Author + information
- Received April 13, 1987
- Revision received July 15, 1987
- Accepted August 5, 1987
- Published online February 1, 1988.
- John M. Herre, MD, FACC∗∗,
- Lewis Wetstein, MD, FACC†,
- Yuh-Lin Lin, MD†,
- A.Scott Mills, MD‡,§,
- Michael Dae, MD∗ and
- Marc D. Thames, MD, FACC§
- ↵∗Address for reprints: John M. Herre, MD, University of California, Room 312M, San Francisco, California 94143-0214.
Transmural myocardial infarction interrupts sympathetic nerves and denervates viable muscle distal to myocardial infarction. The effect of sympathetic stimulation on responses to programmed ventricular stimulation was studied in dogs without myocardial infarction (Group I: n = 5), with transmural anterior wall myocardial infarction (Group II: n = 6) and with nontransmural anterior wall myocardial infarction (Group III: n = 9). Ventricular effective refractory period during sympathetic stimulation decreased by 16 ± 18, 1 ± 2 and 12 ± 8 ms (mean ± SD) in viable muscle of the inferoapical left ventricle in Groups I, II and III, respectively, suggesting efferent sympathetic denervation by transmural myocardial infarction only. Sustained ventricular tachycardia or fibrillation was induced more easily during sympathetic stimulation in six of the six dogs with transmural infarction, but in only two of the nine dogs with nontransmural infarction (p < 0.01).
It is concluded that the partial sympathetic denervation produced by transmural myocardial Infarction enhances the ease of induction of ventricular tachycardia and fibrillation during sympathetic stimulation. A similar mechanism may lead to increased risk for lethal arrhythmias during periods of high sympathetic tone in patients with transmural myocardial infarction.
☆ This study was supported by grants from the Veterans Administration, Washington, D.C., Grants HL30506 and HL34515 from the National Heart, Lung, and Blood Institute National Institutes of Health, Bethesda, Maryland and by a grant from the Academic Senats, University of California, San Francisco, California. This work was presented in part at the 35th Annual Scientific Session of the American College of Cardiology, Atlanta, Georgia, March 1986.
- Received April 13, 1987.
- Revision received July 15, 1987.
- Accepted August 5, 1987.