19. | Principles of Surgery, Companion Handbook

Chapter 18 Acquired Heart Disease

Principles of Surgery Companion Handbook

CHAPTER

18
ACQUIRED HEART DISEASE

Determination of Cardiac Function
Extracorporeal Circulation
Postoperative Complications
Specific Diseases
	Coronary Artery Disease
	Left Ventricular Aneurysm
	Valvular Diseases
Cardiac Tumors
Pericarditis
Arrhythmia Surgery
Pacemakers/Implantable Defibrillators/Intraaortic Balloon Pump/Assist Devices

DETERMINATION OF CARDIAC FUNCTION

Evaluation of cardiac function, both preoperatively and postoperatively, requires an understanding of the heart as a pump. Cardiac output (CO) measures the ability of the heart to supply metabolic substrates and remove waste. CO is proportional to heart rate (HR) multiplied by stroke volume (SV) (that is, CO = HR × SV). CO divided by the patient's body surface area (BSA) equals cardiac index (that is, CI = CO/BSA), which allows a normal value for all patients. SV has three major determinants: preload, afterload, and contractility.

Preload This is measured as the end-diastolic pressure within the ventricle. A normal value is 8 mmHg. Within limits, the ventricle can be volume loaded to increase preload. This results in increased force of contraction. Sarcomere length of 2.2 nm results in maximal force of contraction. In a normal heart, this occurs with an end-diastolic pressure of 14 mmHg. A Swan-Ganz catheter is often used to measure left ventricular end-diastolic pressure. When there are no obstructions between the pulmonary vascular bed and the left ventricle, the wedge pressure reflects left ventricular end-diastolic pressure.

Afterload This is the impedance to left ventricular emptying. The greater the afterload, the lower is the SV. The mean systolic pressure approximates afterload.

Contractility This represents the intrinsic ability of the cardiac muscle to contract and relax. It is measured as a maximal velocity of fiber shortening.

Each of these factors may be manipulated postoperatively to alter CI. Hazard function curves show increased mortality postoperatively with a CI of less than 2 L/min/m². It is important to realize that blood pressure, urine output, temperature, and cerebral function are all unreliable determinants of cardiac function in the postoperative state. If the CI falls below 2 L/min/m², the first intervention is usually to infuse fluid to increase preload to 14–18 mmHg. In stiff ventricles, left ventricular (LV) end-diastolic pressure may need to be 20 mmHg to optimize LV performance. Depending on mean systolic pressure, afterload reduction with vasodilators may be required. Contractility can be improved with the addition of inotropic agents. In severe LV failure, the intraaortic balloon pump may be required.

EXTRACORPOREAL CIRCULATION

Gibbon accomplished the first open heart operation in 1953 using cardiopulmonary bypass. Currently, most centers use a roller pump, originally designed by DeBakey. Since 1985, most centers have used membrane oxygenators. Priming solutions are usually crystalloid or colloid. Hemodilution is allowed to a hematocrit of 20 percent. Starting heparin doses are usually 4 mg/kg, and the activated clotting time is maintained greater than 600 s. Perfusion rate is usually 2.5 L/min/m², keeping mean systematic pressure to at least 50–60 mmHg. Core body temperature is lowered to about 30°C. In most cases, myocardial preservation is obtained using cold crystalloid or blood cardioplegia in combination with body hypothermia (28–30°C) and topical cooling. Myocardial temperatures below 15°C can be obtained, extending the possible cross-clamp time up to 4 h.

POSTOPERATIVE COMPLICATIONS

Bleeding Blood coagulation mechanics are abnormal for at least 18–24 h after coronary artery bypass. Unless bleeding is excessive, transfusion of platelets or fresh frozen plasma is seldom required. Brisk bleeding requires urgent return to the operating room.

Cardiac Tamponade Classic findings include elevated central venous pressure, equalization of diastolic pressures, hypotension, low CI, and mediastinal widening. Findings may be subtle. If a low CI is present and does not respond rapidly to specific treatments, reexploration for cardiac tamponade needs to be considered.

Inadequate Cardiac Index A CI of 2–2.5 L/min/m² early postoperatively is adequate. A CI below 2 L/min/m² requires rapid diagnosis and treatment, since death from inadequate perfusion may occur rapidly.

Preload, afterload, and contractility should be manipulated to optimize LV performance. The combination of fluid resuscitation and afterload reduction often restores cardiac index. Inotropes may be required. An intraaortic balloon pump (IABP) may be required if the preceding interventions fail.

Early postoperative cardiac rhythm disturbances require close attention. Temporary pacing wires are placed on the right ventricle and right atrium before leaving the operating room. Cardiac pacing with atrial or atrioventricular (AV) sequential pacing may be useful to ensure normal sinus rhythm. Premature ventricular contractions should be suppressed medically or overridden with a pacemaker because ventricular fibrillation or ventricular tachycardia can result. Potassium levels should be checked and kept well above 4 mEq/L. Lidocaine given as a bolus (75–100 mg) and infused at 2–4 mg/min can be used. Atrial fibrillation, the most common postoperative arrhythmia, is treated by rate control (calcium-channel or beta blocker) followed by a class IA antiarrhythmic agent; occasionally, electrocardioversion is required for hemodynamic instability.

Respiratory Insufficiency With current pump oxygenators, respiratory insufficiency is uncommon unless severe preexisting disease is present. The simplest numerical expression of this failure is elevation of the A-a gradient, representing the inability of oxygen to diffuse across the alveolar membrane.

Low-Grade Fever Low-grade fevers are common in the first 24–48 h after surgery and are due to pulmonary atelectasis and the use of blood products. After this time, postpericardiotomy syndrome may be present, usually treated with an anti-inflammatory medication. Specific causes, such as infection, need to be sought. The most serious cause is a mediastinal wound infection, which requires prompt return to the operating room. This complication occurs in 1–2 percent of open heart patients.

Renal Failure Urine output should be 0.5–1.0 mL/kg/h. Renal failure is uncommon with postoperative cardiac indices above 2 L/min/m², unless there is preexisting disease. Renal failure may be treated with hemodialysis or peritoneal dialysis.

Central Nervous System Dysfunction Stroke risk is increased in the elderly and patients with atherosclerotic aortas. Every effort should be made to remove air and debris from cardiac chambers before unclamping the aorta. Mean pressures during the pump run should be kept at least 60 mmHg, especially in the elderly.

SPECIFIC DISEASES

Coronary Artery Disease

Atherosclerosis is the fundamental cause, with the basic lesion being a segmental atherosclerotic plaque often localized in the proximal 5 cm of the coronary vessel. Clinical manifestations include angina pectoris, sudden death, myocardial infarction, and congestive heart failure. Angina pectoris is most common, and the differential diagnosis includes anxiety states, musculoskeletal disease, and esophageal reflux. In 25 percent of the patients, symptoms are atypical. Laboratory investigations include a variety of stress tests using electrocardiographic (ECG) monitoring, radionuclide scanning, or echocardiography. Coronary angiography remains the “gold standard.” A stenosis is considered significant when the diameter is reduced by more than 50 percent, corresponding to a reduction in the cross-sectional area of 75 percent. Ventriculography is used to measure ejection fraction (EF), with normal EF 55–70 percent, moderately depressed EF 35–55 percent, and severely depressed EF under 35 percent. Regional wall motion is described as normal, hypokinetic (impaired), akinetic (no visible contraction), and dyskinetic (paradoxical contraction). Positron emission tomographic (PET) or thallium scanning may reveal areas of viable yet nonfunctional myocardium (hibernating) that will benefit from revascularization.

Coronary artery disease can be treated either medically or surgically, which involves coronary artery bypass grafting (CABG). Indications for CABG are determined by symptoms, number of stenotic major coronary arteries, and left ventricular ejection fraction (LVEF).

Coronary surgery (CABG) results in improved survival in patients with unstable symptoms, severe proximal coronary disease (triple-vessel and/or left main), depressed LVEF, or a poor response to stress testing. Unstable situations such as postinfarction angina or structural defects require more urgent intervention. Angioplasty and other intracoronary therapies are used for single and occasionally multivessel disease. Survival is superior for CABG versus angioplasty in diabetic patients, those with triple-vessel disease, and those with double-vessel disease with a tight left anterior decending (LAD) artery stenosis.

Surgical techniques include the use of cold blood cardioplegia with systemic hypothermia and topical cooling. Saphenous vein grafts are used, whereas mammary arteries are preferred, with sequential and bilateral mammary grafts increasing in frequency. Recently, an increased use of other arterial conduits has emerged, including the radial (most common), gastroepiploic, inferior epigastric, and other arteries. Hospital stay is usually 5–7 days, and full return to activity usually occurs in 6–8 weeks. Mortality risk is approximately 1–3 percent, with a morbidity rate of 5 percent and an overall frequency of stroke of 2 percent (up to 10 percent for patients over age 70). Carotid artery surgery is not used unless acute cerebral symptoms (transient ischemic attacks) are present.

Postoperatively, relief of angina is seen in 90–95 percent of patients, correlating with improvement in wall motion abnormalities. Vein graft patency at 1 month exceeds 95 percent, with an attrition rate of approximately 1–2 percent per year up to 5 years. Thereafter, rapid progression of atherosclerotic disease can be seen, and at 10 years, patency rate is about 60 percent. The 10-year patency rate of left internal mammary artery grafts is over 95 percent, whereas the long-term patency of other arterial conduits remains to be determined. Progression of native disease is a major factor, which may be reduced by decreasing the serum cholesterol level. Recurrent angina occurs at a rate of 3–5 percent per patient-year. If LV damage or scarring is present, arrhythmia is usually not improved after CABG. Longevity in patients with coronary artery disease tends to favor operation versus medical treatment when the LVEF is depressed, moderate to severe angina is present, or two or more coronary arteries are stenotic. New developments for the treatment of coronary artery disease include MIDCAB (minimally invasive direct coronary artery bypass (MIDCAB), port-access surgery, transmyocardial laser revascularization (TMLR), and gene therapy.

Left Ventricular Aneurysm

A left ventricular aneurysm (LVA) develops over a period of 4–8 weeks in 10–15 percent of patients after a transmural myocardial infarction. Mural thrombus is present in 50 percent of the patients, whereas emboli and rupture are rare. Most LVAs (>80 percent) are anterolateral. In 30–40 percent of patients, single-vessel disease is present, and large aneurysms impair ventricular function. Longevity is probably related to underlying ventricular function. Distinction must be made at operation between akinetic scar and true aneurysm. Surgical considerations include (1) not disturbing the aneurysm until the aorta is cross-clamped, avoiding emboli, (2) subtotal resection of the aneurysm, maintaining LV muscle and geometry, (3) possible endocardial resection to treat arrhythmias, and (4) appropriate coronary artery grafts to improve global circulation.

Valvular Diseases

MITRAL STENOSIS

Mitral stenosis is almost always due to rheumatic heart disease. Rheumatic fever produces a pancarditis, but it is the endocardial changes that predominate, resulting in scarring of the valve tissue. Turbulent flow results, and hemodynamic changes cause commissural fusion, valve fibrosis, and calcification. Leaflet mobility decreases while the subvalvular apparatus (chordae tendineae) and papillary muscles become thickened, fibrotic, and contracted. Thus the pathologic changes of mitral stenosis do not develop from multiple episodes of rheumatic fever but rather from the turbulent flow resulting from the initial episode. Repair of the mitral valve and decreasing leaflet turbulence may result in a good long-term result.

Normal mitral valve orifice area is 4–6 cm². Reduction to 2–2.5 cm² constitutes mild mitral stenosis (class I). Patients with a cross-sectional area less than 1 cm² are severely disabled (class IV). Mitral stenosis results in the following significant physiologic derangements:

Increased left atrial pressure, enlargement, and eventually atrial fibrillation with a risk of embolization.
Low CO due to a fixed, stenotic orifice.
Variable increases in pulmonary vascular resistance, primarily a result of vasoconstriction in the pulmonary arterioles. In the majority of patients, pulmonary hypertension abates after surgical repair.

The main symptoms in mitral stenosis are exertional dyspnea and fatigue. Dyspnea develops when left atrial pressure rises to exceed the oncotic pressure of plasma leading to transudation of fluid across the pulmonary capillaries. When this interstitial fluid load exceeds lymphatic capacity, pulmonary edema occurs. Systemic emboli occur with increases in left atrial size and atrial fibrillation. Hemoptysis may occur but is usually not severe. Right-sided heart failure occurs later secondary to elevated pulmonary vascular resistance (PVR). Physical examination usually shows cardiac cachexia. Pulmonary congestion is frequent. The “auscultatory triad” includes an increased first heart sound, an opening snap, and an apical diastolic rumble.

The chest radiograph demonstrates a left atrium as a double shadow behind the heart. The usual concavity between the aorta and left ventricle appears as a “straight” left heart border. Mitral valve calcification also may be seen. Pulmonary hypertension causes large pulmonary arteries, and Kerley lines may be present.

Echocardiography (transthoracic or transesophageal) can determine the degree of atrial enlargement, estimate the degree of mitral stenosis, and provide information about leaflet mobility. Cardiac catheterization provides additional information but may not be necessary in patients under age 40 if good echocardiographic data are available. Cardiac catheterization helps delineate the severity of the mitral stenosis, the level of PVR, and the status of the coronary arteries.

Operation should be considered routinely with hemodynamically significant mitral stenosis even if symptoms are minimal. The operative risk is approximately 1 percent, and in early mitral stenosis, reconstruction rather than replacement is often possible (90 percent). The presence of systemic emboli is an indication for surgery because recurrent emboli are common. Most important, mitral stenosis may be repaired successfully regardless of the severity of PVR. The left ventricle in pure mitral stenosis is protected, and PVR is reduced postoperatively in most patients.

MITRAL INSUFFICIENCY

Etiologies include degenerative disease (50 percent), rheumatic fever (20–30 percent), ischemic disease (15–20 percent), endocarditis, congenital abnormalities, and cardiomyopathy. Type I insufficiency due to annular dilatation or leaflet perforation is usually caused by ischemia or endocarditis. Type II insufficiency is secondary to increased leaflet motion with prolapse, commonly of degenerative or ischemic origin. Type III occurs with restricted leaflet motion, usually from rheumatic disease. Annular dilatation is an important component of insufficiency and is usually found with types II and III.

The physiologic derangement of this condition is regurgitation of blood from the left ventricle to the left atrium during systole. This results in decreased forward flow and elevated left atrial pressure, causing pulmonary congestion and volume overload of the left ventricle. The left ventricle undergoes dilatation but may function adequately for long periods of time before failure. A systolic murmur radiating to the axilla is characteristic of mitral regurgitation, becoming pansystolic with increased severity. Symptoms, primarily dyspnea, are mild until late in the course.

Diagnosis and anatomic characterization are made by echocardiography. Cardiac catheterization is indicated in advanced insufficiency and cardiac enlargement, uncertain diagnosis, and when coronary disease is a concern. Timing of the operation is difficult, especially since the symptoms are mild until late in the course. An operation should be done before the onset of LV failure.

Operative Technique The standard operative approach is through a median sternotomy with exposure of the valve through a lateral, transseptal, or superior approach. The atrial appendage should be ligated if atrial fibrillation is present preoperatively. Reconstruction techniques (commissurotomy, repair of subvalvular apparatus) are always preferable to replacement. This preserves LV function and avoids the complications of a prosthetic device. Open, precise repair using cardiopulmonary bypass is preferred to the “blind,” closed commissurotomy. Commissurotomy and repair can be performed if the leaflets are pliable and an adequate opening can be obtained. Carpentier and others have used chordi shortening, chordi transplantation, and quadrangular resection with annuloplasty with excellent results. After discontinuing cardiopulmonary bypass, the repair is evaluated using intraoperative transesophageal echocardiogram or direct measurement of the transvalvular gradient. Significant residual stenosis (gradient 5–7 mm) or regurgitation requires additional procedures or valve replacement.

If reconstruction cannot be accomplished, replacement with a bioprosthesis or mechanical valve is performed. Excision of the valve should preserve the chordae to the posterior leaflet in order to preserve the LV geometry and function (especially in mitral insufficiency). In addition, there is some evidence that posterior leaflet preservation protects against LV rupture in the early postoperative period. Sutures for valve replacement should be placed carefully to avoid the circumflex artery (posterior) and the conduction system (anterior). As with repair, care is taken to remove air from all cardiac chambers before LV ejection.

Antibiotics are given perioperatively and continued until all intracardiac lines are removed. Anticoagulation is started within the first 3 days. With a bioprosthesis, warfarin can be stopped after 3 months if normal sinus rhythm is present and left atrial size has decreased. Currently, no ideal cardiac prosthesis exists. Mechanical valves are durable but thrombogenic, with the frequency of thromboembolism approximately 4 percent per patient-year. The frequency of prosthetic thrombosis is 1 percent per year and necessitates the need for lifelong anticoagulation with its attendant risks. Bioprosthetic valves, however, deteriorate over time, and in 10 years, 20–40 percent of the bioprostheses may require replacement. In general, for patients less than 60 years old who can reliably take warfarin, a metal valve is recommended. Older patients often receive the bioprosthesis.

AORTIC STENOSIS

A normal aortic valve has a cross-sectional area of 2.5–3.5 cm², whereas moderate aortic stenosis is present at 1.0 cm². Valve areas as low as 0.4–0.6 cm² may be found with severe aortic stenosis. The effective valve area is determined by the transvalvular gradient and the CO (Gorlin's formula). Aortic stenosis results in progressive concentric hypertrophy of the left ventricle. Causes of aortic valve stenosis are congenital deformity, rheumatic disease, and acquired calcific disease. Calcified congenital bicuspid valve stenosis (46 percent) is characterized by heavy infiltration with calcium on the leaflets, aorta, and ventricle. Rheumatic aortic stenosis with commissural fusion and calcification accounts for 35 percent. Ten percent of the patients have acquired or sclerotic aortic stenosis, where the leaflets are of normal size without commissural fusion. Leaflet immobility occurs because the bases of the cusps are heavily infiltrated with calcium. In older patients (>40 years old), coronary atherosclerosis occurs in 30–50 percent of patients. Characteristically, there is a long asymptomatic period, up to 10–20 years. The classic symptoms include angina pectoris, syncope, and failure. Once symptoms develop, life expectancy is about 3 years, with sudden death accounting for 15–20 percent of fatalities. Syncope develops in 10 percent of patients and may be related to cerebral blood flow or arrhythmia. Angina unrelated to coronary artery disease occurs in 30–40 percent as a result of left ventricular hypertrophy, elevated LV systolic pressures, and subendocardial ischemia. This problem is obviously made worse with coronary artery disease.

Congestive heart failure is an ominous symptom, with a risk of death of 40 percent over the next 2–3 years. Atrial fibrillation also may occur as ventricular failure progresses. The principal physical finding is a harsh systolic murmur at the base of the heart. A prolonged heave is present at the apical impulse instead of the forceful thrust found in mitral regurgitation or aortic insufficiency. Peripheral pulses have a delayed upstroke. Heart size is usually normal. Echocardiography is the principal diagnostic study demonstrating (1) leaflet mobility and Ca²⁺, (2) transvalvular gradient, (3) degree of ventricular hypertrophy, and (4) ventricular dimensions. Cardiac catheterization with coronary angiography is usually necessary. Valve replacement is indicated for all symptomatic patients, for those demonstrating progressive ventricular decompensation, and for those with critical stenoses. Operative replacement of the aortic valve for significant aortic stenosis remains the best long-term treatment. Valve dilatation with balloon angioplasty is possible but is reserved for nonoperative candidates.

AORTIC INSUFFICIENCY

Aortic insufficiency is caused by a variety of diseases. Bacterial endocarditis commonly results in valvular insufficiency, whereas fever is decreasing in frequency. Annular ectasia is a collagen disease associated with cystic medial necrosis and increases in frequency in the older population. In its most severe form (Marfan syndrome), the aortic root and aorta dilate, producing aortic insufficiency and aneurysmal enlargement of the sinuses of Valsalva and ascending aorta.

Atherosclerotic aneurysms have different underlying pathologies and may cause aortic insufficiency from annular dilatation. Aortic dissection with valve cusp detachment from the aortic wall can result in aortic insufficiency. The clinical course is highly variable depending on the degree and rate of increased aortic insufficiency.

Aortic insufficiency causes diastolic volume overload of the LV. The regurgitant volume may be two to three times the normal stroke volume, 60–70 mL. The LV adaptation is quite different from aortic stenosis, in which concentric muscular hypertrophy occurs. Because of the compensatory mechanism of chamber dilatation, LV end-diastolic pressure and left atrial pressure remain normal until late in the course, when LV failure occurs. Mitral regurgitation might develop at this point as a result of annular dilatation. Death may occur within 4–5 years because of progressive LV failure.

Symptom-free intervals of 8–10 years are common. Symptoms usually develop once LV failure begins in the chronic form. The left ventricle maintains its SV by dilatation, causing massive cardiac enlargement. Anginal symptoms also may be present with severe disease. On physical examination, the murmur is a high-pitched decrescendo diastolic murmur along the left sternal border starting immediately after the second heart sound. Systolic blood pressure remains stable, but diastolic pressure drops. Peripheral pulses increase and often can be visualized because of the widened pulse pressure.

Timing an operation is difficult because once symptoms develop, some degree of LV failure is usually present. Means of detecting the early LV failure have been attempted, and echocardiography, showing an end-systolic dimension greater than 55 mm, has been recommended. A decreased ejection fraction with exercise also has been used to improve surgical results. Even with moderate or severe LV dysfunction, operation is recommended, since death is almost always a certainty otherwise. In this subset of patients, the degree of improvement following surgery is difficult to predict.

Operative Technique Aortic valve surgery is usually performed through a median sternotomy with cardiopulmonary bypass and antegrade or retrograde cardioplegia. A left ventricular vent is placed by way of the right superior pulmonary vein. An aortotomy is performed, and the valve is inspected and completely excised; the annulus is debrided as necessary. Most commonly pledgeted horizontal mattress sutures are placed; alternatively, simple, interrupted figure-of-eight or continuous sutures can be used. Currently, a number of prostheses are available: bioprosthetic valves, including porcine, pericardial, stentless porcine, homograft, and autograft (Ross procedure), and a variety of mechanical valves. Postoperative care includes anticoagulation and observation for arrhythmias. Operative mortality is low (1–2 percent). Five-year survival is 80–90 percent for good ventricles.

TRICUSPID STENOSIS AND INSUFFICIENCY

Distinction needs to be made between organic and functional tricuspid valve disease. Organic tricuspid valve disease is almost always due to rheumatic fever; 10–30 percent of patients with left-sided disease also will have tricuspid valve involvement. The pathology is similar to the more familiar mitral valve disease. Organic tricuspid stenosis is more frequent than insufficiency, which can be caused by endocarditis and trauma. Functional tricuspid valve disease is more common and occurs when normal leaflets do not coapt as a result of annular dilatation. This valvular insufficiency is due to left-sided heart disease with subsequent pulmonary hypertension and right-sided heart failure.

Normal right atrial pressure is 4–5 mmHg. When the tricuspid orifice becomes smaller than 1.5 cm², the atrial pressure rises, with a mean gradient of 5–15 mmHg, resulting in symptoms similar to right-sided heart failure with edema, ascites, and hepatomegaly. A characteristic murmur of tricuspid stenosis is a diastolic murmur at the lower sternum. Inspiration will increase its intensity. A moderate degree of tricuspid insufficiency may be tolerated with little adverse effect. Tricuspid insufficiency produces a systolic murmur at the lower sternum.

Diagnosis of tricuspid valve disease can be accomplished with ultrasound and right-sided heart catheterization. A transvalvular gradient of 4–5 mmHg is significant. At the time of operation, palpation can be a useful indicator of tricuspid insufficiency, whereas both anatomic findings and preoperative symptoms determine the decision for surgical repair. With minor symptoms and anatomic changes, the tricuspid valve should be left alone. If right atrial hypertrophy and/or dilatation is present and the annulus is mildly dilated, repair almost always should be performed. Repair can be accomplished by posterior leaflet annuloplasty, DeVega annuloplasty, or the ring annuloplasty technique of Carpentier. Tricuspid stenosis usually can be handled with a commissurotomy. When leaflet destruction precludes repair, replacement needs to be carried out. Mechanical valves have a higher incidence of thrombotic complications than bioprostheses, which are preferred. When the prosthesis is placed, care must be taken to preserve the septal leaflet, avoiding the complications of heart block. The conduction bundle lies between the coronary sinus and the ventricular septum. With bacterial endocarditis, there is controversy over whether the prosthetic device should be placed at the initial operation or at a later time if right-sided heart failure occurs. Operative mortality is low (1–2 percent). Long-term prognosis depends on underlying myocardial dysfunction.

MULTIVALVULAR DISEASE

With rheumatic heart disease, more than the cardiac valve may be involved. Prominent signs of disease in one valve can readily be masked by disease in other valves. Echocardiography is a valuable tool to determine the contribution of each valve.

CARDIAC TUMORS

Metastases are the most common cardiac tumors, occurring in 4–12 percent of autopsies performed in patients with neoplastic disease. The most frequent primary cardiac tumor is myxoma, comprising 50–60 percent of all primary cardiac tumors. Sarcoma and rhabdomyoma are less common. Benign but extremely rare neoplasms include fibromas, angiomas, lymphomas, and teratomas. Two-dimensional echocardiography is now the keystone of diagnostic studies.

Between 60 and 75 percent of cardiac myxomas develop in the left atrium, almost always from the atrial septum near the fossa ovalis. Most other myxomas develop in the right atrium, and less than 20 have been found in either the right or left ventricle. Myxomas are true neoplasms. They are usually polypoid, arising from superficial layers of the septum, and invasion does not occur. Metastases are rare. The tumor is friable, so emboli can occur. Myxomas cause symptoms by growing large enough to restrict flow or prolapsing through the mitral or tricuspid valve. The tumor is friable in 40–50 percent of patients. Some myxomas produce generalized symptoms resembling an autoimmune disorder, including fever, weight loss, arthralgias, and myalgias.

Treatment is prompt operative removal. A biatrial incision is used for good exposure and complete exploration. The tumor and septum are removed, and the resulting atrial septal defect is closed with a patch. Cardiac rhabdomyomas are probably hamartomas and are most common in children. About 50 percent of patients have tuberous sclerosis of the brain, and the tumor is usually fatal.

PERICARDITIS

Acute pericarditis can be caused by infection, myocardial infarction, trauma, neoplasm, radiation, autoimmune diseases, drugs, and others. Treatment is directed by etiology (e.g., antibiotic therapy for infection or nonsteroidal anti-inflammatory drugs for postinfarction pericarditis) and drainage either by aspiration or operation.

Chronic constrictive pericarditis is usually idiopathic. The physiologic derangement due to limitation of diastolic filling of ventricles results in decreased SV and CO and increased systemic venous pressure. This disease rarely develops after an open heart operation.

Cardiac catheterization results are characteristic, showing the “square root” sign and equalization of pressures. Treatment is surgical removal of pericardial constriction. The approach is through median sternotomy. The pericardium is removed as completely as possible from both ventricles along with the atria and cavae. The plane of resection is usually between the pericardium and epicardium, which, if thickened, may require removal or incision in a gridlike fashion.

ARRHYTHMIA SURGERY

Current ablative therapies are now done for Wolff-Parkinson-White (WPW) syndrome, paroxysmal supraventricular tachycardia, sustained ventricular tachycardia, or atrial fibrillation. The Maze procedure can treat chronic atrial fibrillation successfully.

PACEMAKERS/IMPLANTABLE DEFIBRILLATORS/INTRAAORTIC BALLOON PUMP/ASSIST DEVICES

Technology in this field is changing rapidly. The two most common methods of pacing are R wave–inhibited demand ventricular (VVI) and AV synchronous (DDD). Both require an electrode in the right ventricle, and the second requires an additional wire in the right atrium. These electrodes are usually placed transvenously to engage the endocardial surface. Both methods of pacing prevent syncope by pacing the heart during periods of bradycardia. The latter technique (DDD) allows AV synchrony. Current pacemakers are programmable, allowing rate, pulse amplitude, duration, AV delay, and other variables to be changed. Recently, a code has been developed to describe all pacemakers. Three or more letters are used, representing chamber pace, chamber sensed, and the mode of generator function. Operative techniques usually involve surgical exposure of the cephalic vein, with other options including external jugular, internal jugular, and subclavian percutaneous introduction. Endocardial electrodes require threshold testing, which should be between 0.4 and 0.8 mA and 0.2 and 0.4 V. The most common indicator for pacemaker insertion today is heart block in the elderly (Lev disease). It is uncommon to require a pacemaker after heart block from myocardial infarction. Telephone ECG surveillance is used for pacemaker follow-up, helping to decrease the morbidity from heart block. Another use of cardiac pacemakers and electrodes is the automatic implantable defibrillator, which allows successful detection and termination of malignant ventricular arrhythmias.

Temporary assisted circulation is a valuable clinical modality when transient cardiac injury is present. It is seldom effective if required for more than 2–3 days. Intraaortic balloon pumping (IABP) is an effective method to augment coronary blood flow and decrease LV work. The IABP is alternately inflated during diastole and deflated during systole. CI is usually increased 0.5–0.7 L/min/m². Ischemia of the extremity is the most common complication. If the IABP is not effective, left-sided heart bypass or assist also can be used. Blood is removed from the left atrium or ventricle and returned to the systemic circulation, reducing left-sided work and improving CO. As opposed to the IABP, ventricle assist can be used for prolonged periods of time. Newer devices are implantable and often are used as a bridge to transplantation, some even on an outpatient basis. Research continues on the total artificial heart.

For a more detailed discussion, see Galloway AC, Colvin SB, Grossi EA, Spencer FC: Acquired Heart Disease, chap. 18 in Principles of Surgery, 7th ed.