Author + information
- Received July 26, 1982
- Revision received November 10, 1982
- Accepted November 12, 1982
- Published online April 1, 1983.
- Joseph F. Spear, PhD, FACC*,
- Eric L. Michelson, MD, FACC and
- E. Neil Moore, DVM, PhD, FACC
- ↵*Address for reprints: Joseph F. Spear, PhD, University of Pennsylvania, Department of Animal Biology, 3800 Spruce Street, Philadelphia, Pennsylvania 19104.
Standard microelectrode techniques were used to record transmembrane potentials and determine conduction characteristics in regions of mottled infarcts of canine epicardium, 3 to 5 days or 8 to 15 days after left anterior descending coronary artery occlusion and reperfusion. At 3 to 5 days, resting potential, action potential amplitude, maximal rate of depolarization and action potential duration at 30% repolarization were significantly reduced in the infarcted region. Cells on the epicardial surface showed improvement in resting potential, action potential amplitude and rate of depolarization between 3 to 5 days and 8 to 15 days after infarction. In normal noninfarcted tissues, conduction velocity parallel to fiber orientation was 0.54 ± 0.06 m/s (mean ± standard deviation). Slow conduction in infarcted regions ranged from 0.015 to 0.2 m/s. Action potentials recorded from slowly conducting regions tended to include cells with more depressed amplitude and rate of depolarization than other cells in infarcted regions; they also had inappropriately depressed overshoot relative to their resting potential. Action potentials in slowly conducting areas where local conduction block occurred were associated with prepotentials and notches on their depolarization and repolarization phases. The prepotentials and notches appeared to be caused by electrotonic interactions resulting from microcircuitous conduction around or across inexcitable areas.
These findings demonstrate that areas of slow conduction are heterogenously distributed in the mottled infarct and suggest that disruptions in cell to cell electrical continuity and decreased excitability may contribute to this slow conduction.
This study was supported in part by Grants 5-RO1-HL19045-05, 1-RO1-HL28393-01, 5-RO1-HL25213-02, 2-ROl-HL28393, Clinical Investigatorship Award 5-KO8-HL00709 (Dr. Mich-elson) from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, and a grant from the W.W. Smith Charitable Trust, Philadelphia, Pennsylvania.
- Received July 26, 1982.
- Revision received November 10, 1982.
- Accepted November 12, 1982.
- American College of Cardiology Foundation