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Time course of infarct growth toward the endocardium after coronary occlusion
Abstract:
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.
Insights
After coronary occlusion, arrhythmias originate at the infarct border. This origin shifts toward the endocardium over 24 hours, eventually reaching the Purkinje network.
Area of Science:
- Cardiovascular Physiology
- Cardiac Electrophysiology
- Myocardial Infarction Research
Background:
- Coronary occlusion leads to myocardial infarction, altering cardiac electrical activity.
- The progression and spatial dynamics of infarcts impact arrhythmogenesis.
Purpose of the Study:
- To investigate the electrophysiological and ultrastructural changes in cardiac fibers post-coronary occlusion.
- To determine the evolving site of origin for arrhythmias during myocardial infarction.
Main Methods:
- Isolated subendocardial Purkinje and ventricular muscle fibers were studied at various time points after coronary occlusion.
- Transmembrane potentials and action potentials were recorded.
- Ultrastructural analysis of infarct progression was performed.
Main Results:
- Electrophysiological viability of muscle fibers decreased with infarct age, correlating with infarct migration towards the endocardium.
- Purkinje and surviving ventricular fibers showed reduced resting potential, action potential amplitude, and Vmax, with increased action potential duration.
- Spontaneous diastolic depolarizations were observed in Purkinje fibers in 24-h infarcts.
Conclusions:
- Arrhythmias post-coronary occlusion likely originate at the interface between infarcted and ischemic myocardium.
- The site of arrhythmia origin shifts towards the endocardium over 24 hours, potentially involving the Purkinje network.