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Cellular electrophysiological changes during ischemia in isolated, coronary-perfused cat ventricle with healed
S Kimura1, A L Bassett, J S Cameron
1Department of Medicine, University of Miami, School of Medicine, FL 33101.
Insights
Acute ischemia superimposed on healed myocardial infarction creates electrical differences in heart cells. These electrophysiological inhomogeneities in the infarcted heart may increase the risk of dangerous ventricular arrhythmias.
Area of Science:
- Cardiovascular Physiology
- Cardiac Electrophysiology
Background:
- Healed myocardial infarction (MI) can alter cardiac electrophysiology.
- The effects of superimposed acute ischemia on the electrophysiological properties of infarcted myocardium are not fully understood.
Purpose of the Study:
- To investigate the cellular electrophysiological consequences of acute ischemia in the setting of healed myocardial infarction.
- To compare electrophysiological changes in normal versus infarcted zones during acute ischemia.
Main Methods:
- Isolated, coronary-perfused cat left ventricles from animals with healed MI (2-4 months post-ligation) were used.
- Transmembrane action potentials were recorded from endocardial cells in normal and infarcted zones.
- Acute ischemia was induced by discontinuing coronary perfusion.
Main Results:
- Before ischemia, no significant electrophysiological differences were observed between normal and infarcted zones.
- During ischemia, normal zone cells showed reduced resting potential, action potential amplitude, and duration, with shortened refractory periods.
- Infarcted zone cells exhibited less prominent action potential changes and unchanged refractory periods, leading to significant electrophysiological inhomogeneities.
- Spontaneous rapid ventricular activity occurred in 4/8 preparations with healed MI during prolonged ischemia, but not in normal hearts.
Conclusions:
- Superimposed acute ischemia on healed myocardial infarction induces significant electrophysiological inhomogeneities between normal and infarcted zones.
- These inhomogeneities, particularly altered action potential duration and refractory periods, may serve as a substrate for enhanced arrhythmogenesis in post-MI hearts.
Abstract:
Cellular electrophysiological consequences of acute ischemia superimposed on healed myocardial infarction were studied in isolated, coronary-perfused cat left ventricles 2-4 months after ligation of multiple distal tributaries of the left anterior descending and circumflex coronary arteries. Oxygenated Tyrode's solution was perfused through the left anterior descending and circumflex coronary arteries, and the preparations were superfused with Tyrode's solution gassed with 95% N2-5% CO2. Transmembrane action potentials were recorded from the endocardial cells in normal and infarcted zones. There were no significant differences in measured action potential variables and refractory periods between cells in the normal and infarcted zones before acute ischemia. When coronary perfusion was discontinued ("ischemia"), resting potential, action potential amplitude, and action potential duration were reduced, and the refractory period was shortened progressively in cells of the normal zone. However, the action potential changes were less prominent, and the refractory period was unchanged in cells in the infarcted zone. As a result, there were significant differences in resting membrane potential, action potential amplitude, action potential duration, and refractory period between cells in the normal and infarcted zones at 10 minutes of ischemia. These differences became larger as the ischemic period was prolonged. Spontaneous rapid ventricular activity was observed during the last 20-30 minutes of ischemia in four of eight preparations with healed myocardial infarction, whereas no spontaneous rapid ventricular activity was recorded in any of six normal heart preparations. Our data suggest that superimposition of acute ischemia on healed myocardial infarction produces electrophysiological inhomogeneities that may enhance arrhythmogenesis.