COMPLICATIONS OF MYOCARDIAL INFARCTION AND THEIR MANAGEMENT



In patients who develop mild congestive heart failure with pulmonary congestion during acute myocardial infarction, administration of a di­uretic may be sufficient therapy. Indications for hemodynamic monitoring are listed in Table 7-10. Hemodynamic monitoring allows measure­ment of left ventricular filling pressures (pulmo­nary capillary wedge pressure) and cardiac out­put, and the calculation of systemic vascular resistance. Patients with myocardial infarction may be grouped into subsets based on these mea­surements (Table 7-11). When the normal cardiac index (approximately 2.5 to 3.6 L/min/sq m) is re­duced to 1.8 to 2.2 L/min/sq m, hypoperfusion oc­curs; shock occurs at levels less than 1.8 L/min/ sq m. The normal pulmonary capillary wedge pressure is 10 to 12 mm Hg, but the optimum wedge pressure in a patient with acute myocardial infarction and a relatively noncompliant ventricle is usually 14 to 18 mm Hg.

Even if pharmacological therapy or intra-aortic balloon counterpulsation provides temporary im­provement, patients with cardiogenic shock due to cardiac muscle destruction have a poor prog­nosis. However, patients who have cardiogenic shock secondary to surgically correctable me­chanical factors, for example, acute mitral regur­gitation or acquired ventricular septal defect, have a somewhat more favorable outlook. Myocardial revascularization improves an occasional patient with episodes of profound but reversible my­ocardial ischemia producing hypotension and shock.

Patients with right ventricular infarction may present with hypotension or shock (due to de­creased cardiac output) and signs of right ven­tricular failure. The lungs are clear if left ventric­ular failure or pre-existing pulmonary disease is not present. Tricuspid insufficiency may occur. Fluid administration to raise right ventricular fill­ing pressures and augment left ventricular filling reverses the shock and hypotension, even when jugular venous distention and other manifesta­tions of systemic congestion exist. Right ventric­ular infarction is relatively common in patients with inferior myocardial infarction and is some­times difficult to differentiate from cardiac tam­ponade. Most patients with right ventricular in­farction do well, and their long-term prognosis depends on the extent of left ventricular infarc­tion.

Approximately 20 per cent of patients extend their myocardial infarction within the first five days after infarction. The extension may be as­sociated with recurrent chest pain that is some­times difficult to distinguish from post-myocar-dial infarction pericarditis or recurrent angina. Continued angina and extension of myocardial in­farction are usually unfavorable signs and may be indications for catheterization.

Many patients upon presentation with an acute myocardial infarction have mild to moderate hypertension because of pain, anxiety, and some­times mild congestive heart failure. With relief of pain and treatment of heart failure, hypertension usually disappears within a few hours. However, sustained or severe blood pressure elevation should be treated vigorously to decrease myocar­dial oxygen consumption. Intravenous nitroprus-side may be employed, and oral agents can be sub­stituted as needed.

Rupture of an entire papillary muscle due to myocardial infarction is usually rapidly fatal owing to massive mitral regurgitation. However, rupture of one head of a papillary muscle may be tolerated for a period of time, allowing for diag­nostic evaluation and surgical correction. Some form of papillary muscle rupture occurs in less than 5 per cent of patients with acute infarction. Papillary muscle dysfunction is more common than rupture and occurs when ischemia interferes with contraction of the papillary muscles and nor­mal coaptation of the mitral valve leaflets. The degree of mitral regurgitation from papillary mus­cle dysfunction is usually less than that caused by papillary muscle rupture. Acute medical ther­apy for papillary muscle rupture may require in­otropic agents, diuretics, vasodilators, or intra-aortic balloon counterpulsation. If the patient can be stabilized and weaned from balloon counter­pulsation, surgical mitral valve replacement may be attempted four to six weeks after infarction when infarct scar formation is advanced. How­ever, if hemodynamic stabilization cannot be ob­tained or requires intra-aortic balloon counter­pulsation, early mitral valve replacement should be undertaken.

Rupture of the ventricular septum develops in about 1 per cent of myocardial infarctions and re­sults in marked biventricular failure. It may occur with both inferior and anterior infarctions. It is associated with a holosystolic murmur along the left sternal border and is often difficult to differ­entiate from acute mitral insufficiency. A thrill is more common with ventricular septal defects than acute mitral regurgitation. Right heart (Swan-Ganz) catheterization may be necessary to dis­tinguish acute ventricular septal rupture from mi­tral regurgitation by detecting an oxygen step-up between the right atrium and right ventricle. In­creased pulmonary vascularity due to the left-to-right shunt may be seen on chest x-ray. Two-di­mensional echocardiography can occasionally visualize the ventricular septal defect, but more often a septal aneurysm is demonstrated, with the ventricular septal defect presumably located in the apex of the aneurysm. Contrast echocardiog­raphy may define the defect. Surgical mortality is highest within the first month after infarction, but if ventricular failure is severe, surgery-must be undertaken early.

A ventricular aneurysm is a localized area of thin, scarred myocardium that protrudes beyond and distorts the ventricular cavity . Ven­tricular aneurysms may develop within days of myocardial infarction and gradually stretch, thin, and enlarge over weeks to months. The wall mo­tion of an aneurysm on ventriculography may be akinetic or dyskinetic. Large aneurysms may con­tribute to congestive heart failure by expanding during systole, decreasing the efficiency of blood expulsion. Most patients with ventricular aneu­rysms are asymptomatic. True ventricular aneu­rysms do not rupture. Mural thrombi commonly form in the ventricular aneurysms and appear less likely to embolize in patients who are systemi-cally anticoagulated. Ventricular aneurysms often are associated with ventricular tachyarrhythmias originating from the edge of the aneurysm. Pa­tients with ventricular aneurysms usually dem­onstrate electrocardiographic evidence of trans­mural myocardial infarction, and in many cases there is persistent ST segment elevation in the ECG leads with vectors pointing toward the aneu­rysm. Occasionally, the aneurysm can distort the cardiac silhouette enough to be visible on chest x-ray, appearing as a localized bulge on the sur­face of the left ventricle, sometimes with calcium in the wall. Two-dimensional echocardiography reliably delineates ventricular aneurysms. Refrac­tory congestive heart failure or recurrent systemic emboli despite anticoagulation warrant aneurys-mectomy. Aneurysmectomy alone is usually in­sufficient to control recurrent refractory ventric­ular tachyarrhythmias, which require combined aneurysmectomy with resection.

Rupture of the ventricular free wall is usually rapidly fatal. Rupture usually occurs within the first five days following transmural infarction. The patient’s initial course may be uneventful until the abrupt occurrence of cardiogenic shock and rapid progression to death. Rare patients have survived after successful pericardiocentesis and emergency surgical repair. Occasionally, the course is less acute and blood is walled off within the pericardial space, giving rise to a pseudo-aneurysm. In contrast to true aneurysms, pseu-doaneurysms may rupture and require immediate intervention. The diagnosis of pseudoaneurysm is usually made by echocardiography, showing a narrow-based communication between the ven­tricular cavity and pseudoaneurysm, whereas the communication between a true aneurysm and the ventricular cavity is wide.

Early ambulation and the use of prophylactic subcutaneous minidose heparin have decreased the risk of venous thrombosis and pulmonary em­bolism after myocardial infarction. If deep vein thrombophlebitis or pulmonary embolism is documented, intravenous heparin should be admin­istered for at least seven days and followed by two to six months of oral warfarin. Patients who have systemic emboli also should be treated with in­travenous heparin followed by two to six months of oral warfarin. Consideration should be given to removal of peripheral emboli by surgical embolectomy.

Pericarditis occurs in 7 to 15 per cent of patients within the first week after acute infarction, most frequently in those with transmural infarction of at least moderate size. If a pericardial friction rub is heard, the diagnosis is confirmed, but many pa­tients do not have audible rubs. It is sometimes difficult to distinguish the pain of pericarditis from that of angina pectoris. Anticoagulation should be avoided in patients with active peri­carditis because of the risk of developing hem­orrhagic tamponade. Sinus tachycardia occurring with pericarditis must be differentiated from other causes of sinus tachycardia, for example, he­modynamic deterioration.
A small number of patients, probably less than 5 per cent, develop a late postinfarction syndrome {Dressler’s syndrome) consisting of pericarditis, pericardial effusion, pleural effusion, and some­times fever. The etiology is unknown but may be immunological. Multiple recurrences sometimes occur. If salicylates or nonsteroidal anti-inflam­matory agents are not sufficient, short courses of high-dose corticosteroids provide relief.