New concepts in the pathophysiology of acute myocardial infarction.

Recent findings concerning the pathophysiology of acute myocardial infarction are reviewed and related to the potential for myocardial salvage. The myocardial infarction process can be divided into 2 phases, an early evolving phase (the first 6 hours) and a later convalescent phase. An evolving infarction is associated with an occluded coronary artery; in most cases, a thrombotic occlusion occurs. The human coronary artery normally has an intact endothelium, which has protective vasodilatory and antiplatelet-aggregating effects that are lost when the endothelium is damaged. The endothelium is exquisitely sensitive to trauma and can be damaged by high shear stress produced by narrowing of the coronary arteries that is not associated with reduced coronary blood flow. In addition, during this acute endothelial damage, monocellular infiltration of the coronary arteries has the potential to release factors that may cause platelet aggregation, enhance blood coagulation, attract other white blood cells or exert other effects on the coronary tree. Myocardial damage occurring in the early evolving stage is usually responsive to treatment that either restores myocardial oxygen supply or reduces myocardial oxygen demand. However, coronary events occurring after the first 6 hours usually are not responsive to such treatment. Certain clinical variables may shorten or extend the time period within which damaged myocardium can be saved. The findings suggest important approaches for intervention to modify the acute phase.