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(Circulation. 1973;48:702.)
© 1973 American Heart Association, Inc.

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Slow Ventricular Activation in Acute Myocardial Infarction

A Source of Re-entrant Premature Ventricular Contractions

JOHN P. BOINEAU M.D.¹ JIMMY L. COX M.D.¹

¹ From the Departments of Medicine, Pediatrics, and Surgery, Duke University Medical Center, Durham, North Carolina.

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.

Key Words: Acute myocardial infarction • Ventricular fibrillation • Localized fibrillation • Ischemic heart disease • Prermature ventricular contractions • Sudden death • Re-entry Arrhythmias

Submitted on April 9, 1973
Accepted on June 5, 1973

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