Coronary artery occlusion in dogs caused desynchronization and slowing of ventricular activation, creating local areas of sustained excitation (up to 215 msec) that functioned as sources for PVCs.
The evolution of premature ventricular contractions (PVCs) in acute myocardial infarction was studied by recording bipolar potentials from the left ventricle before and after coronary artery occlusion in dogs. The potentials were recorded from 154 locations in the left ventricular wall as well as at the endocardial and epicardial surfaces. Desynchronization and marked slowing of previously uniform activation was noted and resembled abbreviated, local fibrillation. The dissociation of excitation was either simple, characterized by fragmentation into single delayed spikes, or complex, characterized by numerous spikes. Sustained, desynchronized activity, confined to local myocardial areas, was observed up to 215 msec after the onset of activation. These local areas of sustained excitation functioned as a source of re-entrant activity and were associated with PVCs. Histochemical stains of myocardium indicated a relationship between the inhomogeneous distribution of ischemia (stain) and the desynchronization of the electrical activity.
Boineau et al. (Mon,) conducted a other in Acute myocardial infarction. Coronary artery occlusion vs. Baseline (before occlusion) was evaluated on Evolution of premature ventricular contractions and ventricular activation potentials. Coronary artery occlusion in dogs caused desynchronization and slowing of ventricular activation, creating local areas of sustained excitation (up to 215 msec) that functioned as sources for PVCs.
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