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Mechanisms of acute ischemic contractile failure of the heart. Role of intracellular calcium.

Introduction Ischemic heart disease is usually caused by atheroma in the coronary arteries and results in reduced or absent blood flow to cardiac cells, depriving them of oxygen and metabolic substrates and causing abnormal accumulation ofions or products of metabolism. The consequences of cardiac ischemia include reduced force production, life-threatening disturbances of cardiac rhythm, and ultimately death of the cells. Because of the high prevalence of ischemic heart disease, and its high cost in morbidity and mortality, there has been intense interest in understanding the mechanisms by which ischemia alters the normal functioning of cardiac muscle. The effects of ischemia on contractile performance have been reviewed previously (1, 2) and are only briefly summarized here. When a beating heart is made globally ischemic, there is a rapid decline in developed pressure. This decrease in force production is apparent within 1 min and is generally complete, with little or no developed force, after 5-10 min. After 10-20 min ofischemia, a gradual rise in diastolic pressure becomes apparent (the ischemic contracture), and increases in size as ischemia progresses. If reperfusion is started before or during the early stages ofischemic contracture, eventual recovery ofcontractile function can be virtually complete. However, if reperfusion is delayed until the contracture is well established, muscle damage is accelerated and recovery is poor (3). In addition to reduced force production, the early minutes of ischemia are associated with electrophysiological abnormalities and arrhythmias (4). Arrhythmias also occur during reperfusion. The early fall of force, arrhythmias, and muscle damage all contribute to acute ischemic contractile failure of the heart, which we define as impairment of cardiac function produced by a duration ofischemia within which some recovery is possible if ischemia is reversed (i.e., up to 1-2 h). Recent data, in particular the measurement of intracellular free calcium ([Ca2+]i) during ischemia, has given new insight into the mechanisms producing these effects. In this review we consider the following topics in the light ofthese new measurements: (a) the