Time course of infarct growth toward the endocardium after coronary occlusion.
Transmembrane potentials and ultrastructure of subendocardial Purkinje and ventricular muscle fibers, isolated 1, 3, 5, 6, 14, and 24 h after coronary occlusion were investigated. Action potentials were recorded from progressively fewer layers of muscle cells as the age of the infarct increased. At 14 h little viable muscle remained. The decrease in the number of electrophysiologically viable muscle fibers correlated with structural evidence that the infarct moved with time toward the endocardial surface until only viable Purkinje fibers remained. Purkinje and surviving ventricular muscle fibers demonstrated a progressive decrease in resting potential, action potential amplitude, and Vmax and a progressive increase in action potential duration. Spontaneous diastolic depolarizations were found in Purkinje fibers only in 24-h infarcts and occasionally in cells deep to the endocardial surface, which may have been muscle cells. We hypothesize that during the first 24 h after coronary occlusion arrhythmias originate near the interface of infarcted and ischemic myocardium. As this interface moves toward the endocardium, this site of origin of arrhythmias moves with it until the Purkinje network is reached.
D000818:Animals; D004285:Dogs; D006321:Heart / Q000502:physiology; D006329:Heart Conduction System / Q000648:ultrastructure*; D008564:Membrane Potentials; D009203:Myocardial Infarction / Q000473:pathology*; D009206:Myocardium / Q000648:ultrastructure*; D010210:Papillary Muscles / Q000648:ultrastructure*; D011690:Purkinje Fibers / Q000648:ultrastructure*; D013997:Time Factors