Twenty percent of patients with acute myocardial infarction die before they reach the hospital. Mortality rates in hospitalized patients range from 5% to 15% and are determined chiefly by the size of the infarction and the age and general condition of the patient. Patients developing heart failure or hypotension have high early mortality rates. Several classification criteria have been developed to estimate early prognosis for survival. The most accurate is hemodynamic subsetting (Table 10-3). The prognosis after discharge is determined by three major factors: the degree of left ventricular dysfunction, the extent of residual ischemic myocardium, and the presence of ventricular arrhythmias. The mortality rate in the first year after discharge is approximately 6-8%, with over half of deaths occurring in the first 3 months, chiefly in patients with postinfarction heart failure. Subsequently, the mortality rate averages 4% per year.

A. Risk Stratification
A number of findings indicate increased risk after infarction. These include: (1) postinfarction angina; (2) non-Q wave infarction; (3) heart failure; (4) left ventricular ejection fraction less than 40%; (5) stress-induced ischemia, diagnosed by electrocardiography, scintigraphy, or echocardiography; and (6) ventricular ectopy (> 10 VPB/h).

Patients with postinfarction angina should undergo coronary arteriography. Authorities differ about which tests should be performed routinely in other patients, but in most a noninvasive assessment of left ventricular function and residual ischemia is appropriate. Significant left ventricular dysfunction is most likely with anterior infarction or multiple infarctions. In such patients, noninvasive assessment of left ventricular function by echocardiography or scintigraphy will help assess prognosis and facilitate medical management. If the ejection fraction is less than 40%, coronary angiography may be indicated, as this is a high-risk subset in which revascularization may improve prognosis. ACE inhibitor therapy is also indicated in patients with reduced ejection fractions. Submaximal exercise or pharmacologic stress testing before discharge or a maximal test after 3-6 weeks (the latter being more sensitive for ischemia) helps patients and physicians plan the return to normal activity. Imaging in conjunction with stress testing adds additional sensitivity for ischemia and provides localizing information. Both exercise and pharmacologic stress imaging have successfully predicted subsequent outcome. One of these tests should usually be employed prior to discharge in patients who have received thrombolytic therapy as a means of selecting appropriate candidates for coronary angiography.

Ambulatory electrocardiographic monitoring for arrhythmias is of less clear value; though it has some prognostic value beyond measurements of left ventricular function, no benefit from antiarrhythmic therapy for asymptomatic patients has been demonstrated. Ischemia detected during ambulatory monitoring is an indicator of poor prognosis, but it is unclear how much additional information is obtained in patients who have also undergone exercise testing or scintigraphic studies. The role of other procedures such as assessment of heart rate variability or baroreceptor testing is uncertain.

A conservative approach to postinfarction evaluation would include measurement of left ventricular function in patients with signs of heart failure or large infarctions and a test for ischemia in patients without recurrent chest pain. The latter should occur before discharge if the patient has undergone thrombolytic therapy but may be delayed for 3-6 weeks in most other patients.

B. Secondary Prevention
Postinfarction management should begin with identification and modification of risk factors. Treatment of hyperlipidemia and smoking cessation both prevent recurrent infarction and death. LDL cholesterol levels should be lowered below 100 mg/dL with drug therapy (usually a statin) commencing prior to discharge. Blood pressure control and exercise are also recommended.

Beta-blockers improve survival rates, primarily by reducing the incidence of sudden death in high-risk subsets of patients, though their value may be less in uncomplicated patients with small infarctions and normal exercise tests. No advantage of one preparation over another has been demonstrated except that those with intrinsic sympathomimetic activity have not proved beneficial in postinfarction patients.

Antiplatelet agents are beneficial; aspirin (325 mg daily) is recommended, but clopidogrel (75 mg daily) is also effective. Warfarin anticoagulation for 3 months reduces the incidence of arterial emboli after large anterior infarctions, and according to the results of at least one study it improves long-term prognosis. An advantage to combining aspirin and warfarin has not been demonstrated except perhaps in patients with atrial fibrillation.

Calcium channel blockers have not been shown to improve prognoses overall and should not be prescribed purely for secondary prevention. Antiarrhythmic therapy other than with beta-blockers has not been shown to be effective except in patients with symptomatic arrhythmias. Amiodarone has been studied in several trials of postinfarct patients with either left ventricular dysfunction or frequent ventricular ectopy. Although survival was not improved, amiodarone was not harmful-unlike other agents in this setting. Therefore, it is the agent of choice for individuals with symptomatic postinfarction supraventricular arrhythmias, although emerging data suggest that implantable defibrillators are the preferred option for ventricular arrhythmias.

Cardiac rehabilitation programs and exercise training can be of considerable psychologic benefit, but it is not known whether they alter prognosis.

C. ACE Inhibitors in Patients With Left Ventricular Dysfunction
Patients who sustain substantial myocardial damage often experience subsequent progressive left ventricular dilation and dysfunction, leading to clinical heart failure and reduced long-term survival. In patients with ejection fractions less than 40%, long-term ACE inhibitor therapy prevents left ventricular dilation and the onset of heart failure and prolongs survival. The Heart Outcomes Prevention Evaluation (HOPE) also demonstrated a reduction of approximately 20% in mortality rates and the occurrence of nonfatal myocardial infarction and stroke with ramipril treatment of postinfarction patients without confirmed left ventricular systolic dysfunction. Therefore, ACE inhibitor therapy should be strongly considered in this broader group of patients-and especially in diabetics and patients with even mild systolic hypertension, in whom the greatest benefit was observed.

D. Revascularization
Because of the increasing use of thrombolytic therapy and accumulating experience with PTCA, the indications for revascularization are rapidly evolving. Postinfarction patients who appear likely to benefit from early revascularization if the anatomy is appropriate are (1) those who have undergone thrombolytic therapy and have residual symptoms or laboratory evidence of ischemia, (2) patients with left ventricular dysfunction (ejection fraction < 30-40%) and evidence of ischemia, (3) patients with non-Q wave infarction and evidence of more than mild ischemia, and (4) patients with markedly positive exercise tests and multivessel disease. The value of revascularization in the following groups is less clear: (1) patients treated with thrombolytic agents with little evidence of reperfusion or residual ischemia, (2) patients with left ventricular dysfunction but no detectable ischemia, and (3) patients with preserved left ventricular function who have mild ischemia and are not symptom-limited. Patients who survive infarctions without complications, have preserved left ventricular function (ejection fraction > 50%), and have no exercise-induced ischemia have an excellent prognosis and do not require invasive evaluation.

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_{Ades PA: Cardiac rehabilitation and secondary prevention of coronary heart disease. N Engl J Med 2001;345:892.}

Dargie HJ et al: Effect of carvedilol on outcome after myocardial infarction in patients with left ventricular dysfunction: the CAPRICORN randomized trial. Lancet 2001;357:1385.

Hurlen M et al: Warfarin, aspirin, or both after myocardial infarction. N Engl J Med 2002;347:969.

JAMA patient page: Heart attack. JAMA 1998;280:1462.

Michaels AD et al: Risk stratification after acute myocardial infarction in the reperfusion era. Prog Cardiovasc Dis 2000; 42:273.

Sutton MGS et al: Left ventricular remodeling after myocardial infarction: pathophysiology and therapy. Circulation 2000; 101:2981.

Wright RS et al: Statin lipid-lowering therapy for acute myocardial infarction and unstable angina: efficacy and mechanism of benefit. Mayo Clin Proc 2002;77:1085.