Abstract
Arrhythmias associated with reperfusion of ischemic myocardium may be a major progenitor for sudden cardiac death in man. The electrophysiological basis for arrhythmias associated with reperfusion appears to be heterogeneous electrical recovery, but the precise alterations responsible for malignant versus nonmalignant arrhythmias are unknown. In experimental animals, the highest incidence of malignant arrhythmias after reperfusion occurs after 20 to 30 min of preceding ischemia, a critical time period in which both reversibly and irreversibly injured cells are present, with reperfusion resulting in maximal heterogeneity of recovery of electrical parameters. Although changes in K+, PCO2, and intracellular Ca2+ may be critical in arrhythmogenesis during reperfusion, direct cause-and-effect relationships have not been established. Increases in both alpha-adrenergic responsivity and the density of alpha 1-adrenergic receptors appear to mediate important influences on these malignant arrhythmias, including changes in intracellular calcium. Recent findings also suggest that the accumulation of lysophosphatides in ischemic myocardium may be the responsible moiety for the increase in alpha 1-adrenergic receptors.
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