Electrophysiologic consequences of experimental acute ischemia superimposed on healed myocardial infarction in cats

Abstract

Electrophysiologic studies were carried out in 61 cats studied 2 to 4 months after healing of experimental myocardial infarction, 38 cats studied 90 to 120 minutes after an acute myocardial infarction, and 24 cats in which acute myocardial infarction was superimposed on a 2 to 4 month old healed myocardial infarction (AMI/HMI). The frequency and grade of spontaneous arrhythmias, and the ability to induce sustained ventricular activity in tissue bath, were similar in the cats with acute and those with healed myocardial infarction, but greater in those with acute infarction superimposed on healed infarction. Spontaneous ventricular arrhythmias occurred in 42 percent of the cats with acute infarction, in 31 percent of those with healed infarction, and 62 percent of those with acute infarction superimposed on healed infarction. Similarly, sustained ventricular activity initiated by premature stimuli in tissue bath was achieved in 67 percent of the isolated hearts with acute infarction superimposed on healed infarction compared with 34 percent of the hearts with acute and 33 percent of those with healed infarction. The correlation between spontaneous arrhythmias and inducibility of sustained ventricular activity in tissue bath was significant in all three groups, but attained the highest level of significance in the hearts with healed infarction and those with healed and superimposed infarction. The duration of transmembrane action potentials at 90 percent repolarization (APD 90), recorded from surviving cells overlying an acute infarct, was shorter than that of those recorded from normal cells in the same heart. In contrast, APD 90 values recorded from surviving cells overlying areas of healed infarction were longer than APD 90 values of normal cells. Refractory periods tended to parallel action potential durations, particularly in hearts with healed or healed with superimposed acute infarction. The greatest degree of dispersion of action potential duration and refractory periods was observed in the latter hearts, which also had the greatest incidence of spontaneous arrhythmias and of inducibility of sustained ventricular activity in tissue bath. It is concluded that healing of surviving cells after myocardial infarction leaves in its wake long-term electrophysiologic cell abnormalities. These may interact with a new acute ischemic event to cause greater electrophysiologic instability than observed with acute infarction in the absence of previously injured tissue.