Cardiac electrophysiologic alterations were evaluated 1 to 8 months after partial supracoronary aortic constriction in cats. This procedure induced left ventricular systolic hypertension and hypertrophy with marked connective tissue infiltration. In situ, premature ventricular complexes were observed during or after vagal slowing of sinus rate in 8 (26%) of the 31 experimental animals, while an additional 3 of the 31 developed ventricular fibrillation. No arrhythmias were recorded in 31 normal or 7 sham-operated cats. In vitro, 29% of the left ventricular preparations from cats with pressure overload and 5% from control cats showed spontaneous ectopic activity. During stimulation at cycle lengths of 800 to 1,000 ms, multiple site impalements of subendocardial muscle cells within fibrotic regions revealed heterogeneous electrical abnormalities. These included short action potential duration, low amplitude action potentials generated from low resting potentials, split upstrokes and electrically silent areas. Impalements in nonfibrotic areas of the left ventricle showed prolongation of muscle action potential duration. Long-term disturbances in cellular electrophysiologic properties may favor the development of arrhythmias and thereby contribute to sudden cardiac death in left ventricular hypertension and hypertrophy.

SUMMARY. We studied the characteristics of an electrophysiological border zone detected after healing of experimental myocardial infarction in cats. Thirty-two isolated left ventricles were studied in tissue bath 2-7 months after distal left coronary artery ligation. Action potentials were recorded from endocardial ventricular muscle cells in normal, lateral border and central infarct zones. Action potential duration was prolonged in central infarct zone cells, while action potentials of lateral border zone cells had the shortest duration. Ventricular muscle cells in the border zone also had lower resting potential, action potential amplitude and V max . Slowly rising action potentials (V max < 20 V/ sec) were noted in central infarct zone cells, but more consistently in border zone cells. Functional refractory period of cells in central infarct zone was significantly longer than that recorded from border and normal zone cells. Post-repolarization refractoriness occurred in the majority of border zone cells. Failure of a border zone cell to respond to a premature stimulus during repetitive activity was observed in ten of the 22 preparations in which repetitive activity could be induced. Furthermore, when the coupling interval between driving and premature stimuli was shortened, border zone cells were first to fail to be excited by the premature stimulus. These data indicate that conduction was impaired in the border zone, whereas normal conduction was still possible in central infarct and normal areas. The electrophysiological abnormalities in the endocardial lateral border zone cells of the healed myocardial infarction appear to be the most severe, and the border zone may play an important role in chronic electrophysiological instability observed both in situ and in vitro (Circ Res 51: 486-193, 1982)

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SUMMARY. We studied the effects of a membrane-active antiarrhythmic agent, procainamide (PA), on cellular electrophysiological consequences of ischemic injury to cat ventricular muscle. The left ventricles of 90-to 120-minute acute myocardial infarctions (AMI) (n = 14), and 2-to 4-month healed myocardial infarctions (HMI) (n = 17), were studied by microelectrode techniques in isolated tissue bath. Control action potential duration at 90% repolarization (APD90) recorded from ventricular muscle cells in AMI areas were short (114 ± 4 msec) compared to recordings from cells in normal areas (136 ± 6 msec) (P < 0.001). In contrast, APD90 of cells surviving ischemia in HMI preparations were longer than normals (159 ± 5 vs. 140 ± 5 msec, P < 0.001). After 60 minutes of exposure to PA, the APD90 of all cells was prolonged, but the absolute and relative magnitudes of prolongation were greater in AMI cells (mean = +40 msec, +35%), than in HMI cells (mean = +19 msec, +13%), P < 0.001. The prolongation of APD90 of normal cells was intermediate. Local refractory period changes paralleled APD90 changes. In seven additional HMI preparations, sustained ventricular activity was induced by premature stimulation. APD90 of HMI cells prolonged less than APD90 of normal cells during exposure to PA in these preparations, and decreased differences of APD90 between normal and HMI cells was associated with loss of inducibility of sustained ventricular activity. The effect of tetrodotoxin (TTX) was compared to the effect of PA in four HMI preparations to determine whether impaired delivery of test substances caused only an apparent decreased responsiveness to PA in HMI zones. TTX caused nearly identical prolongations of conduction times in HMI zones and normal zones, whereas PA caused different effects on APD90 in the two zones. In conclusion, PA alters the time course of repolarization of AMI cells more than that of HMI cells, decreasing the dispersion of repolarization in a given AMI or HMI preparation. The decreased dispersion correlated with loss of ability to induce sustained ventricular activity. Finally, the decreased responsiveness of HMI cells to PA does not appear to be due to impaired delivery to cell membranes, but, rather, appears to be a membrane difference persisting in cells which have survived ischemic injury. (Circ Res 50: 386-393, 1982) IN STUDIES of experimental myocardial infarction in cats, we have observed that the cellular electrophysiological abnormalities resulting from acute ischemic injury (90-120 minutes) differ from those which persist long-term (2-4 months) after healing from acute injury (Myerburg et al., 1978; Myerburg et al., in press). Transmembrane action potentials recorded from endocardial cells overlying acute myocardial infarction areas had variable decreases in resting membrane potential, upstroke amplitude, and dV/dt m ax, and shortened action potential durations. In contrast, the majority of surviving endocardial ventricular muscle cells overlying healed myocardial infarction scars were charac...