Acute Myocardial Infarction Complications

A variety of complications can occur after myocardial infarction even when treatment is initiated promptly.

A. Postinfarction Ischemia

Approximately 30% of patients will have angina postinfarction. This is more common in patients with angina prior to infarction and in non-ST segment elevation infarction. Postinfarction angina is associated with increased short- and long-term mortality. The underlying mechanism is usually inadequate blood flow through a recanalized vessel or reocclusion. Vigorous medical therapy should be instituted, including nitrates and beta-blockers as well as aspirin, heparin, and platelet glycoprotein IIb/IIIa antagonists. Most patients with postinfarction angina-and all who are refractory to medical therapy-should undergo early catheterization and revascularization by PTCA or CABG.

B. Arrhythmias

Abnormalities of rhythm and conduction are common.

1. Sinus bradycardia
This is most common in inferior infarctions or may be precipitated by medications. Observation or withdrawal of the offending agent is usually sufficient. If accompanied by signs of low cardiac output, atropine, 0.5-1 mg intravenously, is usually effective. Temporary pacing is rarely required.

2. Supraventricular tachyarrhythmias
Sinus tachycardia is common and may reflect either increased adrenergic stimulation or hemodynamic compromise due to hypovolemia or pump failure. In the latter, beta blockade is contraindicated. Supraventricular premature beats are common and may be premonitory for atrial fibrillation. Electrolyte abnormalities and hypoxia should be corrected and causative agents (especially aminophylline) stopped. Atrial fibrillation should be rapidly controlled or converted to sinus rhythm. Intravenous beta-blockers such as metoprolol (2.5-5 mg/h) or short-acting esmolol (50-200 ug/ kg/min) are the agents of choice if cardiac function is adequate. Intravenous diltiazem (5-15 mg/h) may be used if beta-blockers are contraindicated or ineffective. Digoxin (0.5 mg as initial dose, then 0.25 mg every 90-120 minutes [up to 1-1.25 mg] for a loading dose, followed by 0.25 mg daily if renal function is normal) is preferable if heart failure is present with atrial fibrillation, but the onset of action is delayed. Electrical cardioversion (commencing with 100 J) may be necessary if atrial fibrillation is complicated by hypotension, heart failure, or ischemia, but the arrhythmia often recurs. A short course of a class Ia agent such as procainamide or quinidine may be required in addition to digoxin, a beta-blocker, or a calcium channel blocker to maintain sinus rhythm. Amiodarone (150 mg intravenous bolus and then 15-30 mg/h intravenously, or rapid oral loading with 400 mg three times daily) may be helpful to restore or maintain sinus rhythm.

3. Ventricular arrhythmias
Ventricular arrhythmias are most common in the first few hours after infarction. Ventricular premature beats may be premonitory for ventricular tachycardia or fibrillation but generally should not be treated in the absence of nonsustained ventricular tachycardia (usually more than six consecutive beats). In the latter case, prophylactic lidocaine has been shown to prevent subsequent sustained ventricular tachycardia or fibrillation but does not improve survival in patients who are being monitored. Prophylactic lidocaine may be started as a 1- mg/kg bolus followed by an infusion of 2 mg/min. Toxicity (tremor, anxiety, confusion, seizures) is common, especially in older patients and those with hypotension, heart failure, or liver disease.

Ventricular tachycardia should be treated with a 1- mg/kg bolus of lidocaine if the patient is stable or by electrical cardioversion (100-200 J) if not. If the arrhythmia cannot be suppressed with lidocaine, procainamide (100-mg boluses over 1-2 minutes every 5 minutes to a cumulative dose of 750-1000 mg) or intravenous amiodarone (150 mg over 10 minutes, which may be repeated as needed, followed by 360 mg over 6 hours and then 540 mg over 18 hours) should be initiated, followed by an infusion of 20-80 mg/kg/min. ventricular fibrillation is treated electrically (300-400 J). Unresponsive ventricular fibrillation should be treated with additional amiodarone and repeat cardioversion while CPR is administered.

Accelerated idioventricular rhythm is a regular, wide-complex rhythm at a rate of 70-100/min. It often follows reperfusion and usually does not require specific therapy.

4. Conduction disturbances
All degrees of atrioventricular block may occur in the course of acute myocardial infarction. Block at the level of the atrioventricular node is more common than infranodal block and occurs in approximately 20% of inferior myocardial infarctions. First-degree block is the most common and requires no treatment. Second-degree block is usually of the Mobitz type I form (Wenckebach), is often transient, and requires treatment only if associated with a heart rate slow enough to cause symptoms. Complete atrioventricular block occurs in up to 5% of acute inferior infarctions, usually is preceded by Mobitz I second-degree block, and generally resolves spontaneously, though it may persist for hours to several weeks. The escape rhythm originates in the distal atrioventricular node or atrioventricular junction and hence has a narrow QRS complex and is reliable, albeit often slow (30-50 beats/min). Treatment is often necessary because of resulting hypotension and low cardiac output. Intravenous atropine (1 mg) usually restores atrioventricular conduction temporarily, but if the escape complex is wide or if repeated atropine treatments are needed, temporary ventricular pacing is indicated. The prognosis for these patients is only slightly worse than that of patients who do not develop atrioventricular block.

In anterior infarctions, the site of block is distal, below the atrioventricular node, and usually a result of extensive damage of the His-Purkinje system and bundle branches. New first-degree block (prolongation of the PR interval) is unusual in anterior infarction; Mobitz type II atrioventricular block or complete heart block may be preceded by intraventricular conduction defects or may occur abruptly. The escape rhythm, if present at all, is an unreliable wide-complex idioventricular rhythm. Urgent ventricular pacing is mandatory, but even with successful pacing, morbidity and mortality are high because of the extensive myocardial damage. New conduction abnormalities such as right or left bundle branch block or fascicular blocks may presage progression, often sudden, to second- or third-degree atrioventricular block. Temporary ventricular pacing is recommended for new-onset alternating bilateral bundle branch block, bifascicular block, or bundle branch block with worsening first-degree atrioventricular block. Patients with anterior infarction who progress to second- or third-degree block even transiently should be considered for insertion of a prophylactic permanent ventricular pacemaker before discharge.

C. Myocardial Dysfunction

The severity of cardiac dysfunction is proportionate to the extent of myocardial necrosis but is exacerbated by preexisting dysfunction and ongoing ischemia. Patients who have normal blood pressure, no signs of heart failure, and normal urine output have a good prognosis. Those with hypotension or evidence of more than mild heart failure should have bedside right heart catheterization and continuous measurements of arterial pressure. These measurements permit the accurate assessment of cardiac function, facilitate the correct choice of therapy, and provide important prognostic information. Table 10-3 categorizes patients based upon these hemodynamic findings.

1. Acute left ventricular failure
Basilar rales are common in acute myocardial infarction, but dyspnea, more diffuse rales, and arterial hypoxemia usually indicate left ventricular failure. Since both the physical examination and chest x-ray correlate poorly with hemodynamic measurements and since the central venous pressure does not correlate with the pulmonary capillary wedge pressure (PCWP), right heart catheterization may be essential in monitoring therapy. General measures include supplemental oxygen to increase arterial saturation to above 95% and elevation of the trunk. Diuretics are usually the initial therapy unless right ventricular infarction is present. Intravenous furosemide (10-40 mg) or bumetanide (0.5-1 mg) is preferred because of the reliably rapid onset and short duration of action of these drugs. Higher dosages can be given if an inadequate response occurs. Morphine sulfate (4 mg intravenously followed by increments of 2 mg) is valuable in acute pulmonary edema.

Diuretics are usually effective; however, since most patients with acute infarction are not volume overloaded, the hemodynamic response may be limited and may be associated with hypotension. Vasodilators will reduce PCWP and improve cardiac output by a combination of venodilation (increasing venous capacitance) and arteriolar dilation (reducing afterload and left ventricular wall stress). In mild heart failure, sublingual isosorbide dinitrate (2.5-10 mg every 2 hours) or nitroglycerin ointment (6.25-25 mg every 4 hours) may be adequate to lower PCWP. In more severe failure, especially if cardiac output is reduced, sodium nitroprusside is the preferred agent. It should be initiated only with hemodynamic monitoring; the initial dosage should be low (0.25 ug/kg/min) to avoid excessive hypotension, but the dosage can be increased by increments of 0.5 ug/kg/min every 5-10 minutes up to 5-10 ug/kg/min until the desired hemodynamic response (PCWP < 18 mm Hg, CI > 2.5) is obtained. Excessive hypotension (mean blood pressure < 65-75 mm Hg) or tachycardia (> 10/min increase) should be avoided. Combination of nitroprusside with inotropic agents may be necessary to preserve blood pressure or maximize benefit.

Intravenous nitroglycerin (starting at 10 ug/min) is usually less effective but may lower PCWP with less hypotension. Oral or transdermal vasodilator therapy with nitrates or angiotensin-converting enzyme inhibitors is often necessary after the initial 24-48 hours (see below).

Inotropic agents should be avoided if possible, because they often increase heart rate and myocardial oxygen requirements. Dobutamine has the best hemodynamic profile, increasing cardiac output and modestly lowering PCWP, usually without excessive tachycardia, hypotension, or arrhythmias. The initial dosage is 2.5 ug/kg/min, and it may be increased by similar increments up to 15-20 ug/kg/min at intervals of 5-10 minutes. Dopamine is more useful in the presence of hypotension (see below), since it produces peripheral vasoconstriction, but it has a less beneficial effect on PCWP. Amrinone is a positive inotrope and vasodilator that produces hemodynamic effects similar to those of dobutamine but with a greater decrease in PCWP. However, its longer duration of action makes it less useful in unstable situations. Milrinone is a more potent and newer congener of amrinone with fewer side effects. It should be commenced in a loading dose of 50 ug/kg over 10 minutes, followed by an infusion of 0.375-0.75 ug/kg/min. Digoxin has not been helpful in acute infarction except to control the ventricular response in atrial fibrillation, but it may be beneficial if chronic heart failure persists.

2. Hypotension and shock
Patients with hypotension (systolic blood pressure < 100 mm Hg, individualized depending on prior blood pressure) and signs of diminished perfusion (low urine output, confusion, cold extremities) should be hemodynamically monitored. Up to 20% will have findings indicative of intravascular hypovolemia (due to diaphoresis, vomiting, decreased venous tone, medications-such as diuretics, nitrates, morphine, beta-blockers, calcium channel blockers, and thrombolytic agents-and lack of oral intake). These should be treated with successive boluses of 100 mL of normal saline until PCWP reaches 15-18 mm Hg to determine whether cardiac output and blood pressure respond. Pericardial tamponade due to hemorrhagic pericarditis (especially after thrombolytic therapy or Cardiopulmonary resuscitation) or ventricular rupture should be considered and excluded by echocardiography if clinically indicated. Right ventricular infarction, characterized by a normal PCWP but elevated right atrial pressure, can produce hypotension. This is discussed below.

Most hypotensive patients will have moderate to severe left ventricular dysfunction; pathologic studies indicate that more than 20% of the left ventricle is infarcted (> 40% in cardiogenic shock). If hypotension is only modest (systolic pressure > 90 mm Hg) and the PCWP is elevated, diuretics and an initial trial of nitroprusside (see above for dosing) are indicated. If the blood pressure falls, inotropic support will need to be added or substituted. Such patients may also be treated with intra-aortic balloon counterpulsation (IABC). This device unloads the left ventricle during systole and increases diastolic coronary artery filling pressure. It often facilitates the use of vasodilators in patients who previously did not tolerate them.

Dopamine is the most appropriate pressor for cardiogenic hypotension. It should be initiated at a rate of 2-4 ug/kg/min and increased at 5-minute intervals to the appropriate hemodynamic end point. At low dosages (< 5 ug/kg/min), it improves renal blood flow; at intermediate dosages (2.5-10 ug/kg/min), it stimulates myocardial contractility; at higher dosages (> 8 ug/kg/min), it is a potent a1-adrenergic agonist. In general, blood pressure and cardiac index rise, but PCWP does not fall. Dopamine may be combined with nitroprusside or dobutamine (see above for dosing), or the latter may be used in its place if hypotension is not severe. Amrinone and milrinone have hemodynamic effects similar to those of dobutamine, but their longer duration of action precludes rapid dosage adjustment. Norepinephrine (0.1-0.5 ug/kg/min) is the usual pressor of last resort, since isoproterenol and epinephrine produce less vasoconstriction and do not increase coronary perfusion pressure (aortic diastolic pressure), and both tend to worsen the balance between myocardial oxygen delivery and utilization.

Patients with cardiogenic shock not due to hypovolemia have a poor prognosis, with 30-day mortality rates of 50-80%. If they do not respond rapidly, IABC should be instituted. Surgically implanted ventricular assist devices may be used in extreme cases. Early cardiac catheterization and coronary angiography followed by percutaneous or surgical revascularization offer the best chance of survival, particularly in patients under 75 years of age.

D. Right Ventricular Infarction

Right ventricular infarction is present in one-third of patients with inferior wall infarction but is clinically significant in less than 50% of these. It presents as hypotension with relatively preserved left ventricular function and should be considered whenever patients with inferior infarction exhibit signs of low cardiac output and raised venous pressure. Hypotension is often exacerbated by medications that decrease intravascular volume or produce venodilation, such as diuretics, nitrates, and narcotics. Right atrial pressure and jugular venous pulsations are high, while PCWP is normal or low and the lungs are clear. The diagnosis is suggested by ST segment elevation in right-sided anterior chest leads. The diagnosis can be confirmed by echocardiography or hemodynamic measurements. When hypotension is present, hemodynamic measurements are necessary to monitor therapy. Treatment consists of fluid loading to improve left ventricular filling; inotropic agents may also be useful.

E. Mechanical Defects

Partial or complete rupture of a papillary muscle or of the interventricular septum occurs in less than 1% of acute myocardial infarctions and carries a poor prognosis. These complications occur in both anterior and inferior infarctions, usually 3-7 days after the acute event. They are detected by the appearance of a new systolic murmur and clinical deterioration, often with pulmonary edema. The two lesions are distinguished by the location of the murmur (apical versus parasternal) and by Doppler echocardiography. Hemodynamic monitoring is essential for appropriate management and demonstrates an increase in oxygen saturation between the right atrium and pulmonary artery in Ventricular septal defect and, often, a large v wave with mitral regurgitation. Treatment by nitroprusside and, preferably, IABC reduces the regurgitation or shunt, but surgical correction is mandatory. In patients remaining hemodynamically unstable or requiring continuous parenteral pharmacologic treatment or counterpulsation, early surgery is recommended, though mortality rates are high (15% to nearly 100%, depending on residual ventricular function and clinical status). Patients who are stabilized medically can have delayed surgery with lower risks (10-25%).

F. Myocardial Rupture

Complete rupture of the left ventricular free wall occurs in less than 1% of patients and usually results in immediate death. It occurs 2-7 days postinfarction, usually involves the anterior wall, and is more frequent in older women. Incomplete or gradual rupture may be sealed off by the pericardium, creating a pseudoaneurysm. This may be recognized by echocardiography, radionuclide angiography, or left ventricular angiography, often as an incidental finding. It demonstrates a narrow-neck connection to the left ventricle. Early surgical repair is indicated, since delayed rupture is common.

G. Left Ventricular Aneurysm

Ten to 20 percent of patients surviving an acute infarction develop a left ventricular aneurysm, a sharply delineated area of scar that bulges paradoxically during systole. This usually follows anterior Q wave infarctions. Aneurysms are recognized by persistent ST segment elevation (beyond 4-8 weeks), and a wide neck from the left ventricle can be demonstrated by echocardiography, scintigraphy, or contrast angiography. They rarely rupture but may be associated with arterial emboli, ventricular arrhythmias, and congestive heart failure. Surgical resection may be performed for these indications if other measures fail. The best results (mortality rates of 10-20%) are obtained when the residual myocardium contracts well and when significant coronary lesions supplying adjacent regions are bypassed.

H. Pericarditis

The pericardium is involved in approximately 50% of infarctions, but pericarditis is often not clinically significant. Twenty percent of patients with Q wave infarctions will have an audible friction rub if examined repetitively. Pericardial pain occurs in approximately the same proportion after 2-7 days and is recognized by its variation with respiration and position (improved by sitting). Often, no treatment is required, but aspirin (650 mg every 4-6 hours) or indomethacin (25 mg three or four times daily) will usually relieve the pain. Anticoagulation should be avoided, since hemorrhagic pericarditis may result.

One week to 12 weeks after infarction, Dressler’s syndrome (post-myocardial infarction syndrome) occurs in less than 5% of patients. This is an autoimmune phenomenon and presents as pericarditis with associated fever, leukocytosis, and, occasionally, pericardial or pleural effusion. It may recur over months. Treatment is the same as for other forms of pericarditis. A short course of corticosteroids may help if nonsteroidal agents do not relieve symptoms.

I. Mural Thrombus

Mural thrombi are common in large anterior infarctions but not in infarctions at other locations. Arterial emboli occur in approximately 2% of patients with known infarction, usually within 6 weeks. Anticoagulation with heparin followed by short-term (3-month) warfarin therapy prevents most emboli and should be considered in all patients with large anterior infarctions. Mural thrombi can be detected by echocardiography or CT scan (MRI has yielded frequent false-positive results) but with only moderate reliability, and only a small percentage (up to 25%) embolize, so these procedures should not be relied upon for determining the need for anticoagulation.

Brady WJ et al: Diagnosis and management of bradycardia and atrioventricular block associated with acute coronary ischemia. Emerg Med Clin North Am 2001;19:371.

Crenshaw BS et al: Risk factors, angiographic patterns, and outcomes in patients with Ventricular septal defect complicating acute myocardial infarction. Circulation 2000;101:27.

Goldstein JA: Pathophysiology and management of right heart ischemia. J Am Coll Cardiol 2002;40:841.

Mangrum JM: Tachyarrhythmias associated with acute myocardial infarction. Emerg Med Clin North Am 2001;19:385.

Menon V et al: Management of cardiogenic shock complicating acute myocardial infarction. Heart 2002;88:531.

Prieto A et al: Nonarrhythmic complications of acute myocardial infarction. Emerg Med Clin North Am 2001;19:397.

Rathore SS et al: Acute myocardial infarction complicated by heart block in the elderly: prevalence and outcomes. Am Heart J 2001;141:47.

Sayer JW et al: Prognostic implications of ventricular fibrillation in acute myocardial infarction: new strategies required for mortality reduction. Heart 2000;84:258.

Acute Myocardial Infarction
Essentials of Diagnosis
General Considerations
Clinical Findings
A. Symptoms
B. Signs
C. Laboratory Findings
D. Electrocardiography
E. Chest X-Ray
F. Echocardiography
G. Scintigraphic Studies
H. Hemodynamic Measurements

A. Aspirin
B. Thrombolytic Therapy
C. Acute PTCA and Stenting for ST Segment Elevation Myocardial Infarction
D. Initial Management of Non-ST-Segment Elevation Myocardial Infarction
E. General Measures
F. Analgesia
G. Beta-Adrenergic Blocking Agents
H. Nitrates
I. Angiotensin-Converting Enzyme (ACE) Inhibitors
J. Antiarrhythmic Prophylaxis
K. Calcium Channel Blockers
L. Anticoagulation

A. Postinfarction Ischemia
B. Arrhythmias
C. Myocardial Dysfunction
D. Right Ventricular Infarction
E. Mechanical Defects
F. Myocardial Rupture
G. Left Ventricular Aneurysm
H. Pericarditis
I. Mural Thrombus

Postinfarction Management
A. Risk Stratification
B. Secondary Prevention
C. ACE Inhibitors in Patients With Left Ventricular Dysfunction
D. Revascularization

Provided by ArmMed Media
Revision date: July 4, 2011
Last revised: by Sebastian Scheller, MD, ScD