Acute Myocardial Infarction

Acute Myocardial Infarction

Acute myocardial infarction (AMI) is a serious complication of ischemic heart disease, with an overall mortality rate of 25%. More than one half of these deaths occur shortly after onset, usually due to arrhythmias (ventricular fibrillation). With recent advances in interventional cardiology, the in-hospital mortality rate has been reduced to less than 10–15%. Pump (ventricular) failure is now the lead-ing cause of death after AMI in hospitalized patients.

Most myocardial infarctions occur in patients with more than one severely narrowed (>75% nar-rowing of the cross-sectional area) coronary artery. A transmural infarction occurs in an area distal to a complete occlusion. Patients who die within 24 hours after AMI may demonstrate only coro-nary atherosclerosis on necropsy examination of the heart. The occlusion is nearly always due to throm-bosis at a stenotic atheromatous plaque. Coronary emboli or severe spasm is less commonly the cause. The size and location of the infarct depend on the distribution of the obstructed vessel and whether collateral vessels have formed. Anterior, apical, and septal infarcts of the left ventricle are usually due to thrombosis in the left anterior descending circula-tion; lateral and posterior left ventricular infarcts result from occlusions in the left circumflex system, whereas right ventricular and posterior–inferior left ventricular infarcts result from thrombosis in the right coronary artery. In contrast, subendocardial (nontransmural, or “non–Q wave”) infarctions more often occurs in the setting of reduced myocardial perfusion due to hypotension or intimal hemor-rhage, and less commonly follows coronary plaque rupture and thrombosis.

Following brief episodes of severe ischemia, persisting myocardial dysfunction with only a slow and incomplete return of contractility can be observed. This phenomenon of “stunning” is often thought to occur in areas adjacent to infarcted myocardium and can contribute to ventricular dysfunction following AMI. Relief of the ischemia in these areas can restore contractile function, albeit not immediately. Stunning may be observed follow-ing aortic cross-clamping during cardiopulmonary bypass and present as a reduced cardiac output upon attempted separation from bypass . When severe hypokinesis or akinesis is observed in the setting of severe chronic ischemia, the myocar-dium in these noninfarcted but poorly contractile areas may be said to be “hibernating.” This diagno-sis can be confirmed by observing viable tissue with positron emission tomography, or by showing that the hypocontractile myocardium responds to dobu-tamine during stress echocardiography.

The immediate treatment of AMI is the admin-istration of oxygen, aspirin (160–325 mg), nitro-glycerin (sublingual or spray), morphine (2–4 mg intravenously every 5 min) until the pain is relieved, and in most cases of an ST-segment elevation MI (STEMI) movement of the patient to the cardiac catheterization laboratory. The mnemonic “MONA (morphine, oxygen, nitroglycerin, and aspirin) greets all patients” succinctly states this approach. Because the prognosis following AMI is generally inversely proportionate to the extent of necrosis, the focus in management of an evolving myocar-dial infarction remains on reperfusion. Based on local resources, timing, and anatomic findings dur-ing angiography, angioplasty, stenting, or coronary artery bypass surgery may be preferred. Guidelines for treatment of AMI change on a nearly annual basis and are regularly published by the American College of Cardiology/American Heart Associa-tion and by the European Society of Cardiology; we strongly recommend that they be consulted.

Patients with ST-segment depression or dynamic T-wave changes (non–Q wave infarction; unstable angina) benefit from antithrombin (hepa-rin) and antiplatelet (aspirin) therapy. All patients without contraindications (such as acute heart fail-ure) should receive β blockers. Other medications and treatments such as ACE inhibitors, statins, and cessation of smoking are the key to secondary pre-vention. Patients who have recurrent angina should be given nitrates. If angina persists or if there is a contraindication to β blockers, calcium chan-nel blockers should be administered. Persistent or recurrent angina signals the need for angiography, if it has not already been performed.

Intraaortic balloon counterpulsation is usu-ally reserved for hemodynamically compromised patients with refractory ischemia. Temporary pac-ing following AMI is indicated for Mobitz type II and complete heart block, a new bifascicular block, and bradycardia with hypotension. Emergency treatment of arrhythmias constantly evolves and we recommend that the guidelines for Advanced Car-diac Life Support be followed. In general, ventricu-lar tachycardia, if treated medically is best managed with amiodarone (150 mg intravenous bolus over 10 min). Synchronized cardioversion may be used in patients with ventricular tachycardia and with a pulse. Patients with a stable narrow-complex supra-ventricular tachycardia should be treated with ami-odarone. Patients with paroxysmal supraventricular tachycardia, whose ejection fraction is preserved, should be treated with a calcium channel blocker, ablocker, or DC cardioversion. Medically unstable hypotensive patients should receive cardioversion.

Patients with ectopic or multifocal atrial tachy-cardia should not receive DC cardioversion; instead they should be treated with calcium channel block-ers, a β blocker, or amiodarone.