Complications of Acute Myocardial Infarction

During the healing phase after acute myocardial infarction, disruptions of cardiac anatomy or function may lead to left ventricular aneurysm, left ventricular free wall rupture, acute ventricular septal defect, acute mitral regurgitation, right ventricular myocardial infarction, or pericarditis. The author explains how to recognize and deal with these complications and, where possible, prevent them.

By Jorge A. Martinez, MD, JD

Acute myocardial infarction (AMI) is the result of a dynamic process in which an intraluminal coronary artery plaque ruptures, leading to the formation of a platelet and red blood cell thrombus that occludes the culprit vessel. The occlusion prevents the flow of blood distal to the site, causing anoxia to the myocardium that is no longer supplied by the vessel. The end result is coagulation necrosis and death of the involved myocardium.

During an AMI, the patient may develop systolic dysfunction of the ventricles or arrhythmias, which may adversely affect cardiac output. In the ensuing recovery phase, the patient may suffer acute cardiac decompensation due to anatomic disruptions in the soft, necrotic myocardium or develop symptoms similar to acute ischemia as the healing process affects the pericardium.

This article will discuss common, nonischemic, nonarrhythmic complications of AMI that typically occur during the postinfarction healing period. In general, each complication has characteristic symptoms and physical findings that are the result of a disruption in cardiac anatomy or function. Recognizing the symptoms and physical manifestations of these complications is imperative if they are to be diagnosed, evaluated, and treated successfully.
 

LEFT VENTRICULAR ANEURYSM

Left ventricular aneurysm (LVA) occurs in 5% to 30% of AMI patients who do not undergo emergent revascularization. The aneurysms typically develop in anterior transmural AMI (see image, below). Emergent revascularization can re-establish blood flow through the infarct-related artery. Aggressive blood pressure control during the acute and post-AMI periods is also associated with decreased LVA formation.

Ventricular aneurysm with mural thrombus. Occasionally, this complication presents as a cerebrovascular or peripheral vascular disorder secondary to embolization of the mural thrombus.

The most common locations for LVAs are the apex and anterior wall of the left ventricle, with a size range of one to eight centimeters. Mortality with LVA is six times higher than in patients without an aneurysm. The use of angiotensin-converting enzyme (ACE) inhibitors within twenty-four hours of AMI has been shown to retard ventricular remodeling and resulting LVA formation.

Left ventricular aneurysms form at the infarcted area of the myocardium, where intraventricular pressures stretch the necrotic, noncontracting myocardium. This causes the infarcted segment to dilate and the aneurysm to form. Because the aneurysm is thinner than the viable myocardium and because it does not contract, it bulges outward during systole. The result is a decrease in ventricular stroke volume and a corresponding drop in cardiac output, as well as the pooling of blood in the aneurysm that facilitates thrombus formation.

Mural thrombus formation occurs in approximately 40% of anterior AMI patients who do not receive systemic anticoagulation. Approximately 60% of the thrombi are located in the apex of the left ventricle. The use of systemic anticoagulation during the acute and post-AMI period has reduced the incidence of mural thrombus formation and embolization. Interestingly, when thrombolytic therapy has been employed and reperfusion is achieved, the incidence of mural thrombus formation has been reduced.

Patients with LVA usually experience chest pain days to weeks after their AMI. However, in some cases the initial clinical presentation will involve acute heart failure due to the decrease in effective stroke volume, rupture of the aneurysm, or ventricular arrhythmias. Sudden death may also result from ventricular arrhythmias. These arrhythmias occur because the myocardium adjacent to the aneurysm is irritable and arrhythmogenic. Occasionally, acute cerebrovascular accident or peripheral vascular occlusion due to mural thrombus embolization will be the initial presentation. Importantly, mortality and morbidity associated with LVA is more commonly the result of left ventricular failure or arrhythmias than mural thrombus embolization.

Laboratory studies that assist in diagnosing LVA include a chest x-ray, which may demonstrate cardiomegaly. A characteristic ECG finding is persistent ST-segment elevation in the same leads as a recent AMI. Echocardiography typically shows the aneurysm and may also detect a mural thrombus.

Management of LVA includes aggressive treatment of acute heart failure and ventricular arrhythmias. Patients who suffer a large anterior MI, demonstrate diffuse wall motion abnormalities on echocardiography, or have a history of mural thrombus should receive anticoagulation therapy. Heparin is used acutely to maintain the INR at 1.5 to 2 times normal. Coumadin should then be administered orally for three to six months. Aspirin may be added to the coumadin regimen.

Risk factors for mural thrombus embolization include large anterior wall AMI, AMI complicated by severe left ventricular dysfunction, heart failure, echocardiographic evidence of mural thrombus or left ventricular aneurysm, previous mural thrombus, and atrial fibrillation. In patients with one or more of these risk factors, systemic anticoagulation should be seriously considered. Surgical aneurysmectomy may be necessary if medical therapy fails to control heart failure, arrhythmias, or mural thrombus formation.

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LEFT VENTRICULAR FREE WALL RUPTURE

Left ventricular free wall rupture (LVFWR) occurs in 1% to 8% of AMI patients (see image, below) and is responsible for 8% to 24% of post-AMI deaths. About 30% of LVFWRs occur within the first 24 hours postinfarction and 90% occur within the first 14 days. The highest incidence is in the first four days. Left ventricular free wall rupture is more common in women, patients older than 55 with a first AMI, and those with hypertension. Emergent revascularization is associated with a decreased incidence of LVFWR, with primary angioplasty being more effective than thrombolytic therapy.

Free-wall rupture. This problem is more common in women, patients over age 55 with a first AMI, and hypertensive patients.

The most common rupture site is the junction of necrotic and normal myocardium in transmural anterior or anterolateral AMI. Rupture is seven times more common in the left ventricle than the right ventricle. Death results from acute pericardial tamponade, which is the consequence of rapid, unimpeded blood flow from the ventricular cavity into the pericardial sac.

Patients with LVFWR experience an abrupt onset of chest pain, usually a tearing sensation. Clinical findings resulting from the acute pericardial tamponade include tachycardia, hypotension, pulsus paradoxicus (a drop in peak systolic blood pressure of more than 20 mm Hg on inspiration), narrow pulse pressure, distended neck veins, agitation, confusion, shock, and pulseless electrical activity. Chest x-ray commonly demonstrates cardiomegaly. Electrocardiography reveals tachycardia and occasionally electrical alternans. Echocardiography demonstrates a defect in the ventricular wall, pericardial effusion, and evidence of pericardial tamponade (specifically, collapse of the right atrium, right ventricle, or both during diastole). Doppler echocardiography confirms turbulent blood flow through the ventricular wall defect.

Management of LVFWR hinges on diagnosing and addressing the acute pericardial tamponade. Medical management is rarely successful because the immediate onset of tamponade causes circulatory collapse and cardiac arrest. Consequently, emergent pericardiocentesis and surgical correction of the defect are mandatory. An intra-aortic balloon pump (IABP) may be used as a temporary measure to enhance left ventricular emptying until the patient can be taken to surgery. Medical resuscitation using fluid volume and pressor support may also be initiated.

Arrhythmias should be controlled to maximize cardiac output. Beta blockers, which reduce heart rate, contractility, and ventricular pulsatile forces, will decrease blood volume ejected through the defect. The addition of ACE inhibitors will reduce afterload and promote blood flow through the aorta rather than through the defect.

A variation of LVFWR is pseudoaneurysm, which is a collection of blood in the pericardial sac through a ventricular wall defect. In pseudoaneurysm, blood from the defect does not fill the entire pericardial sac. Instead, because of adhesions between the ventricular wall and the sac, the escaping blood is isolated to a localized area between the wall and the pericardium. This prevents acute pericardial tamponade.

Pseudoaneurysm is more common in inferior and posterior AMI. Typically, patients complain of acute onset of chest pain or discomfort. However, sudden onset of acute heart failure or arrhythmias is not uncommon. Echocardiography demonstrates the ventricular wall rupture and the entrapped blood in the pericardial sac. Definitive treatment is surgical correction of the defect.
 

ACUTE VENTRICULAR SEPTAL DEFECT

A severe complication of AMI is acute ventricular septal defect (VSD), which occurs in 2% of patients (see image, below). It commonly occurs within 24 hours to three weeks of the AMI, with peak incidence at three to five days. It is more common in anteroseptal AMI and in the elderly and patients with hypertension. Approximately 60% of VSDs occur in the anterior septum because the left anterior descending coronary artery, the culprit vessel in anteroseptal AMI, supplies the superior two-thirds of the interventricular septum. The remaining 40% occur in the posterior septum and are associated with a worse prognosis. Ventricular septal defect is more common with poor collateral coronary circulation, multivessel coronary disease, and involvement of the left anterior descending coronary artery. Thrombolytic therapy is associated with a slightly lower incidence of VSD. However, the onset of VSD has been found to occur earlier in the post-AMI period when thrombolytic therapy is employed.

Ventricular septal defect. Patients with poor collateral circulation, multivessel coronary disease, and involvement of the left anterior descending coronary artery are especially susceptible to this complication.

In VSD, the rupture of the interventricular septum results in an immediate shunt from the higher-pressure left ventricle to the lower-pressure right ventricle. Increased volume in the right ventricle causes right ventricular overload and dilation, increased pulmonary artery blood flow, and elevated pulmonary artery pressure. At the same time, the left-to-right shunt causes a loss of left ventricular blood volume with a corresponding decrease in stroke volume. The result is a sudden fall in cardiac output, with hypotension, tissue hypoperfusion, and, in most cases, shock.

Clinical presentation of VSD includes acute chest pain, shortness of breath, sudden tachycardia, biventricular failure, and hypotension. A new-onset holosystolic murmur is often heard. It is usually harsh and in 90% of patients is heard throughout the precordium. A systolic thrill is palpated in 50% of patients. Because of the acute increase in right ventricular and pulmonary artery volumes and pressures, jugular vein distension and an accentuated pulmonary component of the second heart sound are common.

Relevant diagnostic studies include echocardiography, which demonstrates the septal defect, dilated right ventricle, and occasionally tricuspid regurgitation. Doppler echocardiography shows blood flow through the shunt and increased pulmonary artery blood flow. Importantly, right heart catheterization may be used to diagnose VSD. Blood is sampled from the superior vena cava and pulmonary artery. Because of the flow of oxygenated blood from the left ventricle to the right ventricle through the shunt, there will be a 7% to 10% increase in the oxygen saturation in the blood of the right ventricle compared to that of the superior vena cava.

Management of VSD initially involves promoting forward ventricular emptying through the aorta, followed by surgical correction of the defect. Afterload-reducing agents, including ACE inhibitors, nitroprusside, intravenous (IV) nitroglycerin, and hydralazine, can be used to promote left ventricular emptying. Inotropic agents such as dobutamine or milrinone may serve the same purpose; these agents also reduce afterload through peripheral vasodilation. An IABP may be used for severe hypotension or if medical management is unsuccessful. Definitive treatment for VSD is surgical repair.

Survival in VSD is related to the size of the defect, the extent of the left-to-right shunt, and the ability of the right and left ventricles to compensate for changes in blood volume.
 

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ACUTE MITRAL REGURGITATION

Acute mitral regurgitation (AMR) is the result of mitral valve papillary muscle dysfunction or rupture. It occurs in approximately 2% of AMIs, usually within the first two to seven days postinfarction. It is responsible for 5% of post-AMI deaths. Acute mitral regurgitation occurs in both nontransmural and transmural AMI. It is due either to ischemic papillary muscle dysfunction, which results in incompetence of mitral leaflets, or papillary muscle rupture, which results in total incompetence of the mitral valve. Partial papillary muscle rupture is more common than complete rupture.

About 75% of papillary muscle ruptures occur at the posterior papillary muscle because of its vascular supply. The anterior papillary muscle is supplied by the left anterior descending coronary artery and the circumflex coronary artery. Thus, because of its dual blood supply, it rarely ruptures. The posterior papillary muscle has a single blood supply from either the right coronary artery (90%) or the circumflex coronary artery (10%). Accordingly, posterior papillary muscle rupture is more common in inferior and lateral AMI.

Papillary dysfunction or rupture results in a regurgitant jet of blood during systole through the incompetent mitral valve into the left atrium. This regurgitant blood flow fills the atrium and eventually flows back into the pulmonary veins. Thus, AMR is associated with sudden onset of acute pulmonary edema. In complete rupture of the papillary muscle, onset of pulmonary edema is instantaneous and associated with severe pulmonary edema, shock, and death.

The clinical presentation of AMR may range from a new-onset holosystolic murmur in an otherwise hemodynamically stable patient to the sudden onset of shortness of breath, tachycardia, pulmonary edema, hypotension, and shock. Atrial arrhythmias may develop due to distension of the atrium, which is the result of the regurgitant blood flow across the incompetent mitral valve. The increased left ventricular volume causes the left ventricular apical impulse to be displaced. Auscultation of the heart usually reveals an S₃, S₄, and holosystolic murmur. A holosystolic thrill is occasionally palpable.

Chest x-ray usually demonstrates pulmonary edema. Asymmetric pulmonary edema in the upper lobes may be seen if the regurgitant blood flows directly into the pulmonary veins of the right or left upper lobes. Echocardiography reveals flail mitral leaflets and left atrial enlargement. Doppler echocardiography demonstrates the regurgitant blood flowing into the left atrium. Right-heart catheterization demonstrates large V waves in the pulmonary artery and pulmonary capillary wedge pressure tracings.

Medical management of AMR is influenced by the severity of its presentation. If AMR is due to papillary muscle ischemia, enhanced coronary blood flow and afterload reduction with nitroglycerin may be beneficial. In addition, revascularization of the culprit vessel may correct ischemia-induced papillary muscle dysfunction.

In cases where AMR is due to severe papillary muscle dysfunction or papillary muscle rupture, aggressive medical management includes afterload reduction with nitroprusside, IV nitroglycerin, hydralazine, or ACE inhibitors to promote forward ventricular emptying through the aorta. In addition, left ventricular emptying can be enhanced with inotropes such as dobutamine or milrinone. Atrial arrhythmias are often refractory to antiarrhythmic agents and usually require electrical cardioversion. An IABP can be used with severe hypotension or AMR refractory to medical management. Surgery is essential when AMR is secondary to papillary muscle rupture.
 

RIGHT VENTRICULAR MYOCARDIAL INFARCTION

Right ventricular myocardial infarction (RVMI) occurs in 30% to 40% of inferior AMIs and 5% to 10% of anterior AMIs (see ECG, below). It is more common with occlusion of the proximal right coronary artery and is associated with an eight times greater incidence of morbidity and mortality in inferior AMI.

Right ventricular myocardial infarction. Electrocardiography typically shows ST-segment elevation in V3R or V4R when an RVMI has occurred.

The classic clinical findings in RVMI include the triad of hypotension, clear lung fields, and elevated jugular venous pressure. In addition, a right-sided ventricular gallop and evidence of tricuspid regurgitation may be present. These clinical manifestations are the result of several physiologic changes. First, right ventricular ischemia adversely affects right ventricular systolic function. Consequently, the right ventricle is unable to pump an adequate volume of blood to the left ventricle. The reduction in left ventricular volume leads to a decrease in cardiac output. Damage to the right ventricle causes it to dilate in the pericardial sac. The resultant increase in sac pressure impedes the right ventricle's ability to expand and fill during diastole. Increased blood pooling in the right ventricle causes the interventricular septum to bulge into the left ventricle, inhibiting the ability of the left ventricle to fill during diastole. As a result of right ventricular diastolic and systolic dysfunction, a lower pressure gradient exists between the right atrium and right ventricle. Consequently, less blood flows from the atrium into the ventricle during diastole.

Several factors may combine with these pathophysiologic changes to exacerbate the inability of the right ventricle to pump adequate blood volume to the left ventricle. The administration of diuretics or concurrent hypovolemia decreases right ventricular preload. Right ventricular myocardial infarction should always be considered in patients with inferior wall AMI who become hypotensive after receiving diuretics or nitroglycerin. The loss of atrial-ventricular synchrony, as with atrial fibrillation or ventricular tachycardia, eliminates right atrial contraction, reducing the right atrium's contribution to right ventricular end-diastolic volume. Right atrial infarction, common in RVMI, also diminishes the right atrium's ability to contract. Finally, left ventricular failure increases right ventricular afterload and, consequently, decreases the volume ejected from the right ventricle to the left ventricle.

In addition to clinical manifestations, the patient's ECG contributes to the diagnosis of RVMI. Typically, the ECG shows an inferior or posterior AMI. A concurrent right-sided ECG reveals ST-segment elevation in V3R or V4R, which are specific for RVMI. Echocardiography demonstrates a dilated right ventricle, dyskinesis or akinesis of the right ventricle, abnormal septal or right atrial motion, and abnormal flattening of the septum due to right ventricular overload.

Management of RVMI includes reperfusion of ST-segment elevation inferior AMI. Right ventricular preload may be augmented by volume loading and avoiding diuretics. Because of its effect on preload, nitroglycerin should be used with caution. The Trendelenburg position enhances venous return to the right atrium and ventricle. Atrial-ventricular synchrony should be re-established with prompt electrical cardioversion of supraventricular tachycardia, atrial fibrillation, atrial flutter, or ventricular tachycardia. Sequential pacing should be employed in advanced atrioventricular node block. Bradycardia must also be addressed. Inotropic support should be initiated if fluid resuscitation fails to raise blood pressure. Dobutamine is the most effective inotropic agent because it increases ventricular emptying, decreases pulmonary vascular resistance, and reduces right ventricular afterload. Left ventricular failure should be promptly treated in order to reduce right ventricular afterload. Intravenous ACE inhibitors rapidly decrease left ventricular afterload and enhance left ventricular emptying.
 

POST-MYOCARDIAL INFARCTION PERICARDITIS

There are two forms of pericarditis associated with AMI. The first is post-infarction pericarditis (PIP) (see ECG, below), which usually develops within 12 hours to 10 days after a large transmural AMI. It occurs in 6% to 20% of AMI patients who do not receive thrombolytics. The incidence of PIP is reduced by 50% when thrombolytic therapy is utilized.

Acute pericarditis. Electrocardiographic abnormalities in patients with pericarditis after AMI include diffuse, upright T waves unlike the inverted T waves normally seen in myocardial ischemia.

The clinical presentation of PIP includes sharp, persistent, midsternal chest pain that radiates to the shoulders, the interscapular area, or the trapezius muscles. The pain typically increases with inspiration and is relieved by sitting up and leaning forward. A low-grade fever may be present. A friction rub may develop within three days of the AMI. The rub may consist of three components: diastolic, systolic, and presystolic (atrial contraction). Typically, however, only the systolic component is heard. Approximately one-fourth of patients will have a pericardial effusion. Post-infarction pericarditis is associated with a higher post-AMI complication rate and a higher incidence of in-hospital and one- year mortality.

Characteristically, the patient's ECG demonstrates tachycardia, diffuse ST-segment elevation, PR-segment depression in leads I, II, III, and V1, and diffuse, upright T waves in contrast to the inverted T waves normally seen in myocardial ischemia. Echocardiography may reveal a pericardial effusion.

Patients with PIP should be admitted to the hospital and started on high-dose aspirin (650 mg four to six times a day). Steroids and nonsteroidal inflammatory drugs should be avoided because they may interfere with myocardial scarring and promote aneurysm formation. Patients taking anticoagulants should be admitted and their anticoagulants discontinued. They should be observed for signs of hemorrhagic pericarditis and pericardial tamponade.

The second form of post-AMI pericarditis is Dressler's syndrome, which occurs in 1% to 6% of patients. Dressler's syndrome is thought to be the result of an autoimmune response caused by antimyocardial antibodies, which produce a nonspecific inflammatory response throughout the myocardium. It is not seen when fibrinolytics are administered or percutaneous coronary intervention is performed. Compared to PIP, the onset of Dressler's syndrome is delayed, with peak onset at 7 to 11 weeks post-AMI and a range of 1 to 28 weeks post-AMI.

The clinical presentation of Dressler's syndrome is similar to that of PIP except that the syndrome is associated with constitutional symptoms, including low-grade fever, malaise, weakness, myalgia, arthralgia, and anorexia. In addition to a pericardial friction rub, a pleural rub may be present. Electrocardiographic and echocardiographic findings in Dressler's syndrome are similar to those seen in PIP. However, in contrast to PIP, chest x-rays in Dressler's syndrome may demonstrate a pleural effusion, more commonly in the left lung, and pulmonary infiltrates. Also, the white blood cell count and erythrocyte sedimentation rate are usually elevated. Management of Dressler's syndrome is identical to that of PIP.
 

DISRUPTION IN ANATOMY OR FUNCTION

Acute myocardial infarction may be complicated by a number of pathophysiologic mechanisms. Complications such as those discussed in this article are the result of a disruption in cardiac anatomy or function, typically during the post-infarction healing phase. The onset of each of these complications usually results in explicit symptoms and physical manifestations. Thus, a basic knowledge of the complications that occur in the postinfarction period, and the clinical syndrome associated with each, will allow the physician to evaluate and treat the complication in a confident and timely manner.
 

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