Acute Myocardial Infarction

Key Concept/Objective: To recognize that thrombolytic therapy is the treatment of choice for ST elevation myocardial infarction when PCI is not available

Thrombolytic therapy has been widely studied in prospective, randomized, controlled trials involving more than 50,000 patients and has been proved to reduce mortality 29% in patients with ST segment elevation treated within 6 hours after the onset of chest pain. The survival benefi t of thrombolytic therapy is maintained for years. The benefi t of thrombolytic therapy is achieved through rapid restoration of blood fl ow in an occluded coronary artery.

Thrombolytic therapy is strongly recommended for patients with ST segment elevation in two or more contiguous leads who have had less than 6 hours of chest pain; for patients with classic symptoms of infarction in whom a bundle branch block precludes detection of ST segment elevation; and for patients presenting with 6 to 12 hours of chest pain, although the expected benefi ts for this last group of patients are fewer.
The ACC/AHA task force recommends the use of PCI for any patient with an acute STEMI who presents within 12 hours of symptom onset and who can undergo the procedure within 90 minutes of presentation by clinicians skilled in the procedure. When primary PCI is not available or its implementation will be signifi cantly delayed, use of thrombolytic therapy is recommended.

Key Concept/Objective: To know the complications associated with acute myocardial infarction

Although lidocaine has been shown to reduce the occurrence of primary ventricular fibrillation, mortality in patients receiving lidocaine was increased because of an increase in fatal bradycardia and asystole, and prophylactic lidocaine is no longer recommended if defibrillation can rapidly be performed. Beta blockers may reduce the early occurrence of ventricular fibrillation and should be administered to patients who have no contraindications. The treatment of atrial fibrillation in acute myocardial infarction should be similar to the treatment of atrial fibrillation in other settings. If atrial fibrillation recurs, antiarrhythmic agents may be used, although their impact on clinical outcomes is unproven. Mild mitral regurgitation is common in acute myocardial infarction and is present in nearly 50% of patients. The posterior papillary muscle receives blood only from the dominant coronary artery (the right coronary artery in nearly 90% of patients); thrombotic occlusion of this artery may cause rupture of the posterior papillary muscle, resulting in severe mitral regurgitation. Although nearly all patients with right ventricular infarction suffer both right and left ventricular infarction, the characteristic hemodynamic findings of right ventricular infarction generally dominate the clinical course and must be the main focus of therapy.

Key Concept/Objective: To understand the adjuvant medical therapies available for patients with acute myocardial infarction after reperfusion therapy has been administered

Early administration of beta blockers may reduce infarct size by reducing heart rate, blood pressure, and myocardial contractility. It is recommended that all patients with acute myocardial infarction without contraindications receive I.V. beta blockers as early as possible, whether or not they receive reperfusion therapy. Several large, randomized, controlled clinical trials evaluated the use of ACE inhibitors early after acute myocardial infarction; all but one trial revealed a significant reduction in mortality. To determine whether nitroglycerin therapy is beneficial in patients treated with reperfusion, 58,050 patients with acute myocardial infarction in the ISIS-4 trial were randomized to receive either oral controlled-release mononitrate therapy or placebo; thrombolytic therapy was administered to patients in both groups. The results of this study revealed no benefit from the routine administration of oral nitrate therapy in this setting. Previously, routine prophylactic antiarrhythmic therapy with I.V. lidocaine was recommended for all patients in the early stages of acute myocardial infarction. However, studies have revealed that prophylactic therapy with lidocaine does not reduce and may actually increase mortality because of an increase in the occurrence of fatal bradyarrhythmia and asystole.

Key Concept/Objective: To understand that PCI is the therapy of choice in ST segment elevation myocardial infarction

The time to administration of reperfusion therapy is a critical determinant of outcome and one of the few determinants of early clinical outcome under the control of the physician. Many studies have revealed that patients with myocardial infarction treated most rapidly have a lower mortality and, among survivors, reduced infarct size. This observation has led to recommendations that the time between a patient’s presentation to the emergency department and the administration of thrombolytic therapy not exceed 60 minutes; ideally, this period should not exceed 30 minutes. The most critical interval is the time between symptom onset and the achievement of reperfusion, not the time to the initiation of therapy. Thus, therapy that takes longer to initiate may actually be superior if it achieves reperfusion more
rapidly than another therapy that can be initiated more rapidly (e.g., thrombolytic therapy). The American College of Cardiology/American Heart Association (ACC/AHA) Task Force gave a class I recommendation to the use of PCI for any patient with an acute ST segment elevation myocardial infarction (STEMI) who presents within 12 hours of symptom onset and who can undergo the procedure within 90 minutes of presentation by clinicians skilled in the procedure. When primary PCI is not available or its implementation will be signifi cantly delayed, use of thrombolytic therapy is recommended. Reperfusion therapy, whether PCI or thrombolytics, should not await the availability of results of cardiac biomarkers. The immediate implementation of reperfusion therapy without awaiting biomarker data was given a class I recommendation.

Key Concept/Objective: To understand complications of a right ventricular infarction

Right ventricular infarction occurs in approximately one third of patients with acute inferior left ventricular infarction and is hemodynamically signifi cant in approximately 50% of affected patients. Hemodynamically signifi cant right ventricular infarction
associated with anterior infarction or isolated right ventricular infarction is rare. The classic fi ndings associated with hemodynamically signifi cant right ventricular infarction are hypotension with clear lung fi elds and an elevated jugular venous pressure, often
with the Kussmaul sign. Although nearly all patients with right ventricular infarction suffer both right and left ventricular infarction, the characteristic hemodynamic fi ndings of right ventricular infarction generally dominate the clinical course and must be the main focus of therapy. Right ventricular involvement during inferior myocardial infarction is associated with a signifi cant increase in mortality, and aggressive attempts at early reperfusion should be pursued. Prompt recognition of right ventricular involvement is clinically important because therapy that reduces right ventricular fi lling, such as use of nitrates or diuretics, should be avoided.

Key Concept/Objective: To understand the basic principles of thrombolytic therapy

The time between a patient's presentation to the emergency department and the administration of thrombolytic therapy should not exceed 60 minutes. Front-loaded tissue plasminogen activator (t-PA) has been found to be superior to the other thrombolytic regimens. However, some physicians prefer the less expensive streptokinase therapy, particularly for patients at low risk of dying (e.g., those with uncomplicated inferior infarctions) and the elderly, who are more likely to have hemorrhagic complications with t-PA than with streptokinase. Streptokinase is contraindicated in patients who have recently received a dose of streptokinase because of antibodies that form against the drug; these antibodies limit the efficacy of repeat doses and increase the risk of allergic reactions. Thrombolytic therapy has been studied in patients with ECG findings other than ST-segment elevation or bundle branch block and has been found to be either of no use or deleterious. Patients treated with thrombolytic therapy in whom complications do not occur are at low risk for reinfarction and death after discharge, and routine performance of coronary angiography and coronary angioplasty does not reduce the occurrence of these adverse events. Coronary angiography is recommended only for patients with hemodynamic instability or for patients in whom spontaneous or exercise-induced ischemia occurs.

Key Concept/Objective: To recognize the signs, symptoms, and treatment of acute mitral regurgitation

Mitral regurgitation may result from injury to any of the components of the mitral valve apparatus, including the papillary muscles and ventricular walls to which they attach. Mild mitral regurgitation is common in acute myocardial infarction and is present in nearly 50% of patients. Severe mitral regurgitation caused by acute myocardial infarction is rare and generally results from partial or complete rupture of
a papillary muscle. The characteristic murmur of severe chronic mitral regurgitation may not be present with acute rupture of a papillary muscle. Instead, a decrescendo systolic murmur is often present, extending less throughout systole as systemic arterial pressure falls and left arterial pressure rises. In many cases, the signifi cance of the murmur is not recognized. The blood supply of the anterior papillary
muscle arises from branches of both the left anterior descending and the circumfl ex arteries; therefore, rupture of the anterior papillary muscle is rare. However, the posterior papillary muscle receives blood only from the dominant coronary artery (the right coronary artery in nearly 90% of patients); thrombotic occlusion of this artery may cause rupture of the posterior papillary muscle, resulting in severe
mitral regurgitation. Severe mitral regurgitation is 10 times more likely to occur with inferior infarction than with anterior infarction. Acute severe mitral regurgitation is poorly tolerated and generally results in pulmonary edema, often with cardiogenic shock. Prompt surgical repair is recommended. Although the mortality associated with mitral valve surgery is high in this setting, approaching 50%, survival
appears to be greater than with medical therapy alone. Therapy aimed at reducing left ventricular afterload, such as use of IV nitroprusside and an intra-aortic balloon pump, reduces the regurgitant volume and increases forward blood fl ow and cardiac
output and may be helpful as a temporizing measure.

Key Concept/Objective: To recognize the benefi ts of statins in patients with a recent myocardial infarction

Recent studies have demonstrated that in patients with coronary artery disease, lipid-lowering therapy with HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitors reduces not only fatal and nonfatal infarction but also mortality from all causes. The
Scandinavian Simvastatin Survival Study revealed a 42% reduction in cardiac mortality and a 30% reduction in all-cause mortality in 4,444 men and women with coronary artery disease over the 5.4 years of the study. The reductions in mortality were similar in patients in
the lowest and those in the highest quartiles of serum low-density lipoprotein (LDL) cholesterol. It has been demonstrated that postinfarction patients with an LDL cholesterol level at or above 130 mg/dL benefi t from lipid-lowering therapy within as little as 2 years after the initiation of such therapy. Initial measurement of cholesterol should be made within 24 hours after myocardial infarction; measurement of lipids 24 hours or more after myocardial infarction can be misleading in that cholesterol levels may be reduced below baseline levels during this period and remain low for up to 1 month. Early initiation of statins may be more benefi cial than later initiation. Exercise, weight reduction in overweight patients, avoidance of dietary saturated fat and cholesterol, and smoking cessation have all been reported to favorably infl uence blood lipid levels and should be recommended whether or not lipid-lowering medications are prescribed.