Author + information
- Received December 12, 1988
- Revision received March 22, 1989
- Accepted June 7, 1989
- Published online November 15, 1989.
- Marshall S. Stanton, MD,
- Mahmoud M. Tuli, MD,
- Nancy L. Radtke, MD,
- James J. Heger, MD, FACC,
- William M. Miles, MD, FACC,
- Bruce H. Mock, PhD,
- Robert W. Burt, MD,
- Henry N. Wellman, MD and
- Douglas P. Zipes, MD, FACC∗
- ↵∗Address for reprints: Douglas P. Zipes, MD, Indiana University School of Medicine, Krannert Institute of Cardiology, 1001 West 10th Street, Indianapolis, Indiana 46202.
Transmural myocardial infarction in dogs produces denervation of sympathetic nerves in viable myocardium apical to the infarct that may be arrhythmogenic. It is unknown whether sympathetic denervation occurs in humans. The purpose of this study was to use iodine- 123-metaiodobenzylguanidine (MIBG), a radiolabeled guanethidine analog that is actively taken up by sympathetic nerve terminals, to image noninvasively the cardiac sympathetic nerves in patients with and without ventricular arrhythmias after myocardial infarction.
Results showed that 10 of 12 patients with spontaneous ventricular tachyarrhythmias after myocardial infarction exhibited regions of thallium-201 uptake indicating viable perfused myocardium, with no MIBG uptake. Such a finding is consistent with sympathetic denervation. One patient had frequent episodes of nonsustained ventricular tachycardia induced at exercise testing that was eliminated by beta-adrenoceptor blockade. Eleven of the 12 patients had ventricular tachycardia induced at electrophysiologic study and metoprolol never prevented induction. Sympathetic denervation was also detected in two of seven postinfarction patients without ventricular arrhythmias. Normal control subjects had no regions lacking MIBG uptake.
This study provides evidence that regional sympathetic denervation occurs in humans after myocardial infarction and can be detected noninvasively by comparing MIBG and thallium-201 images. Although the presence of sympathetic denervation may be related to the onset of spontaneous ventricular tachyarrhythmias in some patients, it does not appear to be related to sustained ventricular tachycardia induced at electrophysiologic study.
☆ This study was supported in part by the Herman C. Krannert Fund, Indianapolis; by Grants HL-06308 and HL-07182 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; and the American Heart Association, Indiana Affiliate, Inc., Indianapolis.
- Received December 12, 1988.
- Revision received March 22, 1989.
- Accepted June 7, 1989.