Circulation Research · 1975 · 194 citations · 2 references
MedicineCardiologyPhysiologyElectrophysiologyInterventional CardiologyNeurophysiologyAction PotentialsCardiac Action PotentialsCardiac AnatomyCardiac PhysiologyCardiovascular PathophysiologyVentricular ElectrophysiologyElectrophysiological FindingsIschemia-induced Action Potential ChangesPurkinje Fiber Action PotentialsPurkinje Fiber ElectrophysiologyPurkinje FibersUltrastructural AlterationsVentricular Action PotentialsVentricular Depolarization
The electrophysiological properties of subendocardial Purkinje fibers surviving in myocardial infarcts were studied with intracellular microelectrodes in isolated superfused preparations and correlated with subsequent light and electron microscopic studies. Transmembrane action potentials could always be recorded from one or two cell layers of subendocardial Purkinje fibers in infarcted regions 3 days to 7 weeks after coronary artery occlusion; ventricular muscle action potentials were rarely found. Microscopic studies also demonstrated several layers of intact subendocardial Purkinje fibers; the subjacent ventricular muscle cells were irreversibly injured and replaced by scar. At all time intervals, surviving Purkinje fibers had significantly reduced maximum diastolic potentials, action potential amplitudes, and depolarization velocities as well as prolonged action potential durations. These parameters normalized between 24 hours and 7 weeks after coronary artery occlusion. Surviving Purkinje fibers with electrophysiological abnormalities at 24 hours and 3 days contained vast lipid deposits. Lipid was less prevalent at 10 days when action potential characteristics had improved. By 7 weeks, action potentials were nearly normal and lipid was absent. Subendocardial Purkinje fibers surviving in infarcts are subject to conditions which cause electrophysiological and ultrastructural abnormalities. Persistent abnormalities in the electrophysiological properties of these surviving Purkinje fibers may cause persistent altered electrophysiological properties of the infarcted heart.
2
A METABOLIC CAUSE FOR ARRHYTHMIAS DURING ACUTE MYOCARDIAL HYPOXIA
V.A. Kurien · The Lancet · 1970 · 212 citations
Medicine, Cardiology, Physiology +10