Definition

Myocardial infarction or myocardial cell death occurs when a portion of heart muscle is deprived of its blood supply as a result of blockage, acute thrombosis, or spasm of a coronary artery. MI is considered part of a spectrum referred to as ACS. The ACS continuum representing ongoing myocardial ischemia or injury consists of unstable angina, non–ST-segment elevation MI (NSTEMI), and ST-segment elevation MI (STEMI). Patients with ischemic discomfort may or may not have ST-segment or T-wave changes denoted on the ECG.

Pathophysiology

When myocardial oxygen supply (i.e., coronary blood flow) does not meet demand (myocardial oxygen consumption), ischemia or MI may occur. The risk for perioperative MI increases when a patient who has had a previous MI undergoes anesthesia and operation.

ST-segment elevations seen on the ECG reflect active and ongoing transmural myocardial injury. Without immediate reperfusion therapy, most persons with STEMI develop Q waves, reflecting a dead zone of myocardium that has undergone irreversible damage and death. Those without ST elevations are diagnosed either with unstable angina or NSTEMI—differentiated by the presence of cardiac enzymes. Both of these conditions may or may not have changes on the surface ECG, including ST-segment depression or T-wave morphologic changes. MI may lead to impairment of systolic or diastolic function and to increased predisposition to arrhythmias and other long-term complications.

Treatment

As a general rule, initial therapy for acute MI is directed toward restoration of perfusion as soon as possible to salvage as much of the jeopardized myocardium as possible. This may be accomplished through medical or mechanical means, such as PCI or CABG.

Further treatment is based on the following:

Coronary thrombolysis and mechanical revascularization have revolutionized the primary treatment of patients with acute MI, largely because they allow salvage of the myocardium when implemented early after the onset of ischemia. The modest prognostic benefit of an opened infarct-related artery may be realized even when recanalization is induced only 6 hours or more after the onset of symptoms, that is, when the salvaging of substantial amounts of jeopardized ischemic myocardium is no longer likely. The opening of an infarct-related artery may improve ventricular function, collateral blood flow, and ventricular remodeling, and it may decrease infarct expansion, ventricular aneurysm formation, LV dilatation, late arrhythmia associated with ventricular aneurysms, and mortality

Evidence suggests a benefit from the use of β-blockers, ACE inhibitors, angiotensin II receptor blockers, and statins.