cardiorespiratory arrest, nosocomial pneumonia, and eventual death. Eventually nearly all phrenic nerve palsies associated with cardiac surgery resolve, but delays up to 18 months are described.
CHRONIC VENTILATORY DEPENDENCE
The vast majority of cardiac surgical patients are extubated within 24 hours of operation, and younger, low-risk patients often are extubated within a few hours of operation.
A subset of patients requires ventilatory support for more than 3 days for a variety of reasons. Often comorbidity, such as perioperative myocardial infarction, stroke, or renal failure, as opposed to pulmonary problems, is the reason for continuing mechanical ventilation.
Prolonged mechanical ventilation exposes the patient to the risks of nosocomial infections, airway injuries, debilitation, stress ulceration, despondency, and even adverse cardiac events.
Nearly one-third of those ventilated for more than 3 days die of the primary event that necessitated continued ventilation.
Management of these patients is a team effort and usually includes critical care specialists, infectious disease specialists, respiratory and physical therapists, and speech physiotherapists. Provision must be made for nutritional support and infection control. Intravenous catheters must be changed every 3–4 days, and entry sites must receive daily cleansing. Prophylactic measures are needed against stress ulceration, decubitus ulcers, and muscular atrophy. Usually the endotracheal tube using large volume, low pressure cuffs to reduce airway injury is used for the first 2 weeks
. Patients who still require ventilation after 2 weeks generally have tracheostomy with little risk of sternotomy wound contamination.
A weaning protocol is established as soon as possible, and every effort is made to help the patient retain respiratory muscle strength and prevent atrophy. A variety of weaning protocols, including intermittent mandatory ventilation, continuous pressure support, and continuous positive airway pressure, are used. The inspired oxygen tension should be reduced as low as possible to maintain peripheral oxygen saturations > 95 percent. Ventilatory gases must be heated and humidified and ventilators and connecting tubing cleaned or changed frequently. High frequency or “jet” ventilation is used rarely in postoperative cardiac patients. Care requirements for prolonged chronic ventilation incur major costs in both time and money, and unfortunately a high percentage of patients, particularly aged patients, fail to survive.
Adult Respiratory Distress Syndrome (ARDS)
ARDS is a syndrome characterized by refractory hypoxemia, noncompliant lungs, and diffuse and sometimes homogenous infiltrates throughout both lungs on chest X-ray. The hypoxemia is due to a diffuse high permeability pulmonary edema that usually involves the entire lung and fills the alveoli with plasma and scattered red cells. Alveolar surfactant is inactivated by the proteinaceous exudate. Patients develop a high alveolar-arterial oxygen difference and large shunt fraction but do not have high left atrial pressures. The etiology of the syndrome, which may affect up to 1.5 percent of cardiac surgical patients, is not known, but the inflammatory reaction associated with cardiopulmonary bypass is a contributing factor in that extracorporeal perfusion initiates a massive inflammatory response and the production and release of a host of vasoactive substances capable of increasing pulmonary capillary permeability ARDS may occur in sporadic patients after severe trauma, septicemia, acute transient increases in pulmonary venous pressure, and other conditions that fill the alveoli with a proteinaceous fluid. ARDS is associated with severe morbidity and a mortality approaching 50 percent.
Treatment is preventive and supportive. Inspired oxygen is reduced to the lowest levels capable of maintaining adequate oxygen-carrying capacity. Diuresis is vigorously pursued. Cardiac output is maintained at high levels; high filling pressures are avoided. Lungs are ventilated with elevated end-expiratory pressures, reduced tidal volumes, and as low inspired oxygen concentrations as possible. Reduced arterial oxygen tensions are tolerated to reduce inspired oxygen concentrations. Bronchodilators are used to relieve bronchospasm, and secretions are removed by frequent aspiration. Infection is prevented by prophylactic broad spectrum antibiotics, surveillance cultures, and pulmonary toilet. With recovery alveolar fluid and protein are gradually cleared; both the alveolar-arterial oxygen difference and chest X-ray improve concomitantly.
ACUTE RENAL FAILURE
During cardiac surgery the kidneys may be damaged by hypoperfusion because of low systemic blood pressure, low cardiac output, and vasoconstriction from circulating vasoconstrictors and hypothermia and from bombardment by microemboli. Although attenuated by hemodilution, cardiopulmonary bypass reduces renal and plasma flow and creatinine and free water clearance. Severe hemolysis, nephrotoxic drugs, or atheromatous emboli are other uncommon injuries to the kidneys during open heart surgery. Not surprisingly, up to 15 percent of patients develop some evidence of renal dysfunction following cardiac surgery.
Mild renal dysfunction is defined as an increase in blood creatinine of 100–150 percent over baseline without the need for dialysis.
More-severe renal failure occurs in 1.5–4.0 percent of patients and is primarily related to preoperative renal function, postoperative cardiac output, ischemic periods during operation, microemboli, preoperative administration of radiographic contrast materials, and toxic drugs. The need for several transfusions, use of vasopressors, episodes of cardiac arrest or low cardiac output, use of the intra-aortic balloon pump, older age, insulin-dependent diabetes, reduced urine output during cardiopulmonary bypass, and deep hypothermia also correlate with postoperative acute renal failure.Acute renal failure generally is defined as oliguria (urine output less than 400 mL/day), an increase in serum creatinine above 5 mg/dL, glomerular filtration rate less than 30 mL/min/m 2 , or the need for dialysis.
The need for dialysis is estimated to be as high as 1.5 percent of patients who have cardiac surgery, but this incidence undoubtedly reflects the age and preoperative renal status of operated patients. Polyuric renal failure usually develops after recovery from oliguric renal failure and is identified by a high urine volume containing increased concentrations of sodium associated with a rising serum creatinine.
Treatment of acute renal failure requires careful management of fluid balance, avoidance of nephrotoxic drugs, reduction in doses of drugs cleared or excreted by the kidneys, measurements of blood concentrations of potentially toxic drugs, and prevention of infection and other complications. Every effort should be made to optimize cardiac output. Initially if urine is being made, tubular diuretics are given in an attempt to increase urine output. However, if early postoperative fluid accumulation is excessive, fluid may be removed rapidly by continuous arterial venous hemofiltration using femoral percutaneous cannulas if cardiac output is adequate. Venovenous hemodiafiltration is a newer method to correct fluid and electrolyte imbalances and is not dependent on cardiac output.
Plasma potassium concentrations are monitored carefully, and potassium usually is removed from intravenous fluids. High potassium concentrations (> 6.0 meq/L) are aggressively treated with bicarbonate, 50 mL of 50 percent glucose with 10 units of insulin, and 0.5 gm of calcium. Kayexalate ion exchange resins in 25 percent sorbitol given by nasogastric tube or enema are used occasionally, but more often progressive increases in potassium are managed by hemodialysis. Elevated potassium, excess fluid, creatinine over 5 mg/dL, and lethargy generally are indications for hemodialysis on a daily or alternate-day basis. Peritoneal dialysis is now used uncommonly.
Every effort is made to prevent infection, and if unexplained fever, leukocytosis, or reduced cardiac output with peripheral vasoconstriction develops, blood, sputum, and urine cultures are obtained and effective, broad spectrum antibiotics are started or changed without proof of infection. Renal failure patients frequently die of infection before renal function returns and frequently develop serious unrelated complications. Perioperative myocardial infarction is associated with 20 percent of patients with renal failure.
The mortality in patients who develop acute renal failure is approximately 45 percent. Mortality also is elevated in patients with mild renal dysfunction (creatinine > 1.5, < 2.5 mg/dL).
COMPLICATIONS ASSOCIATED WITH CHRONIC RENAL FAILURE
Patients who receive chronic dialysis or have a renal transplant often are eligible for open cardiac surgery but require special management to avoid complications and mortality. Progression of coronary arterial occlusive disease is accelerated by dialysis dependency, and the longevity of bioprosthetic heart valves is substantially reduced. Chronic dialysis patients are susceptible to metabolic and hematologic derangements and require special care of dialysis access catheters and grafts and fluid management. Dialysis patients with azotemia have reduced platelet function, coagulation abnormalities, anemia, and reduced blood protein concentrations and are more susceptible to infection because of suppression of the immune system.
Transplant patients, of course, receive immunosuppressive therapy and also are more susceptible to postoperative infection.
Bleeding is the most common intraoperative complication and occurs in up to 10 percent of patients.] Bleeding is primarily related to platelet dysfunction and mild to moderate thrombocytopenia that produces an increase in preoperative bleeding times. Abnormalities in the structure of von Willebrand factor, an adhesive protein for platelets, also occur in uremic patients. Thus uremic patients require intraoperative and postoperative transfusions of platelets and fresh frozen plasma and may also benefit from desmopressin, which increases factor VIII-von Willebrand factor concentrations. Chronic dialysis patients often receive recombinant erythropoetin to correct chronic anemia. A hematocrit over 25 percent is recommended before operation, and patients may require transfusion.
During operation a dialysis unit in the extracorporeal circuit permits control of potassium and fluid balance. Patients usually are dialyzed the day before operation and also the day afterwards.Venovenous hemodiafiltration also may be useful in these patients if their indwelling arteriovenous fistulas are not serviceable temporarily. During operation these shunts are carefully padded and protected, and no intravenous catheters are inserted in that arm. Renal transplant patients usually need stress dose corticosteroids in the perioperative period, and systemic blood pressure is maintained above 70 mmHg (mean) during cardiopulmonary bypass. Urine output is maintained postoperatively at 50–100 mL/hr by adequate perfusion pressures and diuretics.
A review reports that the overall survival rate for cardiac surgery in chronic dialysis patients is 9 percent. ] More-recent experience reports hospital mortalities 4–5 percent for both revascularization and valve operations. Mortality is increased by the preoperative presence of congestive heart failure and emergency surgery; long-term survival is adversely affected by age above 60 years Actuarial survival at 5 years is 55 percent for chronic dialysis patients; 3-year survival is over 80 percent for renal transplant patients who have open heart surgery. [238 ] , [259 ] , [260 ]
Peripheral Vascular Complications
Peripheral vascular complications in the femoral region are not uncommon because the easy access and size of these vessels encourage insertion of necessary cannulas for monitoring, cardiac catheterization, blood processing (e.g., hemofiltration), and circulatory support. Local hematomas occur frequently if pressure control of removed catheters and cannulas does not stop blood egress. With the rare exception of pending skin necrosis, these hematomas should not be drained; reabsorption may require several weeks. If a large catheter is inserted through a cutdown into the femoral or iliac artery, surgical closure of the artery is recommended at the time of withdrawal. Occasionally arteriovenous fistulas complicate cardiac catheterization. This complication is identified by ultrasound and requires surgical closure. Thrombotic occlusion from percutaneous catheterization or cannulation requires operation to reestablish flow to the lower extremity. A needle, catheter, or cannula may raise an atherosclerotic plaque to compromise or obstruct the vascular lumen. Because these complications occur relatively frequently and are managed relatively easily with few long-term complications, the incidence is not known. Patients who have generalized vascular disease and those who are active smokers are at increased risk of lower extremity vascular complications after open heart surgery. [264 ]
Lower extremity vascular complications occur in approximately 20 percent of patients who require the intra-aortic balloon pump (IABP), and the IABP is responsible for approximately 85 percent of lower leg ischemia after open heart surgery. [264 ] Distal ischemia is more common in patients with low cardiac output or cardiogenic shock and those who require high doses of vasopressors. [265 ] The status of the dorsalis pedis and posterior tibial pulses should be monitored frequently using a portable Doppler probe in patients with an IABP (Fig. 13-10) . Loss of sensation, poor capillary filling, and absence of venous filling are signs of ischemia and prompt steps to immediately relieve the ischemia. If the balloon catheter cannot be removed, it sometimes can be transferred to the other leg. If the preoperative vascular system is normal, the transfer is well tolerated without ischemia in most individuals and reverses the ischemia in the affected leg and foot without operation in approximately 30 percent of patients. [264 ] , [265 ] The majority of patients require surgery to fully restore the circulation. [265 ] This may involve a vascular patch at the site of insertion if the intra-aortic balloon catheter is transferred or removed. More commonly the IABP is not transferred and a cross leg or axillary-femoral prosthetic graft is performed under local anesthesia to restore circulation to the ischemic leg (Fig. 13-5) . [265 ] – [268 ] Twenty-five to thirty percent of patients with ischemia due to the IABP require amputation; overall mortality in this group of patients is approximately 45 percent as opposed to a mortality of 11 percent in postoperative patients with leg ischemia who do not need the IABP. [264 ]
Symptoms of lower leg ischemia also may occur without an IABP in a minority of patients. Approximately two-thirds are caused by thrombotic occlusion secondary to arterial puncture and may be aggravated by vasopressors. [264 ] About one-third of patients develop embolic occlusions, particularly “trash” emboli from dislodgement of atheromata from insertion of catheters into the femoral or iliac arteries and the aorta. If femoral and popliteal pulses are reasonably strong, the foot usually survives, and attempts to remove distal emboli usually are unrewarding. If proximal pulses are diminished or absent, operation is needed. Most of these patients require operation to restore adequate circulation to the lower extremities.
Rarely, heparin-induced thrombocytopenia and thrombosis cause the “white clot syndrome” and vascular occlusion of the small arteries of the extremities (Chapter 9).
Gastrointestinal (GI) complications following cardiac surgery range 0.41–2 percent of patients. [57 ] , [269 ] – [271 ] Often GI complications are part of a constellation of problems in patients with low cardiac output, respiratory failure, renal failure, and/or central nervous system deficits. [272 ] A period of low cardiac output and reduced blood flow to the viscera is thought to contribute to the development of most postoperative GI problems. Although these complications also occur in noncardiac patients, the complications appear more severe after heart operations and are associated with increased morbidity and mortality. [273 ] – [275 ] This severity may, in part, be a result of delays in diagnosis because of anesthetic agents, inability of the sedated, intubated patient to complain, and metabolic disturbances. Early recognition and treatment is imperative for control of GI complications, and postoperative cardiac patients are better able to tolerate early effective operation than to survive major bleeding or abdominal sepsis. [276 ] , [277 ]
The incidence of gastrointestinal (GI) bleeding after open heart surgery ranges 0.35–3 percent. Patients usually bleed during the first month after operation and usually near the end of the first postoperative week. [269 ] , [271 ] , [273 ] , [274 ] Gastritis or peptic ulcer are the most-common causes, although esophagitis, ischemic bowel disease, diverticulitis, and A-V malformations may be responsible. Age and a prior history of GI bleeding are the most reliable predictors of postoperative bleeding. [278 ] H 2 blockade and H + , K + -ATPase inhibitors are recommended for prophylaxis. [278 ]
Melena is the most-common symptom, although hematemesis occurs. [277 ] Upper GI endoscopy is done first because of the prevalence of upper GI bleeding sources. [273 ] , [279 ] Bleeding points are either sclerosed or cauterized, and high doses of H 2 blockers are started. If the patient is stable, gastric resection with or without vagotomy is recommended for rebleeding, but lesser procedures, including reendoscopy, may be done if the age or clinical condition of the patient precludes immediate operation. [274 ] – [276 ] , [278 ] , [279 ] Postcardiotomy bleeding is associated with a high mortality that ranges 7.7–75 percent. [273 ] – [279 ]
Perforated ulcer after heart surgery occurs in 0.02–0.08 percent of patients and in half the patients is found by free abdominal air on a routine chest X-ray. [273 ] , [276 ] , [277 ] , [280 ] Other patients complain of upper abdominal pain and distention. Many patients have a previous history of ulcer disease. These patients are usually treated with an omental patch repair. Mortality ranges 30–50 percent and reflects delay in diagnosis and the general debilitated condition of the patient. [273 ] , [276 ] , [277 ] , [280 ]
Cholecystitis is the second most common GI complication and has an incidence of 0.2–0.5 percent after cardiac operations. These patients usually develop symptoms 5–15 days after operation and complain of fever, nausea, and vague, diffuse abdominal pain associated with a leukocytosis. The pain often is not localized to the right upper quadrant; therefore, the diagnosis often is delayed. Abdominal ultrasonography and nucleotide scanning in combination are more likely to be diagnostic than either test alone. [271 ] , [273 ] , [277 ] , [279 ]
Cholecystitis preferably is treated medically with intravenous fluids, bowel rest, and broad spectrum antibiotics. Because of a high incidence of ischemic injury to the gall bladder, cholecystectomy often is necessary. This is done preferably by laparoscopy. Cholecystostomy seldom suffices. Mortality is high, probably because of delay in diagnosis and the general condition of most afflicted patients soon after cardiac surgery. [273 ] , [274 ] , [276 ] , [279 ]
Twenty-five to thirty-five percent of postoperative cardiac patients develop asymptomatic hyperamylasemia, but only 1–2 percent develop symptomatic pancreatitis, and 0.13–0.6 percent have necrotizing pancreatitis. [281 ] – [283 ] The etiology is unclear; hypoperfusion, microemboli, and hypovolemia have been blamed. [274 ] Autopsy studies of patients who die 1 or more days after operation show evidence of pancreatic injury in 16–25 percent of patients. [283 ] Pancreatitis generally occurs within a few days after operation with symptoms of fever, nausea, epigastric pain, and a leukocytosis and elevated serum amylase and lipase. [271 ] , [283 ] Elevated enzyme levels may not always be specific for pancreatitis; therefore, the diagnosis is confirmed by computed tomography or ultrasound. [283 ]
Patients with hyperamylasemia are monitored to be sure enzyme levels trend lower and symptoms do not occur. Patients with mild pancreatitis are treated by intravenous fluids, nasogastric drainage, and bowel rest until serum amylase levels return to baseline. Necrotizing pancreatitis requires immediate operation with mobilization and debridement of the pancreas, wide drainage, and gastrostomy and feeding jejunostomy. The postoperative course often is complicated. [277 ] , [280 ] Mortality of severe postcardiac pancreatitis is over 50 percent in large series. [273 ] – [275 ] , [277 ] , [282 ] , [283 ]
Older age and generalized peripheral vascular disease may contribute to the development of ischemic colitis, but the complication also seems related to the need for emergency surgery and a period of perioperative hypotension. Evidence of emboli are lacking in pathologic specimens, and the disease typically presents 6 or more days after operation. The incidence of ischemic colitis is estimated to be 0.02–0.3 percent. [57 ] , [273 ] , [277 ] , [279 ] , [280 ] Symptoms usually are insidious with abdominal distention and vague complaints of discomfort and nausea. Severe pain, abrupt distention, vomiting, extreme leukocytosis, melena, and rapid deterioration are late manifestations of the condition. Sigmoidoscopy may provide the diagnosis; laparoscopy is more definitive. Arteriography may show vasospasm of mesenteric vessels, and occasionally individuals without gangrenous bowel benefit from a direct and continuous infusion of papaverine through an angiocatheter placed in the superior mesenteric artery.
At laparoscopy or operation large segments of bowel may be gangrenous or alternatively only patches of bowel ischemic. Necrotic bowel must be excised, but not infrequently the extent of the gangrene precludes salvage of the patient. [272 ] , [274 ] , [277 ] , [279 ] Since many afflicted patients are very old, mortality ranges 50–95 percent. [272 ] , [274 ] , [277 ] , [279 ]
The incidence of divericulitis after open cardiac surgery is 0.13–0.25 percent, and most patients have a prior history of the disease. Perioperative splanchnic hypoperfusion is believed a contributing factor. [269 ] , [272 ] , [279 ] Typically these patients develop fever, leukocytosis, left lower quadrant pain, and abdominal distention; endoscopy or CT scanning may aid the diagnosis. Nearly 50 percent of patients develop abdominal free air and are misdiagnosed as having perforated ulcer. [279 ] Operation is required for perforated diverticulitis; limited colectomy and diverting colostomy are recommended. Without perforation the disease is treated with intravenous antibiotics and bowel rest, usually with successful resolution of the inflammation. [279 ] Patients with perforated diverticulitis face a mortality rate of nearly 25 percent. [279 ]
Fifteen to twenty percent of patients develop transient increases in liver enzymes between the second and fourth postoperative days after cardiopulmonary bypass. The cause is not known but is probably related to blood trauma, hepatic congestion, and perhaps hypoperfusion during bypass. [270 ]
The incidence of hepatic dysfunction after heart surgery is 0.4 percent, but the incidence increases markedly to as high as 35 percent in patients who develop another intra-abdominal complication. [270 ] , [271 ] Progressive hepatic dysfunction manifested by cholestatic jaundice, increasing blood enzyme levels, and refractory coagulopathy develops in 0.03–0.23 percent of patients and usually is associated with multiple organ system failure and is essentially a terminal event. [271 ] , [284 ]
Three to five percent of patients require reexploration for bleeding after open heart surgery, and although up to one-third of patients do not need transfusion of homologous blood, bleeding is a persistent and serious complication that contributes to morbidity and, in debilitated patients, mortality. [285 ] – [285 ] In approximately two-thirds of patients a surgical bleeding source is found. [285 ] Common sites of ongoing hemorrhage include side branches of the internal mammary and gastroepiploic arteries and saphenous vein grafts, graft anastomoses, cannulation sites, aortic and cardiotomy incisions, insertion sites of pacing wires, mammary arterial harvest sites, thymus, and around sternal closure wires. Rarely extraordinary measures, such as packing the chest or girdling the aorta with Teflon felt, are necessary to staunch the bleeding. [289 ] , [290 ] Reexploration for bleeding is more common (~7 percent) in patients with previous operations and in patients having valve procedures. [285 ]
Chest tubes are monitored carefully immediately after operation, and blood is sent for measurement of platelet count, prothrombin time, and partial thromboplastin time unless these measurements were made in the operating room after cardiopulmonary bypass. The patient is warmed, and if bleeding appears somewhat brisk, airway end expiratory pressure is raised to 10–15 cm h 2 o in an attempt to tamponade bleeding sites. [291 ] – [294 ] Hypertension also is controlled. Chest tubes are stripped to prevent obstruction and to insure drainage.
Reexploration is indicated if sudden massive bleeding occurs, if chest tube drainage suddenly accelerates to suggest a surgical cause, or if chest tube drainage persists during the first few hours after operation. If bleeding exceeds 500 mL in the first hour after operation, 400 mL during each of the next 2 hours, 300 mL during each of the first 3 hours, or 1,000 mL in 4 hours, a return to the operating room is recommended. Although a surgical source is found in the majority of patients, one-third appear to have generalized, nonsurgical bleeding that is apparently related to a defect in coagulation. [285 ]
Nonsurgical bleeding problems related to open heart surgery are conveniently categorized as heparin related, platelet related, fibrinolysis, or due to lack of a soluble coagulation protein and are considered in detail in Chapter 9. [295 ] – [310 ] Deficiency of a soluble coagulation protein is rare and is primarily related to preoperative deficiencies; dilution and consumption during cardiopulmonary bypass seldom reduce concentrations to levels that fail to support coagulation. [311 ] Heparin- and platelet-related causes of nonsurgical bleeding are identified by measuring the prothrombin time, partial thromboplastin time, and platelet count immediately after operation. Excess heparin increases the partial thromboplastin time and is treated by additional protamine without fear of a protamine anticoagulation effect. An elevated prothrombin time indicates a defect in the extrinsic coagulation pathway and is treated with fresh frozen plasma (10–15 mL/kg). [366 ] Platelet transfusions (1 U/10 kg) are prescribed in bleeding patients for counts under 80,000/µmL, but platelet transfusions are recommended for bleeding patients soon after operation because of a functional deficit in most of the circulating platelets. Cardiopulmonary bypass routinely increases template bleeding times because of platelet dysfunction for several hours afterward. [303 ] Preoperative aspirin also inhibits platelet function. [307 ] , [312 ]
Fibrinolysis begins with the surgical incision and increases markedly with the onset of cardiopulmonary bypass. [309 ] Heparin fails to completely suppress thrombin formation; therefore, thrombin circulates and converts fibrinogen to fibrin, which is lysed by plasmin. [313 ] The most-effective management of fibrinolysis is prophylaxis by tranexamic acid, epsilon amino caproic acid, or aprotinin (Chapters 8 and 9). [314 ] – [332 ] Antifibrinolytic prophylaxis significantly reduces postoperative blood loss and the need for transfusions in both first time and reoperative patients. [324 ] Because of an abundance of fibrinogen, hypofibrinogemia rarely occurs, and supplemental fibrinogen (cryoprecipitate) usually is used with thrombin to produce topical fibrin clots. Antifibrinolytics preferably are given with the surgical incision; administration after bypass is less effective. [325 ]
The risk of blood-borne pathogens, particularly hepatitis and the human immune deficiency virus (HIV), has progressively decreased (Chapter 9), and modern cardiac surgery uses several different means to reduce postoperative anemia and the need for transfusion. These methods, antifibrinolytics and the availability of recombinant erythropoietin have increased the safety of cardiac operations for Jehovah's Witnesses. [326 ] – [328 ]
CENTRAL NERVOUS SYSTEM
Except for death, central nervous system (CNS) injuries are the most devastating complications of open heart operations. The reported incidence of central nervous system complications varies widely (0.7–5.0 percent) because of differences in definitions, heterogeneity of patient cohorts, timing of evaluations, and other factors. [329 ] – [337 ] Age is a specific risk factor for a postoperative neurologic deficit, and the incidence in patients over 75 years approaches 9 percent. [332 ] , [334 ] , [335 ] Patients with a preoperative history of cerebrovascular disease have a three-fold increased risk of a new neurologic deficit or worsening of a previous deficit. [329 ] , [337 ] The most-common permanent deficit is stroke, but reversible ischemic deficits, encephalopathy and coma, cognitive deficits, and seizures all may occur.
Cerebral macro- and microemboli or a period of hypoperfusion are the most common causes of postoperative CNS injuries. Sources of macroemboli include the ascending thoracic and arch aorta, the carotid arteries, thrombus, calcium, and debris from intracardiac surgery, and air. [329 ] , [332 ] , [336 ] , [337 ] Microemboli are generated by cardiopulmonary bypass (Chapter 9) and by specific surgical maneuvers such as cannulation and lifting the heart. [331 ] , [338 ] , [339 ] Hypoperfusion may occur preoperatively in hypotensive emergency patients but occurs infrequently during cardiopulmonary bypass. [332 ] , [334 ] Postoperatively prolonged hypotension and low cardiac output may cause cerebral dysfunction. [337 ] However, the combination of significant carotid arterial stenosis and hypotension may combine to produce an ischemic injury. The relationship between preexisting carotid disease and open heart surgery is presented in Chapter 20. Currently the possibility of an increase in postoperative CNS injuries during normothermic cardiopulmonary bypass is under intense investigation and is as yet unresolved. [340 ] – [345 ] Neurologic deficits associated with deep hypothermia and circulatory arrest are related to the duration of arrest, the temperature at the time of arrest, hyperglycemia, and possibly the management of blood pH and co 2 (Chapters 9, 10, 38, and 40). Intracranial bleeding is less common and usually complicates an embolus.
Postoperative neurologic deficits are determined early postoperatively initially by gross neurologic examination and later by more-detailed examination. Suspicion of a new or worse neurologic deficit is reason for a neurologic consultation and detailed inventory of the degree of abnormal nervous system function. Invariably either a CT scan or MRI of the brain is ordered. These studies help to differentiate new lesions from old, provide evidence of the probable mechanism of the deficit (embolus with or without associated bleeding, generalized hypoxia, or edema, etc.), and are helpful in formulating a prognosis. [330 ] , [333 ]
Aside from steps to reduce the incidence of macroemboli and to prevent postoperative hypotension and hypoperfusion, attempts to reduce postoperative neurologic dysfunction following open heart surgery are not proven. [330 ] However, during deep hypothermia, retrograde cerebroplegia and limiting the duration of circulatory arrest reduce postoperative neurological deficits (Chapters 9, 10, and 40). The consequences of permanent or severe deficits may be devastating, and patients with permanent lesions face an in-hospital mortality of 15–30 percent. [329 ] – [331 ]
PERIPHERAL NERVE INJURIES
The reported incidence of upper extremity peripheral nerve injuries ranges 1.9–18.3 percent and reflects differences in the evaluation and definition of these injuries. [346 ] – [348 ] A collective review suggests that the true incidence approximates 10 percent. [347 ] Most of these injuries involve the C8 and T1 roots of the brachial plexus, which are injured primarily by stretch or compression during sternal retraction. [349 ] The brachial plexus also can be injured directly from the fractured end of the first rib or by needle trauma from a jugular vein cannulation. Harvest of an internal mammary artery does not increase the likelihood of a brachial plexus injury. Less-common injuries involve the ulnar or, rarely, the radial nerve owing to poor protection during anesthesia. The median nerve may be injured by swelling at the wrist after attempted radial arterial cannulation. [346 ] , [350 ] , [351 ]
Most of these injuries become apparent in the first postoperative week when the patient calls attention to numbness, decreased sensation, or motor deficits of the affected part. Although distressing to patients, nearly all of these injuries resolve spontaneously over 6 to 8 weeks. [347 ] , [349 ] A few are permanent and require more-detailed study and treatment.
Harvesting the saphenous vein often severs or stretches the saphenous nerve that provides sensation to the medial forefoot and ankle. The sensory deficit disappears within a few months and rarely bothers the patient. [346 ] However, injuries to the sciatic, femoral, or common perineal nerves may cause considerable disability. These injuries are reported in 0.1 percent of patients and are owing to needle stick, compression from an improper position of the leg, or lack of protection over the head of the fibula. Injures also are thought to occur from poor perfusion of the lower extremity owing to vasoactive drugs or the intra-aortic balloon pump and may become permanent if the circulation is improved rapidly. [346 ] , [347 ] , [352 ] , [353 ]
Behavioral changes, cognitive dysfunction, sleeplessness, changes in dream patterns, and psychological abnormalities may be documented shortly after operation by careful examination and testing in up to one-half of patients who undergo open heart surgery. [339 ] , [354 ] – [359 ] These changes are more common in older patients and those with previous central nervous system dysfunction and do not correlate with variables in extracorporeal perfusion protocols or equipment [354 ] , [360 ] but roughly correlate with the numbers and size of microemboli detected by carotid ultrasonography during operation. [339 ]
Studies suggest that up to 13 percent of patients develop postoperative psychological disturbances that are clinically manifested by atypical behavior, disorientation, or reduced cognitive functions. [354 ] , [356 ] , [360 ] , [361 ] Hallucinations or delusions may occur in 0.9 percent of patients. Sleep disorders, nightmares, or changes in dream patterns may affect more than one-half of postoperative patients. [357 ] , [362 ] In most patients the changes are transient and gone within a few days or weeks. Changes in cognitive function determined by testing may affect up to 75 percent of patients shortly after operation, but late studies show that the vast majority of patients regain full cognitive function within 6 months to 1 year. [359 ] , [363 ] , [364 ] , [365 ] However, as many as 6.6 percent of patients may demonstrate moderate to severe psychometric abnormalities at late follow-up, and in approximately 1 percent of patients the changes preclude a return to work and normal daily activities. [355 ] , [359 ] , [363 ]
The behavioral changes that are associated with intensive care unit stays longer than 48 hours and that disappear within 48 hours after transfer from the intensive care unit do not appear to have an organic basis but are more likely in postoperative cardiac patients, particularly elderly patients, because of cardiopulmonary bypass, microembolization, and probable metabolic factors.
surgery of the dissecting aorta
The purpose of operation on the acutely or chronically dissected aorta is to eliminate aortic segments at risk for early or late rupture. This requires obliteration of all false channels with reconstitution of blood flow exclusively into the true lumen. Unfortunately, this objective is rarely achieved except for DeBakey type II dissections that involve only the ascending aorta.
Anesthesia and Monitoring
Anesthesia often is induced with midazolam, fentanyl, and pancuronium, and maintained with inhaled isoflurane and intravenous fentanyl. The electrocardiogram, both radial and femoral arterial pressures, and central venous pressures are displayed continuously during operation. In addition, bladder temperature and either nasopharyngeal or tympanic membrane temperature and capillary oxygen saturation by pulse oximetry also are monitored. Radial and femoral arterial catheters, a Swan-Ganz catheter, another large-bore central venous catheter, and one or more peripheral intravenous catheters are inserted and connected to appropriate stopcocks and transducers. A cell saver system for scavenging shed blood often is helpful. Packed cells, fresh frozen plasma, and platelet packs generally are ordered before operation. After induction of anesthesia, the patient is intubated and positioned for the proposed operation.
Comparison of radial and femoral arterial pressures may allow early identification of a malperfusion syndrome. During cardiopulmonary bypass, malperfusion may result from retrograde flow into the false lumen without a proximal entry site; this may cause the “blind pocket” phenomenon and occlude the true lumen. [239 ] , [240 ] The malperfusion is readily identified by a pressure differential between a low right radial and elevated femoral arterial pressures.
Bladder (or rectal) and nasopharyngeal (or tympanic membrane) temperatures are necessary to control the depth of hypothermia. If circulatory arrest is planned, the head is packed in ice to prevent rewarming during periods of arrest and the electroencephalogram often is monitored to assure brain protection. We do not routinely drain cerebrospinal fluid before or after repair of acute or chronic distal aortic dissections.
A double-lumen endobronchial tube considerably improves surgical exposure for procedures on the descending thoracic aorta through a left lateral thoracotomy. Endotracheal tubes with unilateral bronchial catheter blocking devices are less effective. After heparin is administered, manipulation of the deflated lung is kept to a minimum to prevent serious intrapulmonary hemorrhage and loss of gas exchange.
Hemostasis often is a problem, especially after prolonged periods of deep hypothermia in patients with aortic dissections. Shed blood can be aspirated, washed, concentrated, and returned as packed cells. Antifibrinolytic drugs (aprotinin, epsilon amino caproic acid, and tranexamic acid) reduce bleeding significantly. Because of thrombotic concerns aprotinin is deferred until after circulatory arrest; then three million units are given followed by 500,000 units per hour. During cardiopulmonary bypass, one unit of fresh frozen plasma is given every 20 minutes for complicated dissections of the aortic arch. Platelets, fresh frozen plasma, cryoprecipitate, bovine thrombin, and homologous blood should be available. The tendency for diffuse hemorrhage from suture lines and raw surfaces is reduced remarkably with liberal transfusion of fresh frozen plasma and concentrated platelets both during and early after the procedure.
Improvements in suture material, needles, collagen- or gelatin-impregnated grafts, widespread use of Teflon felt, and both fibrin and gelatin resorcinol formalin (GRF) glue have improved technical results considerably over the past several years. [241 ] Thus, it is now rare for a patient to succumb to exsanguinating hemorrhage. Teflon felt is routinely fixed within and without the aorta using a row of continuous mattress sutures followed by a running suture prior to insertion of the graft. This provides a leak-proof gasket at the proximal and distal suture lines. At institutions with access to GRF glue, special clamps and dilators allow easy approximation of dissected layers, and eliminate the need for sutures. [242 ] , [243 ] Polymerization is accelerated by warming the glue, clamps, and Hegar dilators to 40°C. Fibrin glue, provided commercially or made from cryoprecipitate and thrombin, rarely reunites dissected aortic layers.
Various authors use tie-in grafts equipped with a stiff, grooved ring to obviate suturing acutely dissected aortas. [221 ] – [223 ] , [244 ] Our experience with this method is not satisfactory because available graft sizes are limited and the incidence of late complications is substantial.
Extracorporeal Circulation and Cardioplegia
Operations on the proximal ascending aorta and arch always are performed during extracorporeal circulation with a variety of adjunctive measures for cerebral protection. For aortic dissection limited to the ascending aorta, cannulation of the proximal aortic arch and right atrium is employed. When the entire aorta is involved (DeBakey type I dissection), retrograde femoral artery cannulation for cardiopulmonary bypass is used in conjunction with a two-stage venous cannula in the right atrium. For femoral-femoral bypass, the right femoral vein is preferred as the cannula passes more easily from the right-sided femoral system into the cava and right atrium. Pressures are monitored in the femoral artery opposite the cannulation site and preferably, both the right and left radial artery in order to promptly recognize any obstruction to retrograde flow within the arch. [239 ] , [245 ] , [246 ]
A left ventricular (LV) vent invariably is placed through the right superior pulmonary vein. Retrograde blood cardioplegia is administered via a cannula inserted through a pursestring in the right atrium. If retrograde cerebral perfusion is planned, bicaval cannulation is performed, and a bypass line from the arterial cannula to the SVC cannula is added.
Operations involving replacement of the distal ascending aorta or any portion of the aortic arch require special measures to avoid brain injury. The choice of method depends on the amount of time without cerebral circulation required to complete the procedure.
DEEP HYPOTHERMIC CIRCULATORY ARREST
Hypothermic arrest for operative intervention on the aortic arch was first employed by Bernard in 1963 and by Borst in 1964. [226 ] , [247 ] – [251 ] The method is used widely to provide adequate cerebral protection for aneurysms and dissection of the aortic arch. [252 ] – [257 ] Deep hypothermic circulatory arrest reduces cerebral metabolism to 23 percent of its normal value at 20°C and to 17 percent at 15°C; this allows relatively safe periods of circulatory arrest that approach 30 minutes at 20°C and just under 1 hour during deep hypothermia. [258 ] – [260 ] Most authors do not recommend extending hypothermia to below 15°C, as a nonischemic cerebral injury may develop. [261 ]
Svensson and coworkers found the risk of cerebral damage in patients undergoing deep hypothermia for aortic surgery was 4 percent at 30 minutes, 7.5 percent at 45 minutes, and 10.7 percent at 60 minutes. [262 ] Ergin also noted an increased incidence of at least temporary dysfunction after 40–50 minutes of circulatory arrest, and a rise in the stroke rate beyond this time period. [263 ] Possible new ways of extending permissible periods of hypothermic circulatory arrest involve glutamate antagonists and calcium channel blockers. [264 ] , [265 ]
Direct measurement of true brain temperature in humans is not possible; therefore, nasopharyngeal or tympanic membrane temperatures are monitored to reflect brain temperature. Unfortunately, these temperatures do not reliably correlate with the metabolic state of the brain and electroencephalographic (EEG) silence often does not occur at expected temperatures. [262 ] , [266 ] , [267 ] Therefore, both the EEG and a temperature are monitored for patients who require prolonged procedures on the aortic arch. Furthermore, cooling should continue well below the level of EEG silence and for at least 25 minutes. It is our policy to cool to at least 20°C for brief periods of circulatory arrest (up to 20 minutes) and to cool to approximately 15°C or 2–3°C below EEG silence for longer periods.
For deep hypothermic circulatory arrest the patient is cooled on cardiopulmonary bypass without exceeding temperature gradients over 10°C. [268 ] – [272 ] The partial pressure of carbon dioxide is not increased as the temperature drops (alpha stat regimen). Admittedly, the choice of alpha stat management is not universally accepted and pH stat management is preferred by others. [273 ] , [274 ]
During cooling, alpha-adrenergic blockade is instituted to allow a more even decrease in temperature in all parts of the body. Hemodilution and hyperglycemia, which are associated with brain injury, are avoided carefully. [269 ] , [275 ] Methylprednisolone (30 mg/kg) and sodium thiopental (15 mg/kg) are administered before circulatory arrest. [276 ] During the period of circulatory arrest, the head is packed in ice to prevent rewarming to room temperature. As the procedure is being completed, rewarming begins and proceeds to a nasopharyngeal temperature of 36°C and a bladder temperature of at least 34°C. During rewarming, the temperature gradient is not allowed to exceed 10°C. As rewarming occurs, 20 percent mannitol (18 mg/kg) and furosemide (10 mg/kg) are administered to encourage urine output, and sodium bicarbonate is given to correct the pH value to normal. To eliminate possible air collection in the distal aorta, the circulation is never completely arrested and at least 100–200 mL/min of blood flow into the femoral artery is maintained. This is interrupted if exposure is difficult.
Retrograde perfusion of the superior vena cava is described elsewhere (see Chapter 10) and is helpful for maintaining a desired brain temperature and for flushing debris from aortic arch vessels.
Retrograde cerebral perfusion probably provides little nutritive flow.
On occasion, when excessively long procedures on the arch are anticipated, selective antegrade perfusion is used. This procedure is performed easily by inserting a right-angle cannula into the innominate artery proximal to the bifurcation.
Atraumatic bulldog clamps are used to occlude the innominate, carotid, and subclavian arteries. Antegrade flow is maintained to the brachiocephalic circulation at approximately 1 L/min while both radial arterial catheters are monitored to maintain a mean blood pressure of 70 mmHg. Monitoring the pressure in the left radial artery assures adequate flow through the circle of Willis. An additional cannula can be inserted into the left carotid artery if necessary.
If arch involvement is uncertain at the outset of operation and the time required for circulatory arrest unknown, cooling proceeds in two stages. First, temperature is reduced to 20°C, and the circulation is interrupted. The aorta is opened in the mid ascending portion and the interior including the arch is inspected. If the inner cylinder is intact, the distal open reconstruction and anastomosis proceeds immediately by suturing the graft to the proximal portion of the reconstituted arch. Antegrade circulation usually is re-established through a cannula placed in the graft in less than 15 minutes. However, if the inner cylinder of the arch is disrupted or if individual brachiocephalic vessels require reconstruction, the clamp on the ascending aorta is replaced and cooling is continued to 15–17°C or 3°C below EEG silence. While cooling continues, the proximal portion of the operation is accomplished.
Operative Techniques for Proximal Dissections
Median sternotomy is the standard incision for all procedures on the ascending thoracic aorta and for most transverse arch procedures. The incision may be extended into one or both of the supraclavicular spaces if arch branches require further exposure. During re-operation for ascending aortic dissection, median sternotomy may be hazardous and the patient should be cannulated for cardiopulmonary bypass before opening the sternum. When the aortic arch requires replacement, the anterior wall is exposed and the arch is retracted inferiorly to expose the origins of the arch branches. The left phrenic and vagus nerves always are identified at the distal arch and retracted anteriorly. A fourth rib anterolateral incision is added only when a portion of the descending aorta is included.
REPLACEMENT OF THE AORTIC ROOT AND ASCENDING AORTA
The entire ascending aorta is replaced with a gelatin-impregnated Dacron graft and an open anastomosis to the arch is performed in every case of acute proximal dissection. Aortic regurgitation which is encountered in 50–75 percent of patients with acute proximal aortic dissection is most commonly managed by resuspension of the commissures, reconstitution of the layers of the aortic root, and anastomosis to an appropriate sized graft.] More recently, valve-sparing procedures whereby the valve is mounted in a Dacron graft to eliminate the sinuses of Valsalva have been proposed, but this procedure remains controversial.
The ascending aorta in acute dissection appears bluish purple and blood may seem to seep through the aortic wall. Because the ascending aorta may rupture, manipulation is not recommended until body temperature is substantially reduced to allow for a safe period of cerebral protection if the aorta ruptures. Once body temperature is reduced, the heart fibrillates and must be protected from distension.
The aorta is separated from the pulmonary artery and clamped in the mid ascending portion using a Fogarty aortic clamp. Retrograde cardioplegia is begun. The proximal aorta is opened and transected approximately 5 mm distal to the highest point of the commissures. Once this is done, 4-0 Teflon pledgeted polypropylene sutures with a finely tapered needle are passed at the apex of each commissure from inside the aortic lumen, to outside through a second pledget
These are tied, to resuspend the valve commissures. A running horizontal mattress suture is used to fasten two Teflon felt strips inside and outside the circumference of the aorta without pursestringing. This is followed by a running (over and over) 4-0 Prolene suture that seals the inner layer of felt against the outer layer, with the aortic wall sandwiched between and the outer layer of felt (thus providing a leak-proof gasket). Alternatively the root can be glued using GRF glue. Reconstruction of the aortic root requires 10–15 minutes; core cooling may proceed during this period if the aortic arch is involved.
When the patient's core temperature reaches 20–22°C, the ascending aortic clamp is removed and the interior of the distal ascending aorta and arch is inspected. If the inner cylinder remains intact, the layers of the dissection are reconstituted, using intimal and adventitial layers of Teflon felt to compress the dissected walls of the aorta between
. Once the layers are reunited, a graft of appropriate size is beveled and sutured to the three-layered arch using a continuous 4-0 Prolene suture. The repair is always extended to the proximal arch to facilitate late replacement of the arch if this is required later
After the distal suture line is completed, the graft is deaired, clamped, and extracorporeal circulation is resumed after a cannula is inserted into the graft for antegrade perfusion. This compresses dissected aortic layers together in most patients. Rewarming proceeds while the distal graft is joined to the proximally reconstructed aortic root. Occasionally it is useful to fold a segment of the adventitia over either the proximal or distal suture line for additional hemostasis.
When the dissection reaches either coronary ostium without disrupting the cylinder of the coronary vessel proper, repressurization of the root usually eliminates any potential space between the layers. However, if the ostium is completely surrounded by the dissection, it is preferable to excise a button with a 4-mm margin of aortic wall. The layers are then united using GRF glue and a 5-0 Prolene suture or between donuts of Teflon felt. The ostial button is anastomosed to a tube graft or composite graft without torsion or tension. Partial disruption of a coronary ostium is repaired with continuous 5-0 Prolene suture leaving the ostium in continuity with the aortic wall. Aortocoronary bypass grafting is the last resort if the ostium is very small and torn or if damage is irreparable.
The St. Jude valve conduit is preferred because the suturing ring is thin and minimizes the distance between the graft and coronary ostia. Furthermore, new-generation composite valves are packaged using an impervious ascending aortic graft. Placement of pledgeted sutures for attachment of graft to annulus is critically important. Everting 2-0 pledgeted sutures are employed and great care is taken to place the sutures exactly shoulder-to-shoulder along the perimeter of the annulus and corresponding valve sewing ring . A minimal amount of diseased aortic wall is retained to decrease the chance of late complications involving the coronary buttons. Once the valve is tied to the annulus, the coronary ostia are attached to the graft by either the side-to-side Bental technique or the preferred button technique . Continuous 4-0 or 5-0 Prolene suture, usually reinforced with Teflon felt, is used. A Cabrol interostial coronary graft or an ultra short (1.5-cm) graft-to-left-main extension occasionally is employed when low-lying ostia cannot be mobilized. The remnants of the ascending aorta are closed over the graft to protect the prosthesis against infection or if reoperation becomes necessary. Graft inclusion should not be used to achieve hemostasis.
ACUTE DISSECTION INVOLVING THE AORTIC ARCH
Disruption of the inner arch cylinder occurs in 10–30 percent of patients with acute dissection and portends an ominous prognosis. The aortic arch should be inspected during a short period of hypothermic circulatory arrest in every proximal dissection.
Limited tears in the dissecting membrane within the arch are managed by placing the distal anastomosis beyond the site of disruption during circulatory arrest. Fortunately, this is the most common problem and tears tend to be located away from the origin of the cephalic branches.
In more severe cases, the true channels of one or more of the supra-aortic vessels are completely separated from the arch and are supplied through secondary entry ports
. In the most severe circumstance, a completely separated true lumen may prolapse distally to cause obstruction. These problems are managed by subtotal or, more commonly, total replacement of the arch with reconnection of some or all of the supra-aortic vessels to the prosthesis
In acute dissections the supra-aortic branches are anastomosed individually to separate openings in the arch graft rather than as a unit
One, two, or three separate anastomoses may be required. In addition, supra-aortic vessels themselves may require repair using GRF glue or Teflon felt.
For subtotal or total arch replacement, the tubular portion of the arch is freed to approximately 2 cm beyond the level of the planned distal anastomosis. Arch branches are dissected free and the dissected layers of the aortic wallare divided near the origins of the brachiocephalic vessels. The aortic dissecting membrane is excised and individual arteries, usually the innominate and carotid, are divided just beyond their origins. Next the dissected layers of the transected descending thoracic aorta are reunited using either GRF glue or internal and external Teflon felt strips. Separate running mattress and over-and-over prolene sutures are recommended to produce a firm seal. When the tear extends distally into the descending thoracic aorta, after the dissected layers are reapproximated, a short elephant trunk is added to the graft to provide a more secure seal. Brachiocephalic vessels usually are anastomosed directly to separate openings in the graft. Alternatively, if the anatomy is favorable, the patch of arch vessels may be sewn to a single opening in the graft after the dissected layers of the patch are reapproximated either with GRF glue or Teflon felt strips
CHRONIC AORTIC ARCH DISSECTION
For chronic dissections or postdissection aneurysms isolated to the proximal arch, an open distal anastomosis is made at the junction of the ascending and transverse arches. The graft is anastomosed beyond the site of any true arch tear. When brachiocephalic vessels are involved, flow to the true lumens is re-established with replacement of the arch. Sometimes, individual arch grafts may be required. Occasionally a chronic dissection membrane that involves and partially occludes the brachiocephalic vessels or proximal descending thoracic aorta may be fenestrated. The distal anastomosis always is made to the outer layer of the aorta.
Operative Techniques for Distal Dissections
Ischemic injury to the spinal cord and/or intra-abdominal organs is a disastrous complication of dissected thoracic or thoraco-abdominal aortic repairs.
The risk of spinal cord damage is higher for repair of acute dissection than for arteriosclerotic aneurysms because chronically occluded intercostal arteries in aneurysm patients may stimulate development of spinal cord collaterals that partially protect against ischemic injury. Moreover, the friable dissected aortic wall of an acute dissection presents a greater technical challenge.
Several protocols are designed to predict or prevent spinal cord ischemia, but none have attained widespread use because of inconsistent efficacy and false-negative and-positive results. Intraoperative monitoring of sensory or motor evoked potentials and preoperative imaging of the great radicular artery attempt to predict cord ischemia.
Cooling the spinal cord by surface, intrathecal, or whole- body hypothermia using extracorporeal circulation attempt to prevent cord ischemia. Intraoperative cerebrospinal fluid withdrawal is designed to maximize the pressure difference between the residual arterial circulation and the cord during aortic occlusion, but clinical benefit remains undecided. This method also risks intrathecal bleeding during heparinization from a traumatic puncture. Pharmacologic agents to prevent spinal cord damage include oxygen free radical scavengers, prostaglandin E, dextrorphan, corticosteroids, and sodium thiopental, but none have provided reliable protection in patients.
Three important principles are now recognized to reduce the risk of spinal cord and organ ischemia. First, maintain perfusion of vessels downstream to the distal graft anastomosis and prevent proximal hypertension. Second, promptly revascularize all important aortic side branches. Third, reduce spinal cord and visceral organ temperature during the period of ischemia. These principles evolved from prior experience with simple, proximal aortic cross-clamping followed by expeditious anastomosis of major aortic branches to the graft. This experience produced unpredictable ischemic injuries to the spinal cord and visceral organs, and complications owing to hypertension proximal to the clamp.
Our current routine for replacement of the distal aorta incorporates extracorporeal circulation for all interventions. When only the descending thoracic aorta or thoraco-abdominal aorta is replaced, centrifugal pump bypass from the left atrium or pulmonary vein to the left femoral artery is used to maintain full perfusion of the distal circulation. Cooling to 30°C is accomplished via an inline heater-cooling circuit or surface cooling. The safety, simplicity, and lack of heparin requirement are important advantages of left heart bypass.
For complex procedures on the descending thoracic aorta, cardiopulmonary bypass via the femoro-femoral route allows cooling the patient to any desired temperature. The ascending aorta also is cannulated and the left or main pulmonary artery also may be cannulated to provide adequate venous drainage. These cannulations enable full cardiopulmonary bypass, deep hypothermia, and periods of circulatory arrest. Deep hypothermic circulatory arrest may be required for the proximal anastomosis when a proximal aortic clamp cannot be safely placed, when brachiocephalic vessels require repair, or when the dissection proceeds retrograde and requires reconstitution of the dissected layers prior to graft anastomosis.
The patient is placed in the right lateral decubitus position with the left pelvis tilted posteriorly for femoral vessel access. The fourth interspace usually provides adequate access to the aortic arch for the proximal anastomosis and the mid-descending aorta for the distal suture line. For additional exposure, the fifth or the sixth ribs may be notched either anteriorly or posteriorly. If the distal anastomosis is made beyond the eighth interspace, a second thoracotomy is added. If the anterior part of the incision slants toward the costal arch, only a single skin incision is required.
A single skin incision and two thoracic incisions are used to expose extensive dissections (Crawford type I or II). The lower thoracic incision extends across the costal arch onto the abdominal wall. The retroperitoneum is entered just below the costal arch and bluntly freed from the posterior muscles and abdominal wall. By carefully avoiding tears in the peritoneum the intra-abdominal organs, especially the spleen, are protected from injury. The diaphragm is divided radially, leaving a 2-cm margin along the chest wall. For malperfusion syndrome involving the infradiaphragmatic aorta a tenth rib retroperitoneal approach is useful.
When the thorax is entered, care is taken to avoid injury to either the aorta or lung. Particularly in acute dissection, overtraction of the ribs is avoided until the patient is fully prepared for extracorporeal circulation. Except for sites selected for cross-clamping, no attempt is made to free the lung from aortic adhesions. When the lung is inadvertently injured, air and blood leaks are repaired carefully and sometimes reinforced with strips of pericardium.
DISTAL ARCH AND DESCENDING THORACIC AORTA
The most common site of aortic rupture in acute distal dissection is the proximal third of the vessel. Because replacement of this segment comprises the majority of acute dissections, the overall risk of spinal cord complications for distal dissections is low.
The proximal clamp is placed between the left carotid and subclavian arteries. The vagus nerve is encircled with a Silastic band and the recurrent nerve is identified. The left subclavian and carotid arteries are exposed by incising the overlying pleura and the subclavian artery is encircled with umbilical tape.
The mediastinum is cleared between the subclavian and left carotid arteries down to the trachea to free the posterior circumference of the arch. Blood pressure should be maintained below 100 mmHg during this dissection to minimize the risk of rupture. Ultimately, the arch is freed to the point where the index finger and thumb can squeeze the posterior wall. If the arch ruptures during this dissection, the site of hemorrhage is compressed and full hypothermic cardiopulmonary bypass is instituted to perform the repair during circulatory arrest.
The proximal descending thoracic aorta is first freed for about 6 cm, by dividing visible intercostal arteries between clips. The distal aorta is mobilized at the appropriate level, with care to avoid important intercostal vessels and the thoracic duct. The pericardium is incised posterior to the phrenic nerve for access to the left atrium or the upper left pulmonary vein. An end-hole atrial cannula is advanced into the mid-atrium for left heart bypass. The left femoral artery is cannulated. Flow rates are adjusted to maintain equal arterial blood pressures in the upper and lower portions of the body during the procedure. This usually requires approximately 1.5–2.0 L/min in adults. After establishing left heart bypass, lidocaine is administered and the patient is cooled slowly to 30°C. The aorta is clamped between the left carotid and subclavian arteries; the latter is occluded with a tourniquet. A longitudinal incision is used to enter the false channel, which is cleared of thrombus to recognize and stop any backbleeding from right-sided intercostal and bronchial arteries. Single or multiple dissecting membranes are identified and completely removed. The aorta then is completely divided at the junction of the arch and descending portion, to facilitate the anastomosis and control anastomotic bleeding. Transection also improves visualization of the recurrent laryngeal nerve to avoid entrapment in the posterior suture line.
The aortic wall dissection usually originates at the origin of the left subclavian artery where the primary entry tear also is located. After excising the dissection membrane, the anastomosis is made to uninvolved aorta. A gelatin-impregnated Dacron graft is sized to the diameter of the distal aorta and proximally beveled to the corresponding aortic diameter. A Teflon felt strip is included in the suture line, even if a nondissected cuff is available. Continuous 3-0 or 4-0 Prolene incorporating large bites of the aortic wall is run from the posterior anastomosis upward. The suture line incorporates the origin of the left subclavian artery, with full-thickness bites along the left margin. If the subclavian artery is dissected, the false channel is closed by the anastomosis. When the graft is anastomosed to the mid arch, a separate (8-mm) graft is placed between the aortic prosthesis and the distal subclavian artery.
The anastomosis is tested by first releasing the subclavian artery and then unclamping the aorta with the distal graft occluded. Any anastomotic bleeding is seen and repaired easily.
The distal aortic wall layers always are reconstituted in an acute dissection by using external and internal strips of Teflon felt. Approximation of the dissected layers causes the true channel of the distal vasculature to re-expand and avoids malperfusion of vital organs. The graft is sutured to the repaired distal aorta using 3-0 or 4-0 continuous Prolene and generous bites of aorta. The distal aortic clamp is released first, leaks are repaired, then the proximal clamp is released slowly.
Rewarming is begun during completion of the distal anastomosis. After termination of extracorporeal bypass, the left atrium is decannulated, and the pericardial incision is loosely closed. Likewise, the cannula in the femoral artery is removed, and the vessel is repaired. The aortic remnants are firmly sutured around the graft to control diffuse bleeding until hemostasis is achieved and to protect the graft if a pleural space infection occurs.
When the proximal two-thirds of the descending thoracic aorta requires replacement, the intercostal arteries arising from the excluded aortic portion are sacrificed without fear of spinal cord complications.
When replacement of the entire descending thoracic aorta is required, all sizable intercostal vessels, below the first six pairs, are connected to the graft. For these extensive repairs moderate hypothermia is used and the aorta is clamped sequentially after each branch anastomosis to minimize ischemic injuries.
If the mid-arch layers are separated, they are reconstituted, either between layers of Teflon felt or with GRF glue, under hypothermic circulatory arrest. Proximal arch involvement must be identified prior to incising the aorta to allow for adequate cooling. Conversion of a planned left heart bypass with moderate hypothermia to full bypass and deep hypothermia and circulatory arrest requires addition of an oxygenator/heat exchanger to the bypass circuit and cannulation of both the left femoral artery and ascending aorta. The left femoral vein may be cannulated with advancement of the catheter over a wire to the right atrium. If adequate venous drainage is not obtained, a right-angle cannula (Polystan, Kopenhagen, Denmark) (10-mm ID) placed through the pulmonary artery into the right ventricle improves drainage dramatically. The proximal anastomosis then proceeds as described for proximal dissections.
In patients with chronic dissection, the distal graft-to-aorta anastomosis always is made to the outer coat of the vessel because multiple downstream re-entries ensure perfusion of all side branches. It is helpful to distend the graft under pressure to its final length and configuration prior to trimming the distal end. A distal elephant trunk prosthesis occasionally is helpful for aneurysmal chronic dissections.
Operative intervention for acute dissection of the thoracoabdominal aorta is indicated for replacement of a ruptured aortic segment or for relief of distal organ malperfusion. Total cardiopulmonary bypass with ascending aortic and left femoral arterial cannulation and deep hypothermic circulatory arrest are used to prevent spinal cord and visceral organ ischemia. A femoral venous catheter advanced to the right atrium and pulmonary arterial catheter is used for venous drainage.
The aorta is exposed from the arch to its bifurcation. The proximal anastomosis is done first the specific technique is determined by the extent of the dissection into the aortic arch and has been described earlier for exposure through a left thoracotomy incision. After completion of the anastomosis, the cross-clamp is moved distally on the graft
. A perfusion catheter is inserted through the proximal graft to perfuse the upper body and, later, vessels anastomosed to the proximal graft. The first six pairs of thoracic intercostal vessels are clipped or oversewn to prevent backbleeding. Large lower intercostal arteries are sutured to the graft as a patch.
During circulatory arrest, a longitudinal incision is made in the left posterolateral wall of the aorta to the aortic bifurcation
. After accumulated thrombus is removed from the false lumen, the dissection membranes are excised. A small rim of intima-media is left around the orifices of visceral, renal, and large lower intercostal and lumbar arteries.
Backbleeding from the aortic bifurcation, visceral, or renal vessels is controlled with balloon catheters. Usually, the celiac, right renal, superior mesenteric, and right-sided lumbar arteries originate from a nondissected strip of the aorta. However, the left renal artery characteristically originates from the false lumen. A 4-mm rim of aortic wall is left around the origin of the left renal artery.
The celiac, superior mesenteric, right renal, and all large intercostal and lumbar arteries above L3 are reattached as a unit to a single opening in the graft
. The lower lumbar arteries and the inferior mesenteric artery are suture-ligated. The left renal artery and any other major vessels arising from the false lumen are attached to separate openings in the graft.
A continuous 3-0 or 4-0 Prolene suture with full-thickness aortic bites is used for the unit anastomosis; finer sutures are used for attachment of the left renal artery and other individual branches.
Occasionally a short interposition graft is needed to reattach the left renal artery without tension.
If visceral or renal arteries are involved in the dissection, they must be repaired to allow perfusion of the true lumen after connection to the aortic graft. This usually is achieved by taking deep suture bites of the vessel orifice to simultaneously reapproximate the dissecting membrane to the outer aortic coat and connect the branch to the graft. When the inner cylinder of visceral vessel is disrupted, the true lumen is reconstituted with a running fine Prolene suture before it is anastomosed to the graft. In very rare cases, individual arteries require bypass, usually because of distal occlusion or aneurysm formation.
Once the visceral vessels are reperfused, the graft is anastomosed to the aortic bifurcation
Significant backbleeding is controlled using balloon catheters rather than cross-clamping the aorta. Dissected layers at the aortic bifurcation are reconstituted using Teflon felt or GRF glue prior to anastomosis to the graft.
After all anastomoses are completed, perfusion is restarted and rewarming is begun. Leaks are controlled by separate sutures. The bowel is examined carefully for ischemia; often a Doppler probe is helpful because of vasospasm after these long, complicated procedures.
Malperfusion of Aortic Branches
Involvement of aortic branches in the process of dissection is not uncommon. Indeed, branch occlusion may be prominent in the clinical presentation. In a large autopsy series, main coronary artery involvement occurred in 7 percent of cases, dissected supra-aortic branches in 42 percent, and visceral vessels (celiac trunk, superior mesenteric, and renal arteries) were affected in 27 percent. Distally the iliac and femoral vessels were involved in 26 percent (46) of patients.
Clinical series show a lower incidence of symptomatic branch ischemia. Symptomatic dissection into the main coronary arteries occurs in 4.7 percent, into supra-aortic branches in 9.3 percent, into visceral vessels in 8.7 percent, and into the legs in 11.7 percent.
Thus, the initial clinical presentation of aortic dissection may include myocardial ischemia, stroke, sudden paraplegia, acute abdomen, and ischemic extremities, and may obscure the correct diagnosis of dissection.
Although perfusion of the lower extremities is often relieved by reuniting the true and false lumens by repair of the aorta, malperfusion of visceral branches may persist with disastrous consequences
The dissection involves major branch arteries in several ways
. Compression of the true channel by overexpansion of the false is the most common mechanism of vascular obstruction. The true channel of an individual branch vessel may undergo complete dehiscence from the aorta if the dissection completely encircles the origin. Intussusception of the dissected inner wall commonly occludes a branch but reentries may cause spontaneous relief. In rare cases, the entire circumference of the aorta may intussept distally to cause severe organ ischemia. If the entry tear is close to the origin of a branch vessel, a mobile flap of the aortic dissecting membrane can cause occlusion.
Although malperfusion in acute dissection often disappears spontaneously, intervention to relieve distal ischemia may be required. Fenestration of the dissecting membrane to equalize the pressure in both vascular channels decreases the obstruction caused by an overexpanded false channel. This was the first and still is the most commonly performed procedure for malperfusion. Ostial reconstruction particularly is appropriate for obstructed coronary arteries. As a last resort, formal bypass procedures, such as aorto-mesenteric or aorto-renal grafting, occasionally are required, after an unsuccessful membrane fenestration.
For patients at substantial operative risk with thoracoabdominal or aorto-iliac obstruction, extra-anatomic (axillo-bifemoral) bypass can restore lower body perfusion. In acute distal dissection, relief of a thoracoabdominal malperfusion may be the only intervention required beyond medical management. For chronic proximal or distal dissection, replacement of a stenotic aortic segment is a satisfactory method to alleviate malperfusion.
Membrane fenestration using endovascular interventional procedures is attractive in these critically ill patients because prompt relief of vascular obstruction can be obtained without anesthesia or the need for surgery. These procedures can precede emergency operation on the aorta to promptly relieve potentially lethal organ ischemia. Usually, an angioplasty balloon catheter is advanced through a small fenestration, inflated, and withdrawn to rupture the dissecting membrane. The dissecting membrane also can be punctured by moving a special catheter upstream and using a septostomy blade to create a large tear in the membrane to restore flow in the distal true lumen.
Percutaneous transluminal angioplasty can dilate a chronically narrowed dissected aorta.Expandable stents to reestablish blood flow in dissected branch vessels also is possible.
In acute dissection obstruction of either or both carotid arteries, usually by overexpansion of the false lumen in the aortic arch or occasionally from a dissected main carotid artery, is an ominous finding. When the inner cylinder is intact, as is usual, flow improves after closing the false channel and redirecting flow into the true lumen. When the inner cylinder of a dissected innominate or carotid artery is disrupted, excision of that vessel from the arch, reconstitution of the dissected layers, and reimplantation onto the arch graft is recommended. Extra-anatomic bypass operations involving the carotid arteries rarely are performed but have been successful.
For aortic arch malperfusion in chronic dissection, fenestration of the dissecting membrane just beyond the origin of the arch vessel usually is sufficient. Occasionally the dissection extends peripherally into the distal main or carotid bifurcation to produce persistent chronic malperfusion, often manifested by transient ischemic attacks (TIAs). In this instance, the dissecting membrane is resected at the beginning of the stenotic portion, the downstream layers are reconstructed, and the vessel is closed with a patch.
Complete collapse and obstruction of the true lumen of the arch can occur at the onset of retrograde cardiopulmonary bypass owing to overperfusion and expansion of the false lumen. This problem must be alleviated by rapid recannulation of the proximal true lumen using a second arterial line kept readily available for this purpose. Either transapical or direct aortic cannulation using a brief period of circulatory arrest can be employed. The transapical approach with a tourniquet surrounding the ascending aorta is preferred.
When the entire true channel of the ascending aorta collapses during systole and causes coronary malperfusion, repair of the root eliminates the problem.
Delamination in the aortic root may extend to or encircle the main coronary ostia and occasionally continue distally along the proximal coronary artery. This problem is eliminated by reconstituting the layers of the aortic root either with Teflon felt or GRF glue. After root reconstruction, the ostia may appear persistently narrowed; however, when the inner cylinder is intact, the apparent stenosis disappears with pressurization. Rarely, the vessel may be torn at its origin and require meticulous reconstruction with fine sutures and glue. In the majority of these patients, the affected coronary ostium can be salvaged and anastomosed to the aortic graft either directly or with the button technique. When the ostium is disrupted severely and cannot be reconstructed, ascending aortic graft-coronary bypass is required.
Relief of abdominal organ malperfusion may require a variety of interventions. These include replacement of the aorta, membrane fenestration, and extra-anatomic bypass of individual vessels. Even severe thoracoabdominal malperfusion often resolves with ascending aortic repair.
When simple reconstitution of the proximal aorta does not relieve visceral malperfusion, the most frequently performed procedure is aortic membrane fenestratio
. The infrarenal aorta is exposed at the diaphragmatic hiatus, generally using the retroperitoneal approach.
The aorta is controlled either manually or with a soft vascular clamp and is occluded below the renal arteries. The vessel is incised through the nondissected portion, which usually is the right anterior wall. The nondissected wall appears normal, whereas the freshly dissected portion appears dark blue. This incision avoids the need to close the friable outer dissected aortic wall. The dissection membrane is incised and partially excised, as far upstream as possible, and well below the renal vessels exposed by briefly removing the infrarenal clamp. The dissected layers are reconstituted below the renal arteries between layers of Teflon felt or with GRF glue. After completion of the fenestration the aortotomy usually is closed directly; occasionally an infrarenal tube graft is required.
Fenestration of individual vessels is sometimes needed, if the dissection membrane extends beyond the ostium of the obstructed branch. When an individual vessel, usually the superior mesenteric or celiac, requires fenestration, left atrio-femoral or femoral-femoral bypass is employed with moderate cooling to 30°C. Ideally, the membrane is completely removed but usually the downstream dissected wall layers must be reunited by suturing or gluing the false lumen. Patch closure of the arteriotomy is preferred to avoid narrowing the vessel.
If membrane excision does not re-establish perfusion to the ischemic organ, extra-anatomic bypass is required. The iliac artery rather than the dissected aorta can be utilized for inflow.
Lower extremity ischemia from obstruction of the terminal aorta or pelvic vessels also may spontaneously resolve after aortic repair. When unilateral malperfusion of a lower extremity persists and percutaneous catheter-based membrane fenestration fails or is unavailable, femoro-femoral PFTE (polyfluorotetraethylene) or Dacron bypass is the preferred method of revascularization.
In the absence of proximal inflow, axillo-femoral with or without a cross-femoral bypass graft is employed.
Postoperative management of patients with acute and chronic dissections is basically similar to other complex open cardiac procedures
. Invasive monitors, placed in the operating room, are followed with special attention to the stability of vital signs, chest tube bleeding, arterial blood gases, urine output, and temperature. Initially, the patient remains sedated; as the patient emerges from anesthesia, a gross neurologic assessment is made. The patient usually remains intubated until fully awake and respiratory, hemodynamic, and bleeding concerns are resolved.
Baseline laboratory studies include an ECG, portable chest x-ray, complete blood count, arterial blood gas, and serum electrolytes and glucose. Chest tube drainage is replaced; persistent bleeding is managed by blood replacement products, indicated tests and therapeutic drugs, and occasionally by surgical exploration. A cell saver that returns washed cells to the patient is safer than one that returns filtered, anticoagulated shed blood.
Operation rarely eliminates all dissected aorta and usually a perfused false lumen remains in some distal segments. Postoperative management must maintain strict control of blood pressure and dp/dt using vasoactive drugs. Adequate flow to vital organs is maintained. Mechanical ventilation and continuous narcotics and sedatives may facilitate control of hypertension.
Often an unstable patient with dissection undergoes operative repair without complete evaluation; thus malperfusion of distal aortic branches may be unrecognized until postoperatively. Close attention to peripheral pulses, urine output, and other organ-dependent parameters is recommended. When doubt regarding perfusion of a particular vascular bed exists, Doppler ultrasound followed by prompt angiography may be lifesaving.