TITLE: COMPLICATIONS OF ACUTE MYOCARDIAL INFARCTION
AUTHORS: DAVID TSCHOPP, MD -- Department of Cardiovascular Medicine
   SORIN J. BRENER, MD -- Department of Cardiovascular Medicine
REVIEWED: JANUARY 19, 2005
Print Tables From This Chapter
Complications of acute myocardial infarction (MI) include ischemic, mechanical, arrhythmic, embolic, and inflammatory (pericarditis) disturbances. Nevertheless, circulatory failure from either severe left ventricular (LV) dysfunction or one of the mechanical complications of MI accounts for most fatalities.
ISCHEMIC COMPLICATIONS

PREVALENCE

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

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

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

Postinfarction Angina
Angina that occurs within a few hours to 30 days after acute MI is defined as postinfarction angina. The incidence of postinfarction angina is greatest in patients with non-ST-segment elevation MI (approximately 25%) and in those treated with fibrinolytics, compared with mechanical revascularization.
PATHOPHYSIOLOGY
Reinfarction occurs more frequently when an IRA reoccludes than when it remains patent; however, reocclusion of an IRA does not always cause reinfarction because collateral circulation may be abundant. After fibrinolytic therapy, reocclusion is found on 5% to 30% of angiograms and is associated with worse outcome.

The pathophysiologic mechanism of postinfarction angina is similar to that of unstable angina and should be managed as such. Patients with postinfarction angina have a worse prognosis (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 creatine kinase (CK) and occasional new ECG 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 to substantiate the diagnosis. CK-MB, the myocardial component of CK, is a more useful marker for tracking ongoing infarction than troponins, given their shorter half-life. Rising and falling CK-MB levels suggest infarct expansion or recurrent infarction. Elevations of CK-MB greater than or equal to 50% more than a previous nadir are diagnostic for reinfarction.
THERAPY

Medical therapy with aspirin, heparin, nitrates, and beta-adrenergic blockers is indicated for patients who had an MI and have ongoing ischemic symptoms. An intra-aortic balloon pump (IABP) should be inserted in patients with hemodynamic instability or severe LV systolic dysfunction. Coronary angiography should be preformed in patients who are stabilized with medical therapy. Emergency angiography should be undertaken in unstable patients. Revascularization, either percutaneous or surgical, is associated with improved prognosis.
MECHANICAL COMPLICATIONS
Mechanical complications of acute MI include ventricular septal rupture (VSR), papillary muscle rupture or dysfunction (causing mitral regurgitation), cardiac free wall rupture, pseudoaneurysm, LV failure with cardiogenic shock, right ventricular (RV) failure, ventricular aneurysm, and dynamic LV outflow tract (LVOT) obstruction.
VENTRICULAR SEPTAL RUPTURE
PREVALENCE

VSR occurred among 1% to 2% of patients after acute MI in the prethrombolytic era.2 The incidence has dramatically decreased with reperfusion therapy. The GUSTO 1 trial demonstrated a VSR incidence of approximately 0.2%.3 VSR is more likely to occur in patients who are older, female, hypertensive, nonsmokers, and who have anterior infarction, increased heart rate, and worse Killip class at admission. VSR may develop as early as 24 hours after MI; it was commonly seen 3 to 7 days after MI in the prefibrinolytic era and currently is seen 2 to 5 days after MI.2 Fibrinolytic therapy is not associated with increased risk of VSR.4
PATHOPHYSIOLOGY

With anterior MI, this defect usually occurs at the border of preserved and infarcted myocardium in the apical septum; with inferior MI, it affects the basal posterior septum. 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 channels 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 generally is 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.

An ECG may show atrioventricular (AV) nodal or infranodal conduction delay abnormalities in approximately 40% of patients. Echocardiography with color-flow imaging is the test of choice for diagnosis of VSR (Figure 1). Echocardiography can define LV and RV function (important determinants of mortality) as well as the size of the 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 also can be diagnosed by demonstrating a step-up in oxygen saturation in the right ventricle and pulmonary artery (PA) on PA catheterization. The location of the step-up is important, as there have been rare case reports of peripheral PA step-ups due to acute mitral regurgitation (MR). Diagnosis involves fluoroscopically guided measurement of oxygen saturation in the superior and inferior vena cava, right atrium, right ventricle, and pulmonary artery. A step-up in oxygen saturation of greater than 8% occurs in VSR between the right atrium and the PA with a left-to-right shunt across the ventricular septum. A shunt fraction can be calculated as follows:

Qp/Qs = Sao2-Mvo2/Pvo2-Pao2

Where Qp = pulmonary flow, Qs = systemic flow, Sao2 = arterial oxygen saturation, Mvo2 = mixed venous oxygen saturation, Pvo2 = pulmonary venous oxygen saturation, and Pao2 = pulmonary arterial oxygen saturation, Qp/Qs greater than or equal to 2 suggests a considerable shunt, which is likely to be poorly tolerated by the patient.
THERAPY
Early surgical closure is the treatment of choice, even if the patient's condition is stable. Initial reports suggested that delaying surgery was likely to result in improved surgical mortality. These benefits were likely the result of selection bias,5 as the mortality rate among patients with VSD treated medically is 24% at 72 hours and 75% at 3 weeks.6 Therefore, patients should be considered for urgent surgical repair.

Cardiogenic shock and multisystem failure from VSR are associated with high mortality. This further supports early surgical intervention before complications develop.7 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 due to increased technical difficulty and frequently the need for mitral valve repair or replacement in the patients with MR.8 Regardless of the infarct location and hemodynamic condition of the patient, surgery should always be considered as it is associated with a lower mortality rate than conservative management.9

Intensive medical management should be started to support the patient before surgery. Unless there is significant aortic regurgitation, an IABP should be inserted emergently as a bridge to a surgical procedure. The IABP will decrease systemic vascular resistance and shunt fraction while increasing coronary perfusion and maintaining blood pressure. After insertion of an IABP, vasodilators can be used with close hemodynamic monitoring. Vasodilators also reduce left-to-right shunting and increase systemic flow by reducing systemic vascular resistance. The vasodilator of choice is intravenous (IV) nitroprusside, which is started at 0.5 µg/kg/min to 1.0 µg/kg/min and titrated to an MAP of 60 mm Hg to 75 mm Hg.
PAPILLARY MUSCLE RUPTURE
(ACUTE MITRAL REGURGITATION)
PREVALENCE
Acute MR after acute MI predicts poor prognosis. Nevertheless, MR of mild to moderate severity is found in 13% to 45% of patients after acute MI.10,11 Although most MR is transient and asymptomatic, MR caused by papillary muscle rupture is a life-threatening complication. Fibrinolytic agents decrease the incidence of rupture, however, rupture may occur earlier in the post-MI period. In the prefibrinolytic era, papillary muscle rupture had been reported to occur between day 2 and day 7; however, the SHOCK Trial Registry demonstrated a median time to papillary muscle rupture of 13 hours.12 Papillary muscle rupture is found in 7% of patients in cardiogenic shock and contributes to 5% of the mortality after acute MI.13
PATHOPHYSIOLOGY

MR can occur as a result of multiple mechanisms including:

  1. mitral annular dilatation secondary to LV dilatation,
  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 papillary muscle as a result of papillary muscle infarction.14

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.15 The anterolateral papillary muscle has a dual blood supply, being perfused by the left anterior descending and left circumflex coronary arteries. In 50% of patients, the infarct is relatively small.
SIGNS AND SYMPTOMS
Complete transection of the papillary muscle 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 a posterior papillary muscle rupture is present, the murmur radiates to the left sternal border and may be confused with the murmur of VSR or aortic stenosis. The intensity of the murmur does not always predict the severity of MR. In patients with severe failure, poor cardiac output, or elevated left atrial pressures, the murmur may be soft or absent.
DIAGNOSTIC TESTING
The ECG usually shows evidence of recent inferior or posterior MI. The chest radiograph reveals 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 may be particularly useful. Additionally, hemodynamic monitoring with a PA catheter may reveal large V waves (greater than 50 mm Hg) in the pulmonary capillary wedge pressure (PCWP).
THERAPY
Patients with papillary muscle rupture should be rapidly identified and should receive aggressive medical treatment while being considered for surgery. Medical therapy includes vasodilator therapy. Nitroprusside is useful in the treatment of acute MR because it decreases systemic vascular resistance, thereby reducing the regurgitant fraction and increasing the forward stroke volume and cardiac output. Nitroprusside can be started at 0.5 µg/kg/min to 1.0 µg/kg/min and titrated to an MAP of 60 mm Hg 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 insertion of an IABP.

Patients with papillary muscle rupture should be considered for emergency surgery because the prognosis is dismal among medically treated patients. Coronary angiography should be performed before surgical repair, as revascularization during mitral valve replacement (MVR) is associated with improved short-term and long-term mortality.16
FREE WALL RUPTURE
PREVALENCE
Free wall rupture (Figure 2) occurs in 3% of MI patients and accounts for approximately 10% of mortality after MI. Cardiac rupture occurs within 5 days of MI in 50% of patients and within 2 weeks of MI in 90%. Free wall rupture occurs only among patients with transmural MI. Risk factors include advanced age, female sex, hypertension, first MI, and poor coronary collateral vessels.
PATHOPHYSIOLOGY
Although free wall rupture accounts for part of the early (first 24 hours) mortality risk among patients treated with fibrinolytic agents, the overall incidence of free wall rupture is not greater in patients treated with fibrinolytics.17 Any wall can be involved, but cardiac rupture most commonly occurs in 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 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 (days 5-10) and is located at the border zone of the infarction and normal myocardium. The reduction in Type III ruptures due to fibrinolytic therapy results 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 LVOT obstruction, which leads to increased wall stress.18
SIGNS AND SYMPTOMS
Sudden onset of chest pain with straining or coughing may herald the onset of myocardial rupture. Acute rupture patients often develop electromechanical dissociation, shock, and sudden death. Other patients may have a more subacute course as a result of a contained rupture (pseudoaneurysm). They may complain of pain consistent with pericarditis, nausea, and develop hypotension. In a study evaluating 1,457 patients with acute MI, 6.2% of patients had free wall rupture. Approximately one third of these patients presented with a subacute course.19

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 ECG. Additionally, a large number of patients develop transient bradycardia just before rupture.
DIAGNOSTIC TESTING
Although there is often insufficient time for diagnostic testing in the management of patients with acute rupture, echocardiography is the test of choice. Echocardiography may demonstrate a pericardial effusion with findings of cardiac tamponade. These findings include right atrium and RV diastolic collapse, dilated inferior vena cava, and marked respiratory variation in mitral and tricuspid inflow. Additionally, a PA catheter may reveal hemodynamic signs of tamponade, with equalization of the right atrium, RV diastolic pressure, and PCWP.
THERAPY
The goal of therapy is to diagnose the problem quickly and perform early emergency cardiac surgery to correct the rupture. Emergency pericardiocentesis may be performed on patients with tamponade and severe hemodynamic compromise while arrangements are being made for transport to the operating room. Pericardiocentesis may be dangerous due to reopening of the communication with the pericardium as the intrapericardial pressure is relieved. Medical management has no role in the treatment of these patients except for vasopressors to maintain blood pressure as the patient is transported to the operating room.
PSEUDOANEURYSM
PATHOPHYSIOLOGY
Pseudoaneurysm is caused by a contained rupture of the LV free wall. The aneurysm may remain small or undergo progressive enlargement. The outer walls are 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 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 and heart failure. Some patients may have systolic, diastolic, or to-and-fro murmurs related to blood flow across the narrow neck of the pseudoaneurysm during 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 ECG. The diagnosis can be confirmed by echocardiography, magnetic resonance imaging, or computed tomography.
THERAPY
Spontaneous rupture may occur without warning in approximately one third of patients with a pseudoaneurysm. Therefore, surgical intervention is recommended to prevent sudden death for all patients, regardless of symptoms or the size of the aneurysm.
LEFT VENTRICULAR FAILURE
AND CARDIOGENIC SHOCK
PREVALENCE
Some degree of LV dysfunction is expected after an acute MI. The degree of dysfunction correlates with the extent and location of myocardial injury. Patients with small and more distal infarctions may have discrete regional wall motion abnormalities with preserved overall LV function due to hyperkinesis of unaffected segments. Risk factors for development of cardiogenic shock include prior MI, older age, female sex, diabetes, and anterior infarction.

Killip and Kimball20 developed a classification scheme to predict a patient's prognosis based on their hemodynamic profile. Patients were classified into four hemodynamic subsets-from no evidence of congestive heart failure to cardiogenic shock (Table 1). They reported an 81% mortality rate in the patients presenting with cardiogenic shock.

Forrester et al21 classified patients by their hemodynamic profile with a PA catheter. The parameters used included PCWP and cardiac index. They reported a 50% mortality rate in the most compromised subset (PCWP greater than 18 mm Hg, cardiac index less than 2.2 L/min/m2). GUSTO I reported that 0.8% of patients clinically developed cardiogenic shock. In those receiving fibrinolytics, the mortality rate remained high at 58%.22
PATHOPHYSIOLOGY
Patients may develop cardiogenic shock in association with an acute MI from multiple etiologies, including large LV infarction, severe RV infarction, VSR, free wall rupture, acute MR, and pharmacologic depression of LV function (alpha blockers in proximal left anterior descending MI). Patients with cardiogenic shock as a result of acute MI typically have severe multivessel disease with involvement of the left anterior descending arteries.23 Generally, at least 40% of the LV mass is affected in patients who present in cardiogenic shock as a result of a first MI.24 In patients with prior MIs and depressed LV function, a smaller acute insult may result in cardiogenic shock.
SIGNS AND SYMPTOMS
Patients who present in Killip class 3 often have respiratory distress, diaphoresis, and cool clammy extremities in addition to the typical signs and symptoms of acute MI. Patients in Killip class 4 (cardiogenic shock) may have severe orthopnea, dyspnea, oliguria, and 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 is a common physical finding in association with pulmonary rales and elevated jugular venous pressures.
DIAGNOSTIC TESTING
Patients with cardiogenic shock due to acute MI generally have extensive ECG changes, demonstrating a large infarct, diffuse ischemia, or multiple prior infarcts. If these changes are not present, then another cause of shock should be considered. Chest radiograph can reveal pulmonary edema, and laboratory tests often demonstrate lactic acidosis, renal failure, and arterial hypoxemia.

The patient in cardiogenic shock should be monitored with a PA catheter and an arterial line. These help distinguish between primary LV failure and other mechanical causes of cardiogenic shock. Echocardiography determines the extent of dysfunctional myocardium and helps identify mechanical complications.
THERAPY
A patient in cardiogenic shock should immediately have an IABP placed to reduce afterload, improve cardiac output, and improve coronary perfusion.

Medical therapy with vasodilators (nitroglycerin, nitroprusside, and angiotensin-converting enzyme [ACE] inhibitors) and diuretics should be used as tolerated. IV nitroglycerin is the drug of choice among vasodilators because it is anti-ischemic and less likely to produce coronary steal than nitroprusside. The starting dose is 10 µg/min to 20 µg/min; the dose may be increased by 10 µg/min every 2 to 3 minutes to a goal MAP of 70 mm Hg. IV nitroprusside can be added if further reduction in afterload is necessary. Nitroprusside is started at 0.5 µg/kg/min to 1.0 µg/kg/min and is also titrated to an MAP of approximately 70 mm Hg. Patients with low blood pressures (MAP less 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 within the first 12 hours of an MI if the patient is not already in cardiogenic shock.25,26 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 in cardiogenic shock should be treated with short-acting IV medications until they are stabilized.

Patients with mild pulmonary edema MI can be treated with diuretics such as furosemide administered intravenously and adjusted for creatinine and history of diuretic usage. Beta-adrenergic agonists such as dobutamine or dopamine may be needed for patients with severe heart failure and hypotension. Nevertheless, this therapy should generally be reserved for patients who do not respond to IABP and maximal medical therapy, or those with RV infarct.

Phosphodiesterase inhibitors such as milrinone may be beneficial to some patients. 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 20 µg/min to maintain a MAP of about 70 mm Hg.

Percutaneous revascularization of IRA has been associated with an improved prognosis in patients with cardiogenic shock, reducing the mortality rate from 80% to 50%. Generally, intervention has been performed on only the IRA, although some report multivessel percutaneous revascularization with more complete revascularization for patients with refractory shock after IRA recanalization.27,28

Emergency surgical revascularization is indicated in 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 need for cardiac transplantation.
RIGHT VENTRICULAR FAILURE
PREVALENCE
Mild RV dysfunction is common (approximately 40% of cases) after MI of the inferior or inferior-posterior wall; however, right heart failure occurs in only 10% of patients with inferior or inferior-posterior wall MI, normally only in infarcts involving the proximal right coronary artery.
PATHOPHYSIOLOGY
The degree of RV dysfunction depends on the location of the right coronary artery occlusion. Only proximal occlusions (proximal to the acute marginal branch) of the right coronary artery result in marked dysfunction. The degree of RV involvement also depends on the amount of collateral flow from the left coronary artery. Because the right ventricle is thin walled and has a low oxygen demand, there is coronary perfusion during the entire cardiac cycle; therefore, widespread irreversible infarction is rare.29

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.30 Patients with severe RV failure also may present with symptoms of low cardiac output, including diaphoresis, cool and clammy extremities, and altered mental status. Additionally, they often have oliguria and hypotension.

Physical examination reveals elevated jugular venous pressures, a right-sided S3 gallop, and normal lung exam. The presence of jugular venous pressure greater than 8 cm water and Kussmaul's sign (an exaggerated increase in jugular venous distention with inspiration) is both highly sensitive and specific for severe RV failure. A rare but clinically important complication of an RV infarct is right-to-left shunting, which is manifested by RV infarction and hypoxemia when RA pressures exceed LA pressures in patients with a patent formen ovale.

Electrocardiographically, patients present with inferior ST elevation in conjunction with ST elevation in V4R. These findings have a positive predictive value of 80% for RV infarction.31 Chest radiograph results usually are normal.
DIAGNOSTIC TESTING
Echocardiography is the diagnostic study of choice for RV infarction. It can detect RV dilatation and dysfunction as well as LV inferior wall dysfunction. It is also helpful in excluding cardiac tamponade, which may hemodynamically mimic RV infarction. The hemodynamic profile of acute RV infarct is similar to an acute pulmonary embolism.

Hemodynamic monitoring with a PA catheter reveals high right atrial pressures with a low PCWP (unless severe LV dysfunction is present) because RV failure results in underfilling of the left ventricle and low cardiac output. In some patients, RV dilatation 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 PCWP. A right atrial pressure greater than 10 mm Hg and a right atrial pressure to PCWP ratio of 0.8 or more strongly suggest RV infarction.32,33
THERAPY
Volume loading to increase LV preload and cardiac output is the key to management of RV infarction. Some patients may require several liters in 1 hour to reach a target PCWP of 15 mm Hg. These patients should have hemodynamic monitoring with a PA catheter. The target central venous pressure for fluid administration is approximately 15 mm Hg. When volume loading is insufficient to improve cardiac output, treatment with inotropic agents is indicated. Administration of dobutamine increases the cardiac index and improves RV ejection fraction.34

Patients may benefit from reperfusion therapy because patients who undergo successful reperfusion of RV branches have enhanced RV function and lower 30-day mortality.35 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 minute.

Although only case reports have shown that IABPs improve cardiac index 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 LV filling. Most patients with RV infarction spontaneously improve after 48 to 72 hours. An RV assist device is indicated for patients who remain in cardiogenic shock despite these measures.
VENTRICULAR ANEURYSM
PREVALENCE
Patients with apical transmural MIs are at greatest risk of aneurysmal formation; however, patients with posterior-basal infarcts may also develop aneurysms. 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 with inhibition of infarct expansion. Even late reperfusion limits infarct expansion through multiple mechanisms, including immediate change in infarction characteristics, preservation 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 dilatation are associated with persistent occlusion of an IRA. The aneurysm consists of a stretched portion of the myocardium, containing all three layers and connected with the ventricle by a wide neck.
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 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, are less compliant than acute aneurysms, and are less likely to expand during systole. Patients with chronic aneurysms may have heart failure, ventricular arrhythmias, and systemic embolism, or 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 ECG findings include ST elevation, which persists despite reperfusion therapy, and Q waves (Figures 3). ST elevations that persist for more than 6 weeks suggest a chronic ventricular aneurysm. A chest radiograph may reveal a localized bulge in the cardiac silhouette (Figure 4). Echocardiography accurately depicts the aneurysmal segment and may also demonstrate the presence of a mural thrombus. Additionally, echocardiography is useful in differentiating true aneurysms from pseudoaneurysms. True aneurysms have a wide neck, whereas pseudoaneurysms have a narrow neck in relation to the fundus of the aneurysm. Magnetic resonance imaging may also be useful in delineating the aneurysm.
THERAPY
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 12 to 24 hours of the onset of acute MI, as infarct expansion starts early. Corticosteroids and nonsteroidal anti-inflammatory agents should be avoided in the acute setting because they have been demonstrated 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 initially treated with IV heparin with a target partial thromboplastin time of 50 to 70 seconds. Warfarin is started simultaneously. Patients should be treated with warfarin at a target international normalized ratio of 2-3 for 3 to 6 months. Whether patients with large aneurysms without thrombus should receive anticoagulants is controversial. 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. These patients may be subsequently observed with echocardiography. Anticoagulation may be reinitiated if a thrombus develops.

Refractory heart failure and refractory ventricular arrhythmias in patients with aneurysms is an indication for surgical resection. Surgical resection may be followed by either conventional closure or newer techniques to restore LV geometry. Revascularization is beneficial for patients with viable myocardium around the aneurysmal segment.
DYNAMIC LEFT VENTRICULAR
OUTFLOW OBSTRUCTION
PREVALENCE
Dynamic LVOT obstruction is an uncommon complication of acute anterior MI. It was first described in a case report by Bartunek et al.18
PATHOPHYSIOLOGY
This event is dependent on compensatory hyperkinesis of the basal and mid segments of the left ventricle. Predictors of enhanced regional wall motion in noninfarct zones are the absence of multivessel disease, female gender, and higher TIMI flow (Thrombolysis in Myocardial Infarction trial) 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 drawn anteriorly toward the septum (Venturi effect). This leads to further outflow tract obstruction as well as mitral regurgitation.

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, patients older than 70 years of age, and in those without prior MI.
SIGNS AND SYMPTOMS
Patients may have respiratory distress, diaphoresis, and cool and 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. They also 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/or tachycardia can also be present.
DIAGNOSTIC TESTING
Echocardiography is the diagnostic test of choice. It accurately depicts the hyperkinetic segment and the LVOT obstruction as well as the systolic anterior motion of the mitral leaflet.
THERAPY
Treatment centers on decreasing myocardial contractility and heart rate while expanding intravascular volume and modestly increasing afterload. 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 normal saline solution to increase preload and decrease LVOT obstruction and the systolic anterior motion of the mitral leaflet. The patient's hemodynamic and respiratory status should be monitored closely during this therapeutic intervention with a Swan-Ganz catheter. Vasodilators, inotropic agents, and IABP should be avoided.
ARRHYTHMIC COMPLICATIONS
Dysrhythmia is the most common complication after acute MI. It is related to the formation of re-entry circuits at the confluence of the necrotic and viable myocardium. Premature ventricular contractions occur in approximately 90% of patients. The incidence of ventricular fibrillation is approximately 2% to 4%. Although lidocaine reduces the rate of primary ventricular fibrillation in patients with MI, there is no survival benefit, and there may be excess mortality. Therefore, lidocaine is not recommended as prophylactic therapy.36 Amiodarone may be used in patients with MI and frequent premature ventricular contractions, nonsustained ventricular tachycardia, or post-defibrillation for ventricular fibrillation. Amiodarone is administered as a bolus of 150 mg, then 1 mg/min IV for 6 hours followed by 0.5 mg/min. During cardiac arrest (ventricular fibrillation or pulseless ventricular tachycardia), the bolus should be increased to 300 mg (may repeat 150-mg boluses every 10 minutes to maximum dose of 24 grams). Ventricular arrhythmias not responsive to amiodarone may be treated with lidocaine (1 mg/kg bolus to a maximum of 100 mg followed by 1 mg/min to 4 mg/min drip)37 or procainamide. Polymorphic ventricular tachycardia is a rare complication of acute MI that can be treated with amiodarone, lidocaine, and/or procainamide as described for monomorphic ventricular tachycardia.

Recently, the risk of sudden cardiac death after MI has been evaluated. A significant correlation exists between significant systolic dysfunction and potential for sudden cardiac death. Implantable defibrillators have been shown to reduce mortality in patients with a prior MI and an ejection fraction of less than 30%, regardless of whether ventricular dysrhythmia is present.38

Supraventricular arrhythmias occur in less than 10% of patients with acute MI. Patients who develop these arrhythmias tend to have more severe ventricular dysfunction and worse outcome. Incipient heart failure should be suspected and treated in patients presenting with new atrial arrhythmias in the setting of an 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 RV infarction. Infranodal conduction disturbances with wide complex ventricular escape rhythms occur most frequently in large anterior MIs and portend a very poor prognosis.

Transvenous pacing is indicated in patients who present with asystole, Mobitz type II, second-degree AV block, or with complete AV block. Consideration for transvenous pacing should be given in patients with new onset bifascicular and trifascicular block in the setting of acute MI. Pacing is not indicated for patients with sinus bradycardia or AV dissociation and a more rapid ventricular escape rhythm as long as the patient is maintaining adequate hemodynamics. Initial treatment for these rhythm disturbances is IV atropine at a dose of 0.5 mg 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 less than 2%. This figure increases in patients with anterior wall MIs. 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.39
PATHOPHYSIOLOGY
Most emboli arise from the left ventricle as a result of wall motion abnormalities or aneurysms. Atrial fibrillation may also contribute to systemic embolic complications.
SIGNS AND SYMPTOMS
The most common clinical presentation 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 embolism. Focal neurologic deficits occur in patients with central nervous system emboli. Peripheral emboli cause limb ischemia, renal infarction, or mesenteric ischemia. Limb pain in a cold pulseless extremity is indicative of limb ischemia, and flank pain and hematuria are characteristic of renal infarction. Mesenteric ischemia causes severe abdominal pain, out of proportion to physical findings, and bloody diarrhea.
THERAPY
IV heparin should be started immediately with a target partial thromboplastin time of 50 seconds to 70 seconds and continued until the international normalized ratio is in the therapeutic range. Warfarin therapy should also be started immediately, with a goal international normalized ratio of 2-3 and continued for at least 3 to 6 months for patients with mural thrombi and those with large akinetic areas detected during echocardiography.
PERICARDITIS
PREVALENCE
The incidence of early pericarditis after acute MI is approximately 10%. The inflammation usually develops 24 to 96 hours after MI.40 Dressler's syndrome, or late pericarditis, occurs in 1% to 3% of patients 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 not known, but an autoimmune mechanism has been suggested.
SIGNS AND SYMPTOMS
Most patients with early pericarditis report no symptoms. Patients with symptoms (from either early or late pericarditis) report progressive, severe chest pain that lasts for hours. The symptoms are postural (worse in the supine position) and can be alleviated when the patient sits up and leans forward. The pain tends to be pleuritic in nature and, therefore, is exacerbated with deep inspiration, coughing, and swallowing. Radiation of pain to the trapezius ridge is nearly 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 exam 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; in 10%, it is uniphasic. A pericardial effusion may cause fluctuation in the intensity of the rub.

Evolving MI ECG changes may mask the diagnosis of pericarditis. Pericarditis produces generalized ST-segment elevation, which appears on ECG tracings in a concave upward or saddle-shaped pattern. As pericarditis evolves, T waves become inverted after the ST segment becomes isoelectric. On the other hand, in acute MI, T waves may become inverted when the ST segment is still elevated. Four phases of ECG abnormality have been described in association with pericarditis (Table 2).41

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

Aspirin is the therapy of choice for post-MI pericarditis in doses of 650 mg every 4 to 6 hours. Nonsteroidal anti-inflammatory drugs and corticosteroids should be avoided for 4 weeks after the acute event. These agents may interfere with myocardial healing and contribute to infarct expansion.42 In late pericarditis, nonsteroidal anti-inflammatory drugs and even corticosteroids may be indicated if severe symptoms persist beyond 4 weeks after MI. Colchicine may be beneficial in patients with recurrent pericarditis.
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    43.

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