Complications of Acute
Myocardial Infarction

Adam W. Grasso

Sorin J. Brener

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Complications of acute myocardial infarction (MI) include ischemic, mechanical, arrhythmic, embolic, and inflammatory (pericarditis) disturbances (Table 1). Nevertheless, circulatory failure from severe left ventricular (LV) dysfunction or one of the mechanical complications of MI accounts for most fatalities.

Table 1: Complications of Acute Myocardial Infarction
Complication Type Manifestations
Ischemic Angina, reinfarction, infarct extension
Mechanical Heart failure, cardiogenic shock, mitral valve dysfunction, aneurysms, cardiac rupture
Arrhythmic Atrial or ventricular arrhythmias, sinus or atrioventricular node dysfunction
Embolic Central nervous system or peripheral embolization
Inflammatory Pericarditis

 

Ischemic complications

These can include infarct extension, recurrent infarction, and recurrent angina.

Prevalence

Infarct extension is a progressive increase in the amount of myocardial necrosis within the infarct zone of the original MI. This may manifest as an infarction that extends and involves the adjacent myocardium or as a subendocardial infarction that becomes transmural.

Reocclusion of an infarct-related artery (IRA) occurs in 5% to 30% of patients following fibrinolytic therapy. These patients also tend to have a poorer outcome. 1 Reinfarction is more common in patients with diabetes mellitus or prior MI.

Infarction in a separate territory (recurrent infarction) may be difficult to diagnose within the first 24 to 48 hours after the initial event. Multivessel coronary artery disease is common in patients with acute myocardial infarction. In fact, angiographic evidence of complex or ulcerated plaques in noninfarct-related arteries is present in up to 40% of patients with acute MI.

Angina, which occurs from a few hours to 30 days after acute MI, is defined as postinfarction angina. The incidence of postinfarction angina is highest in patients with non–ST-elevation MI (approximately 25%) and those treated with fibrinolytics compared with mechanical revascularization (percutaneous coronary intervention [PCI]).

Pathophysiology

Reinfarction occurs more frequently when the IRA reoccludes than when it remains patent; however, reocclusion of the IRA does not always cause reinfarction because of abundant collateral circulation. After fibrinolytic therapy, reocclusion is found on angiograms of 5% to 30% of patients and is associated with a worse outcome.

The pathophysiologic mechanism of postinfarction angina is similar to that of unstable angina and should be managed in a similar manner. Patients with postinfarction angina have a worse prognosis with regard to sudden death, reinfarction, and acute cardiac events.

Signs and Symptoms

Patients with infarct extension or postinfarction angina usually have continuous or recurrent chest pain, with protracted elevation in the creatine kinase (CK) level and, occasionally, new electrocardiographic changes.

Diagnostic Testing

The diagnosis of infarct expansion, reinfarction, or postinfarction ischemia can be made with echocardiography or nuclear imaging. A new wall motion abnormality, larger infarct size, new area of infarction, or persistent reversible ischemic changes help substantiate the diagnosis. CK-MB is a more useful marker for tracking ongoing infarction than troponin, given its shorter half-life. Re-elevation and subsequent decline in CK-MB levels suggest infarct expansion or recurrent infarction. Elevations in the CK-MB level of more than 50% over a previous nadir are diagnostic for reinfarction.

Treatment

Medical therapy with aspirin, heparin, nitrates, and beta blockers is indicated in patients who have had a myocardial infarction and have ongoing ischemic symptoms. An intra-aortic balloon pump (IABP) should be inserted promptly in patients with hemodynamic instability or severe LV systolic dysfunction. Coronary angiography should be performed in patients who are stabilized with medical therapy, but emergency angiography may be undertaken in unstable patients. Revascularization, percutaneous or surgical, is associated with improved prognosis.

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Mechanical complications

Mechanical complications of acute MI include ventricular septal rupture, papillary muscle rupture or dysfunction, cardiac free wall rupture, ventricular aneurysm, LV failure with cardiogenic shock, dynamic left ventricular outflow tract obstruction, and right ventricular failure.

Ventricular Septal Rupture

Independent predictors of ventricular septal rupture (VSR) are shown in Box 1.

Box 1: Independent Predictors of Ventricular Septal Rupture Occurrence
Older age
Female gender
Nonsmoker
Anterior infarct
Worse Killip class on admission
Increasing heart rate on admission

 

Prevalence

VSR formerly occurred in 1% to 2% of patients after acute MI in the prethrombolytic era (Figs. 1 and 2). The incidence has dramatically decreased with reperfusion therapy. 2 The GUSTO-I trial has demonstrated an incidence of VSR of approximately 0.2%. 3,4

VSR may develop as early as 24 hours after MI but was commonly seen 3 to 7 days after MI in the prefibrinolytic era and 2 to 5 days currently. Fibrinolytic therapy is not associated with an increased risk of VSR. 2,5

Pathophysiology

The defect usually occurs at the junction of preserved and infarcted myocardium in the apical septum with anterior MI and in the basal posterior septum with inferior MI. VSR almost always occurs in the setting of a transmural MI and is more frequently seen in anterolateral MIs. The defect may not always be a single large defect; it can be a meshwork of serpiginous channels that can be identified in 30% to 40% of patients.

 
Signs and Symptoms

Early in the disease process, patients with VSR may appear relatively comfortable, with no clinically significant cardiopulmonary symptoms. Rapid recurrence of angina, hypotension, shock, or pulmonary edema may develop later in the course.

Diagnosis

Rupture of the ventricular septum is often accompanied by a new harsh holosystolic murmur best heard at the left lower sternal border. The murmur is accompanied by a thrill in 50% of cases. This sign is generally accompanied by a worsening hemodynamic profile and biventricular failure. Therefore, it is important that all patients with MI have a well-documented cardiac examination at presentation and daily thereafter.

An electrocardiogram (ECG) may show atrioventricular (AV) nodal or infranodal conduction delay abnormalities in approximately 40% of patients. Echocardiography with color flow imaging is the best method for diagnosing VSR. There are two types of VSR, which can best be visualized in different echocardiographic planes. A basal VSR is best visualized in the parasternal long axis with medial angulation, apical long axis, and subcostal long axis. An apical VSR is best visualized in the apical four-chamber view. Echocardiography can define LV and right ventricular (RV) function—important determinants of mortality—as well as the size of defect and degree of left-to-right shunt by assessing flow through the pulmonary and aortic valves. In some cases, it may be necessary to use transesophageal echocardiography to assess the ventricular septal defect.

VSR can also be diagnosed by demonstrating an increase in oxygen saturation in the right ventricle and pulmonary artery (PA) on PA catheterization. The location of the increase is significant, because there have been case reports of peripheral PA increases because of acute MR. Diagnosis involves fluoroscopically guided measurement of oxygen saturation in the superior and inferior vena cava, right atrium, right ventricle, and pulmonary artery. An increase in oxygen saturation of more than 8% occurs between the right atrium and right ventricle and pulmonary artery, with a left-to-right shunt across the ventricular septum. A shunt fraction can be calculated as follows:

where = pulmonary flow, = systemic flow, Sao2 = arterial oxygen saturation, Mvo2 = mixed venous oxygen saturation, Pvo2 = pulmonary venous oxygen saturation, and Pao2 = pulmonary arterial oxygen saturation. of more than 2 suggests a large shunt, which is likely to be poorly tolerated by the patient.

Treatment

Early surgical closure is the treatment of choice, even if the patient's condition is stable. Initial reports have suggested that delaying surgery is likely to result in improved surgical mortality. 6 These benefits were probably the result of selection bias, 7 because the mortality rate in patients with VSD treated medically is 24% at 72 hours and 75% at 3 weeks. Therefore, patients should be considered for urgent surgical repair.

There is a high surgical mortality associated with cardiogenic shock and multisystem failure. This further supports earlier operation before complications develop. 8 Mortality is highest in patients with basal septal rupture associated with inferior MI (70%, compared with 30% in patients with anterior infarcts). The mortality rate is higher because of increased technical difficulty and the frequent need for mitral valve repair or replacement in the patients with mitral regurgutation. 9 Regardless of the location and hemodynamic condition of the patient, surgery should always be considered, because it is associated with a lower mortality rate than conservative management. 10

Intensive medical management should be started to support the patient before surgery. Unless there is significant aortic regurgitation, an IABP should be inserted urgently as a bridge to a surgical procedure. The IABP will decrease the systemic vascular resistance (SVR) and shunt fraction while increasing coronary perfusion and maintaining blood pressure. After insertion of the IABP, vasodilators can be used, with close hemodynamic monitoring. Vasodilators can also reduce left-to-right shunting and increase systemic flow by reducing SVR. Nevertheless, caution should be exercised to avoid a greater decrease in pulmonary vascular resistance than in SVR and a consequent increase in shunting. The vasodilator of choice is intravenous (IV) nitroprusside, which is started at 0.5 to 1.0 μg/kg/min and titrated to a mean arterial pressure (MAP) of 60 to 75 mm Hg.

Mitral Regurgitation

Prevalence

Mitral regurgitation (MR) after acute MI predicts poor prognosis, as demonstrated in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial. Nevertheless, MR of mild to moderate severity is found in 13% to 45% patients following acute MI. 11–14 Whereas most MR is transient in duration and asymptomatic, MR caused by papillary muscle rupture (Fig. 3) is a life-threatening complication of acute MI. Fibrinolytic agents decrease the incidence of rupture; however, when present, rupture may occur earlier in the post-MI period than in the absence of reperfusion. Although papillary muscle rupture was reported to occur between days 2 and 7 in the prefibrinolytic era, the SHOCK Trial Registry demonstrated a median time to papillary muscle rupture of 13 hours. 15 Papillary muscle rupture is found in 7% of patients in cardiogenic shock and contributes to 5% of the mortality after acute MI. 16,17

Pathophysiology

Mitral regurgitation can occur as a result of a number of mechanisms, including the following: (1) mitral valve annular dilation secondary to LV dilation; (2) papillary muscle dysfunction with associated ischemic regional wall motion abnormality in close proximity to the insertion of the posterior papillary muscle; and (3) partial or complete rupture of the chordae or papillary muscle. 16

Papillary muscle rupture is most common with an inferior MI. The posteromedial papillary muscle is most frequently involved because of its single blood supply through the posterior descending coronary artery. 18 The anterolateral papillary muscle has dual blood supply, being perfused by the left anterior descending (LAD) and left circumflex coronary arteries. In 50% of patients with papillary muscle rupture, the infarct is relatively small.

Signs and Symptoms

Complete transection of the papillary muscles is rare and usually results in immediate pulmonary edema, cardiogenic shock, and death. Physical examination demonstrates a new pansystolic murmur, which is audible at the cardiac apex and radiates to the axilla or the base of the heart. If there is a posterior papillary muscle rupture, the murmur radiates to the left sternal border and may be confused with the murmur of VSD or aortic stenosis (intensity of the murmur does not always predict the severity of MR). In patients with severe heart failure, poor cardiac output or with elevated left atrial pressures, the murmur may be soft or absent.

Diagnostic Testing

The ECG usually shows evidence of a recent inferior or posterior MI. The chest radiograph shows evidence of pulmonary edema. Focal pulmonary edema can occur in the right upper lobe when flow is directed at the right pulmonary veins.

The diagnostic test of choice is two-dimensional echocardiography with Doppler and color flow imaging. In severe MR, the mitral valve leaflet is usually flail. Color flow imaging can be useful in distinguishing papillary muscle rupture with severe MR from VSR. Transthoracic echocardiography may not fully appreciate the amount of MR in some patients with posteriorly directed jets. In these patients, transesophageal echocardiography (TEE) may be particularly useful.

Hemodynamic monitoring with a PA catheter may reveal large V (more than 50 mm Hg) waves in the pulmonary capillary wedge pressure (PCWP). Nevertheless, patients with VSR can also have large V waves as a result of augmented pulmonary venous return in a left atrium of normal size and decreased compliance. Further complicating the diagnostic picture, patients with severe MR and reflected V waves in the PA tracing may have an increase in oxygen saturation in the PA. 19 Mitral regurgitation can be distinguished from VSR with a Swan-Ganz catheter by two characteristics. First, prominent V waves in the PCWP tracing preceding the incisura on the PA tracing are almost always secondary to severe MR. Second, blood for oximetry should be obtained with fluoroscopic control from the central PA rather than from more distal branches to identify a significant increase in oxygen content associated with VSR.

Treatment

Patients with papillary muscle rupture should be rapidly identified and receive aggressive medical treatment while being considered for surgery. Medical therapy includes vasodilator therapy. Nitroprusside is useful in the treatment of patients with acute MR. Nitroprusside directly decreases SVR, thereby reducing the regurgitant fraction and increasing the forward stroke volume and cardiac output. Nitroprusside can be started at 0.5 to 1.0 μ/kg/min and titrated to a MAP of 60 to 75 mm Hg. An IABP should be inserted to decrease LV afterload, improve coronary perfusion, and increase forward cardiac output. Patients with hypotension may tolerate vasodilators after the insertion of an IABP.

Patients with papillary muscle rupture should be considered for emergency surgery, because the prognosis is dismal in medically treated patients. Coronary angiography should be performed before surgical repair, because revascularization during MVR is associated with improved short-term and long-term mortality. 17,20 Additional surgical candidates include patients with moderate MR who do not improve with afterload reduction.

Free Wall Rupture

Prevalence

Free wall rupture occurs in 3% of MI patients and accounts for approximately 10% of mortality after MI (Fig. 4). The timing of cardiac rupture is within 5 days in 50% of patients and within 2 weeks of MI in 90% of patients. Free wall rupture occurs only among patients with transmural MI. Risk factors include advanced age, female gender, hypertension, first MI, and poor coronary collateral vessels.

Pathophysiology

Free wall rupture accounts for part of the early hazard in patients treated with fibrinolytic agents. Nevertheless, the overall incidence of free wall rupture is not higher in patients treated with fibrinolytics. 21–23 Although any wall can be involved, cardiac rupture most commonly occurs at the lateral wall.

Free wall rupture occurs at three distinct intervals, with three distinct pathologic subsets. Type I increases with the use of fibrinolytics. It occurs early (within the first 24 hours) and is a full-thickness rupture. Type II rupture occurs 1 to 3 days post-MI and is a result of erosion of the myocardium at the site of infarction. Type III rupture occurs late and is located at the border zone of the infarction and normal myocardium. The reduction in type III ruptures as a result of the advent of fibrinolytics has resulted in no change in the overall free wall rupture rate. It has been postulated that type III ruptures can occur as a result of dynamic left ventricular outflow tract obstruction and the resultant increased wall stress. 24

Signs and Symptoms

Sudden onset of chest pain with straining or coughing may suggest the onset of myocardial rupture. Acute rupture patients often have electromechanical dissociation and sudden death. Other patients may have a more subacute course as a result of a contained rupture. They might complain of pain consistent with pericarditis, nausea, and hypotension. In a study evaluating 1457 patients with acute MI, 6.2% of patients had free wall rupture. Approximately one third of these patients presented with a subacute course. 22

Jugular venous distention, pulsus paradoxus, diminished heart sounds, and a pericardial rub suggest subacute rupture. New to-and-fro murmurs may be heard in patients with subacute rupture or pseudoaneurysm. A junctional or idioventricular rhythm, low-voltage complexes, and tall precordial T waves may be evident on the ECG. Additionally, a large number of patients have transient bradycardia just before rupture, as well as other manifestations of increased vagal tone.

Diagnostic Testing

Although often there is not enough time for diagnostic testing in the management of patients with acute rupture, echocardiography is the test of choice. Echocardiography will demonstrate a pericar-dial effusion with findings of cardiac tamponade. These findings include right atrium and RV diastolic collapse, dilated inferior vena cava, and marked respiratory variations in mitral and tricuspid inflow. Additionally, a Swan-Ganz pulmonary catheter may reveal hemodynamic signs of tamponade, with equalization of the right atrium, RV diastolic, and pulmonary capillary wedge pressures.

Treatment

The goal of therapy is to diagnose the problem and perform early emergency open heart surgery to correct the rupture. Emergency pericardiocentesis may be performed immediately on patients with tamponade and severe hemodynamic compromise while arrangements are being made for transport to the hospital. The procedure may be dangerous because of reopening of communication with the pericardium as the intrapericardial pressure is relieved. Medical management has no role in the treatment of these patients, except for the use of vasopressors to maintain blood pressure temporarily as the patient is rushed to the operating room.

Pseudoaneurysm

Pathophysiology

Pseudoaneurysm is caused by contained rupture of the LV free wall. The aneurysm may remain small or undergo progressive enlargement. The outer wall is formed by the pericardium and mural thrombus. The pseudoaneurysm communicates with the body of the left ventricle through a narrow neck, the diameter of which is by definition less than 50% of the diameter of the fundus.

Signs and Symptoms

Pseudoaneurysms may remain clinically silent and be discovered during routine investigations. However, some patients may have recurrent tachyarrhythmia, systemic embolization, and heart failure. Some patients may have systolic, diastolic, or to-and-fro murmurs related to the flow of blood across the narrow neck of the pseudoaneurysm during LV systole and diastole. A chest radiograph may show cardiomegaly, with an abnormal bulge on the cardiac border. There may by persistent ST-segment elevation on the ECG. The diagnosis may be confirmed by echocardiography, magnetic resonance imaging (MRI), or computed tomography.

Treatment

Spontaneous rupture can occur without warning in approximately one third of patients with a pseudoaneurysm. Therefore, surgical intervention is recommended for all patients, regardless of symptoms or the size of the aneurysm, to prevent sudden death.

Left Ventricular Failure and Cardiogenic Shock

Prevalence

Some degree of left ventricular dysfunction is to be anticipated after an acute MI. The degree of dysfunction correlates with the extent and location of myocardial injury. Patients with small, more distal infarctions may have discrete regional wall motion abnormalities with preserved overall left ventricular function because of hyperkinesis of unaffected segments. 25 Prior MI, older age, female gender, diabetes, and anterior infarction are risk factors for the development of cardiogenic shock. 26,27

Killip and Kimball 28 have developed a classification scheme to categorize patients' prognosis based on their hemodynamic profile. Patients were classified into four hemodynamic subsets, from no evidence of congestive heart failure (CHF) to cardiogenic shock ( Table 2 ). They reported an 81% mortality rate in patients presenting in cardiogenic shock.

Table 2: Incidence of Heart Failure in Acute Myocardial Infarction
Killip Class Characteristics Patients (%)
I No evidence of congestive heart failure 85
II Rales, jugular venous distention, or S3 13
III Pulmonary edema 1
IV Cardiogenic shock 1

Forrester and collleagues 29,30 classified patients by their hemodynamic profile with a pulmonary artery catheter using PCWP and cardiac index. They reported a 50% mortality rate in the most compromised subset (PCWP more than 18 mm Hg; cardiac index less than 2.2 L/min/m2). Results of the GUSTO-I trial have indicated that 7-8% of patients develop cardiogenic shock clinically. Fibrinolysis did not materially affect mortality, which remains high at 58%. 31,32

Pathophysiology

Patients may develop cardiogenic shock in association with an acute MI of multiple causes, including large LV infarction, severe RV infarction, ventricular septal rupture, free wall rupture, acute mitral regurgitation, or pharmacologic depression of left ventricular function (beta blockers in proximal left anterior descending MI). Patients with cardiogenic shock as a result of acute MI typically have severe multivessel disease, with significant involvement of the LAD artery. 33,34 Generally, at least 40% of the left ventricular mass is affected in patients who present in cardiogenic shock as a result of a first MI. 35,36 In patients with prior MIs and depressed left ventricular function, a smaller acute insult may result in cardiogenic shock (Fig. 5).

Signs and Symptoms

Patients who present in Killip class III often have respiratory distress, diaphoresis, and cool clammy extremities, in addition to the typical signs and symptoms of acute MI. Patients in Killip class IV (cardiogenic shock) may have severe orthopnea, dyspnea, and oliguria and may have altered mental status, as well as multisystem organ failure from hypoperfusion. It may be possible to palpate an area of dyskinesia on the precordium. Additionally, an S3 gallop, pulmonary rales, and elevated jugular venous pressure are common findings on physical examination.

Diagnostic Testing

Patients with cardiogenic shock caused by acute MI generally have extensive electrocardiographic changes demonstrating a large infarct, diffuse ischemia, or multiple prior infarcts. If these changes are absent, another cause of shock should be considered. Chest radiography reveals pulmonary edema. Laboratory tests may demonstrate lactic acidosis, renal failure, and arterial hypoxemia.

The patient in cardiogenic shock should be monitored with a pulmonary artery catheter and an arterial line. These may help distinguish between primary LV failure and other mechanical causes of cardiogenic shock (see earlier).

Echocardiography helps determine the extent of dysfunctional myocardium. It also helps identify other mechanical complications of MI that may be contributing to cardiogenic shock.

Treatment

A patient in cardiogenic shock should have an IABP placed urgently to reduce afterload, improve cardiac output, and enhance coronary perfusion. Medical therapy with vasodilators (e.g., nitroglycerin, nitroprusside and angiotensin-converting enzyme [ACE] inhibitors) and diuretics should be used as tolerated. Intravenous nitroglycerin is the first-line drug of choice among vasodilators because it is less likely to produce coronary steal than nitroprusside and protects against ischemia. The starting dose is 10 to 20 mg/min and it may be increased by 10 mg/min every 2 to 3 minutes to a goal MAP of 70 mm Hg. Intravenous nitroprusside can be added if further reduction in afterload is necessary. Nitroprusside is started at 0.5 to 1.0 μg/kg/min and is also titrated to a MAP of approximately 70 mm Hg. Patients with low blood pressures (MAP lower than 70 mm Hg) may not tolerate vasodilators.

ACE inhibitors improve LV performance and decrease myocardial oxygen consumption by reducing the cardiac preload and afterload of patients with heart failure and acute MI. ACE inhibitors can reduce infarct expansion if started in the first 12 hours of an MI if the patient is not already in cardiogenic shock. It is recommended that captopril be started early, at 6.25 mg every 8 hours, with each dose subsequently doubled as tolerated to a maximal dose of 50 mg every 8 hours. Patients with mild pulmonary edema MI can be treated with diuretics such as IV furosemide, adjusted for creatinine and history of diuretic use. β-Adrenergic agonists such as dobutamine or dopamine may be needed for patients with severe heart failure and cardiogenic shock. Nevertheless, this therapy should generally be reserved for those who have failed IABP and maximal vasodilator therapy or for those with a right ventricular infarct. Phosphodiesterase inhibitors such as milrinone may be beneficial for some patients. The bolus may be omitted in patients with marginal blood pressures. Patients without adequate MAP may not tolerate milrinone. Some patients may need norepinephrine to maintain arterial pressure. Norepinephrine is started at 2 μg/min and titrated to maintain the MAP at approximately 70 mm Hg.

PCI or emergency coronary bypass surgery has been associated with an improved prognosis in patients in cardiogenic shock, reducing the mortality rate from 80% to 50%. Multivessel revascularization should be attempted in shock patients. 10

Emergency surgical revascularization is indicated for patients with severe multivessel disease or substantial left main coronary artery stenosis. Other surgical modalities that may be considered include LV or biventricular assist devices or extracorporeal membrane oxygenation as a bridge to heart transplantation. Some patients may gradually be weaned from assist devices after recovery of the stunned portion of myocardium, without the need for cardiac transplantation.

Right Ventricular Failure

Prevalence

Mild RV dysfunction is common (approximately 40%) after MI of the inferior or inferoposterior wall; however, hemodynamically significant RV impairment occurs in only 10% of patients with inferior or inferoposterior wall MI (Fig. 6).

Pathophysiology

The degree of RV dysfunction depends on the location of the right coronary artery (RCA) occlusion. Only proximal occlusions (proximal to the acute marginal branch) of the RCA result in marked dysfunction. 37 The degree of RV involvement also depends on the amount of collateral flow from the LAD and the degree of blood flow through the thebesian veins. Because the right ventricle is thin-walled and has lower oxygen demand, there is coronary perfusion during the entire cardiac cycle; therefore, widespread irreversible infarction is rare.

Signs and Symptoms

The triad of hypotension, jugular venous distention with clear lungs, and absence of dyspnea has high specificity but low sensitivity for RV infarction. 38 Severe RV failure may manifest with symptoms of a low cardiac output state, including diaphoresis, cool clammy extremities, and altered mental status. Patients often have oliguria and hypotension. Other causes of severe hypotension in the setting of an inferior MI include bradyarrhythmia, acute severe mitral regurgitation, and ventricular septal rupture.

Patients with isolated RV failure have elevated jugular venous pressure and RV S3 heart sound in the setting of a normal lung examination. The presence of jugular venous pressure higher than 8 cm of water and Kussmaul's sign is highly sensitive and specific for severe RV failure. A rare but clinically important complication of RV infarction is right-to-left shunting secondary to increased pressures in the RA and RV and opening of the foramen ovale. This should be considered in patients with right ventricular infarction and hypoxemia.

Electrocardiographically, patients present with inferior ST elevation in conjunction with ST elevation in the V4R lead. These findings have a positive predictive value of 80% for right ventricular infarction. 39 The chest radiograph is usually normal.

Diagnostic Testing

Echocardiography is the diagnostic study of choice for RV infarction. It will demonstrate RV dilation and dysfunction and usually LV inferior wall dysfunction. It is also helpful in excluding cardiac tamponade, which may mimic RV infarction hemodynamically. The hemodynamic profile of acute RV infarct can also be diagnostic of an acute pulmonary embolism in the absence of an ischemic event.

Hemodynamic monitoring with a pulmonary artery catheter reveals high right atrial pressures with a low PCWP, unless severe LV dysfunction is also present, because RV failure results in underfilling of the left ventricle and a low cardiac output. In some patients, RV dilation can cause decreased LV performance on the basis of flattening or bowing of the septum into the left ventricle and restriction of ventricular filling, with elevation of the PCWP. A right atrial pressure of higher than 10 mm Hg and a right atrial pressure–to–PCWP ratio of 0.8 or more strongly suggest RV infarction. 40

Treatment

Volume loading to increase left ventricular preload and cardiac output is key to the management of RV infarction. Some patients may require several liters in 1 hour to reach a target PCWP of 15 mm Hg. It is important to have hemodynamic monitoring with a pulmonary artery catheter in these patients, because overzealous fluid administration can further decrease LV output. This occurs as a result of septal shift toward the left ventricle and an intrapericardial pressure shift. The target central venous pressure for fluid administration is approximately 15 mm Hg. When volume loading is insufficient to improve cardiac output, inotropes are indicated. Administration of dobutamine increases cardiac index, improves RV ejection fraction, and is better than afterload reduction with nitroprusside. 1

Patients may benefit from reperfusion therapy, because patients who undergo successful reperfusion of RV branches have enhanced RV function and a lower 30-day mortality rate. 41,42 Patients with RV infarction and bradyarrhythmias or loss of sinus rhythm may have significant improvement with AV sequential pacing. Optimal pacer settings tend to be longer AV delays (approximately 200 msec) and a heart rate of 80 to 90 beats per min.

Although there have only been case reports of IABP improving the cardiac index (CI) in combination with dobutamine, an IABP may be useful, even though it acts primarily on the left ventricle. Pericardiectomy may be considered for patients with refractory shock because it reverses the septal impingement on left ventricular filling. Most patients with RV infarction improve after 48 to 72 hours. An RV assist device is indicated for patients who remain in cardiogenic shock in spite of these measures.

Ventricular Aneurysm

Prevalence

Patients with apical transmural MIs are at higher risk of aneurysmal formation, followed by those with posterior-basal infarcts. Patients who do not receive reperfusion therapy are at greatest risk of developing this complication (10% to 30%).

Pathophysiology

The early open artery hypothesis states that early reperfusion results in improved myocardial salvage and prevents infarct expansion. Even late reperfusion limits infarct expansion through a number of mechanisms, including immediate change in infarction characteristics, preservation of small amounts of residual myofibrils and interstitial collagen, accelerated healing, the scaffold effect of a blood-filled vasculature, and elimination of ischemia in viable but dysfunctional myocardium. Infarct expansion and progressive LV dilation are associated with persistent occlusion of an IRA. The aneurysm consists of a stretched portion of the myocardium, containing all three layers and connected to the ventricle by a wide neck. The differences between a pseudoaneurysm (false aneurysm) and true aneurysm are highlighted in Table 3 .

Table 3: Differences Between True and False Ventricular Aneurysms
Parameter True Aneurysm False Aneurysm
Cause Infarction Rupture
Incidence 1%-5% Rare
Neck Wide Narrow
Wall All three layers—scar Pericardium and thrombus
Rupture Very rare Common
Signs and Symptoms

Congestive heart failure and even cardiogenic shock can develop as a result of a large LV aneurysm. Because acute aneurysms expand during systole, contractile energy generated by a normal myocardium is wasted and puts the entire ventricle at a mechanical disadvantage. Chronic aneurysms persist for more than 6 weeks after the acute event and are less compliant than acute aneurysms and less likely to expand during systole. Patients with chronic aneurysms may have heart failure, ventricular arrhythmias, and systemic embolization, or they may be asymptomatic. Palpation of the precordium may reveal a dyskinetic segment of the ventricle. An S3 gallop may be heard in patients with poor ventricular function.

Diagnostic Testing

Typical electrocardiographic findings include ST elevation, which may persist despite application of reperfusion therapy and Q waves. When electrocardiographic changes (ST elevation) persist for more than 6 weeks, patients may have a chronic ventricular aneurysm. A chest radiograph may reveal a localized bulge in the cardiac silhouette. Echocardiography is the gold standard and accurately identifies the aneurysmal segment. It may also demonstrate the presence of a mural thrombus. Additionally, echocardiography is useful in differentiating true aneurysms from pseudoaneurysms. MRI may also be useful and diagnostic for delineating the aneurysmal section.

Treatment

Congestive heart failure with acute aneurysms is managed with IV vasodilators. ACE inhibitors have been shown to reduce infarct expansion and unfavorable LV remodeling. ACE inhibitors are best started within the first 12 to 24 hours of onset of acute MI, because infarct expansion starts early. Corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided in the acute setting because they have been shown to induce infarct expansion and aneurysm formation in experimental models. Heart failure with chronic aneurysms can be managed with ACE inhibitors, digoxin, and diuretics.

Anticoagulation with warfarin sodium is indicated for patients with a mural thrombus. Patients should be treated initially with IV heparin, with a target partial thromboplastin time (PTT) of 50 to 70 seconds. Warfarin is started simultaneously. Patients should be treated with warfarin at a target international normalized ratio (INR) of 2 to 3 for 3 to 6 months. It is controversial whether patients with large aneurysms without thrombus should receive anticoagulants. Many clinicians prescribe anticoagulants for 6 to 12 weeks after the acute phase. Patients with LV aneurysms and a low global ejection fraction (less than 40%) have a higher stroke rate and should take anticoagulants for at least 3 months after the acute event. They may be subsequently observed with echocardiography. Anticoagulation may be reinitiated if a new thrombus develops.

Refractory heart failure or refractory ventricular arrhythmias in patients with aneurysms is an indication for surgical resection. Surgical resection may be followed by conventional closure or newer techniques to maintain LV geometry. Revascularization is beneficial for patients with a large amount of viable myocardium around the aneurysmal segment.

Dynamic Left Ventricular Outflow Tract Obstruction

Prevalence

Dynamic left ventricular outflow tract obstruction is an uncommon complication of acute anterior MI, as first described in a case report by Bartunek and associates. 43

Pathophysiology

This event is dependent on compensatory hyperkinesis of the basal and midsegments of the left ventricle in patients with distal infarcts. Predictors of enhanced regional wall motion in noninfarct zones are the absence of multivessel disease, female gender, and higher flow in the infarct-related vessel. The increased contractile force of these regions decreases the cross-sectional area of the LVOT. The resulting increased velocity of blood through the outflow tract can produce decreased pressure below the mitral valve and result in the leaflet being displaced anteriorly toward the septum (Venturi effect). This results in further outflow tract obstruction as well as mitral regurgitation because of systolic anterior motion of the anterior mitral valve leaflet.

It has been postulated that this complication can play a role in free wall rupture. LVOT obstruction leads to increased end-systolic intraventricular pressure. This in turn leads to increased wall stress of the weakened, necrotic, infarcted zone. This fatal complication occurs most frequently in women, older patients (older than 70 years), and in those without prior MI.

Signs and Symptoms

Patients may have respiratory distress, diaphoresis, and cool clammy extremities in addition to the typical signs and symptoms of acute MI. Patients with severe obstruction may appear to be in cardiogenic shock with severe orthopnea, dyspnea, and oliguria and may have altered mental status from cerebral hypoperfusion. Patients present with a new systolic ejection murmur heard best at the left upper sternal border, with radiation to the neck. Additionally, a new holosystolic murmur can be heard at the apex, with radiation to the axilla as a result of systolic anterior motion of the mitral leaflet. An S3 gallop, pulmonary rales, hypotension, and tachycardia can also be present.

Diagnostic Testing

Echocardiography is the diagnostic test of choice and accurately depicts the hyperkinetic segment, the LVOT obstruction as well as the systolic anterior motion of the mitral leaflet (SAM).

Treatment

Treatment centers on decreasing myocardial contractility and heart rate while expanding intravascular volume and increasing afterload (modestly). Beta blockers should be added slowly with careful monitoring of heart rate, blood pressure, and Svo2. Patients can receive gentle IV hydration with several small (250-mL) aliquots of saline to increase preload and decrease LVOT obstruction and SAM. The patient's hemodynamic and respiratory status should be monitored closely during this therapeutic intervention with a pulmonary artery catheter. Vasodilators, inotropes, and IABP should be avoided because they can increase LVOT obstruction.

Arrhythmic Complications

Ventricular arrhythmia is a common complication of acute MI, occurring in almost all patients, even before monitoring is possible. It is related to the formation of re-entry circuits at the confluence of the necrotic and viable myocardium. Premature ventricular contractions (PVCs) occur in approximately 90% of patients. The incidence of ventricular fibrillation is approximately 2% to 4%. Although lidocaine has been demonstrated to reduce the rate of primary ventricular fibrillation in patients with MI to some extent, there is no survival benefit and there may be excess mortality. Therefore, it is not recommended that patients receive prophylactic therapy. 33b Amiodarone may be used in patients with MI and frequent PVCs, nonsustained ventricular tachycardia post-MI, or post–defibrillation for ventricular fibrillation. The recommended dosing is a bolus of 150 mg and then administration of 1 mg/min for 6 hours, followed by 0.5 mg/min. When starting this medication for ventricular fibrillation or pulseless ventricular tachycardia (VT), the bolus should be increased to 300 mg (the 150-mg bolus can be repeated in 10 minutes). Ventricular arrhythmias not responsive to amiodarone may be treated with lidocaine (1-mg/kg bolus to a maximum of 100 mg, followed by a 1- to 4-mg/min drip) 44 or procainamide. Polymorphic VT is a rare complication of acute MI and can be treated with amiodarone, lidocaine, or procainamide, or a combination, as described for monomorphic VT. It is usually associated with recurrent ischemia.

The importance of ventricular fibrillation in the setting of MI has been re-evaluated in the context of the interaction between severe systolic dysfunction and the potential for sudden cardiac death. Implantable defibrillators have been shown to reduce mortality in patients with an ejection fraction (EF) lower than 30%, regardless of the presence of ventricular dysrhythmia. 45

Supraventricular arrhythmias occur in less than 10% of patients with acute MI. Because patients who develop these arrhythmias tend to have more severe ventricular dysfunction, they have a worse outcome. Although isolated right atrial infarction or small inferior infarcts leading to atrial arrhythmias are not associated with higher mortality rates, the appearance of atrial arrhythmias usually heralds the onset of heart failure in the setting of acute MI.

Bradyarrhythmias, including AV block and sinus bradycardia, occur most frequently with inferior MI. Complete AV block occurs in approximately 20% of patients with acute right ventricular infarction. Infranodal conduction disturbances with wide complex ventricular escape rhythms occur most frequently in large anterior MIs and portend a very poor prognosis.

Temporary transvenous pacing is indicated in patients who present with asystole, Mobitz type II second-degree AV block, or complete AV block. Consideration for transvenous pacing should be given to patients with bifascicular or trifascicular block in the setting of acute MI. 46 Pacing is not indicated for patient in sinus bradycardia or AV dissociation with a slow sinus rate and a more rapid ventricular escape rhythm as long as the patient is maintaining adequate hemodynamics. If mild symptoms exist, the initial treatment for these rhythm disturbances is IV atropine, 0.5 to 1.0 mg. This may be repeated every 5 minutes, to a maximum dose of 2 mg.

Embolic Complications

Prevalence

The incidence of clinically evident systemic embolism after MI is lower than 2%. The incidence increases in patients with anterior wall MI. The overall incidence of mural thrombus after MI is approximately 20%. Large anterior MI may be associated with mural thrombus in as many as 60% of patients. 47,48

Pathophysiology

Most emboli arise from the left ventricle as a result of wall motion abnormalities or aneurysms. Atrial fibrillation in the setting of is-chemia may also contribute to systemic embolization.

Signs and Symptoms

The most common clinical manifestation of embolic complications is stroke, although patients may have limb ischemia, renal infarction, or intestinal ischemia. Most episodes of systemic emboli occur in the first 10 days after acute MI. Physical findings vary with the site of the embolism. Focal neurologic deficits occur in patients with central nervous system emboli. Limb ischemia manifests with limb pain in a cold pulseless extremity. Renal infarction manifests with flank pain and hematuria. Mesenteric ischemia manifests with abdominal pain out of proportion to physical findings and bloody diarrhea.

Treatment

IV heparin should be started immediately with a target PTT of 50 to 70 seconds and continued until the INR is in therapeutic range. Warfarin sodium therapy should also be started immediately, with a goal INR of 2 to 3, and continued for at least 3 to 6 months for patients with mural thrombi and for those with large akinetic areas detected by echocardiography.

Pericarditis

Prevalence

The incidence of early pericarditis after acute MI is approximately 10%. The inflammation usually develops between 24 and 96 hours after MI. 49,50 Dressler's syndrome, or late pericarditis, occurs with an incidence between 1% and 3%, 1 to 8 weeks after MI.

Pathophysiology

The pathogenesis of acute pericarditis is an inflammatory reaction in response to necrotic tissue. As such, acute pericarditis develops more often in patients with transmural MI. The pathogenesis of Dressler's syndrome is unknown, but an autoimmune mechanism has been suggested.

Signs and Symptoms

Most patients with early pericarditis report no symptoms. Patients with symptoms from early or late pericarditis describe progressive, severe chest pain that lasts for hours. The symptoms are postural—worse in the supine position—and are alleviated by sitting up and leaning forward. The pain tends to be pleuritic in nature and is therefore exacerbated with deep inspiration, coughing, and swallowing. Radiation of pain to the trapezius ridge is almost pathognomonic for acute pericarditis. The pain also may radiate to the neck and, less frequently, to the arm or back. A pericardial friction rub on examination is pathognomonic for acute pericarditis; however, it can be ephemeral. The rub is best heard at the left lower sternal edge with the diaphragm of the stethoscope. The rub has three components—atrial systole, ventricular systole, and ventricular diastole. In about 30% of patients, the rub is biphasic and in 10%, it is uniphasic. A pericardial effusion may cause fluctuation in the intensity of the rub.

Evolving MI changes may mask the diagnosis of pericarditis. Pericarditis produces generalized ST-segment elevation, which is concave or saddle-shaped. As pericarditis evolves, T waves become inverted after the ST segment becomes isoelectric. Conversely, in acute MI, T waves may become inverted when the ST segment is still elevated. Four phases of electrocardiographic abnormalities have been described in association with pericarditis 51 ( Table 4 ).

Table 4: Electrocardiographic Changes of Pericarditis
Stage Electrocardiographic Change
I ST elevation, upright T waves
II ST elevation resolves, upright to flat T waves
III ST isoelectric, inverted T waves
IV ST isoelectric, upright T waves

A pericardial effusion on echocardiography is strongly suggestive of pericarditis. Nevertheless, the lack of an effusion does not rule out pericarditis.

Treatment

Aspirin is the therapy of choice for post-MI pericarditis, 650 mg every 4 to 6 hours. NSAIDs and corticosteroids should be avoided less than 4 weeks after the acute event. These agents may interfere with myocardial healing and contribute to infarct expansion. In late pericarditis, NSAIDs and even corticosteroids may be indicated if severe symptoms persist beyond 4 weeks after MI. Colchicine may be beneficial for patients with recurrent pericarditis.

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References

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Suggested Readings

  • American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction): ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summary: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation. 110: 2004; 588-636.
  • Aspirin plus coumarin versus aspirin alone in the prevention of reocclusion after fibrinolysis for acute myocardial infarction: Results of the Antithrombotics in the Prevention of Reocclusion In Coronary Thrombolysis (APRICOT)-2 Trial. Circulation. 106: 2002; 659-665.
  • Effect of thrombolytic therapy on the risk of cardiac rupture and mortality in older patients with first acute myocardial infarction. Eur Heart J. 26: 2005; 1705-1711.
  • Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation. 101: 2000; 27-32.
  • Reperfusion for right ventricular infarction. N Engl J Med. 338: 1998; 978-980.
  • Current management of ischemic mitral regurgitation. Mt Sinai J Med. 72: 2005; 105-115.
  • Medical therapy of acute myocardial infarction by application of hemodynamic subsets (second of two parts). N Engl J Med. 295: 1976; 1404-1413.
  • Frequency, patient characteristics, and outcomes of mild-to-moderate heart failure complicating ST-segment elevation acute myocardial infarction: Lessons from four international fibrinolytic therapy trials. Am Heart J Jan. 145: 2003; 73-79.
  • Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 346: 2002; 877-883.
  • Cardiogenic shock due to acute severe mitral regurgitation complicating acute myocardial infarction: A report from the SHOCK Trial Registry. Should we use emergently revascularize occluded coronaries in cardiogenic shock?. J Am Coll Cardiol. 36: 2000; 1104-1109.