Author + information
- Received August 22, 1988
- Revision received April 26, 1989
- Accepted May 10, 1989
- Published online November 1, 1989.
- James B. Martins, MD∗,
- William Kim, MD and
- Melvin L. Marcus, MD, FACC
- ↵∗Address for reprints: James B. Martins, MD, Cardiovascular Division, The University of Iowa, Iowa City, Iowa 52242. USA
The purpose of this study was to investigate the electrophysiology of acute ischemia in hypertrophic as compared with nonhypertrophic myocardium. Left circumflex coronary artery occlusion was produced in anesthetized open chest dogs. Of 40 dogs studied, 22 were normotensive and 18 had chronic hypertension produced by a single kidney renal clamp procedure. Recordings of electrograms and extrastimulus testing were performed in endocardial and epicardial sites in both normal and ischemically damaged zones documented by triphenyltetrazolium chloride.
In the hypertrophy group, there was greater endocardial to epicardial conduction delay in ischemic zones, mean ± SEM 57 ± 4 ms versus 31 ± 2 ms in the normotensive group (p < 0.05). Also, sustained monomorphic ventricular tachycardia was inducible in seven of eight dogs with hypertrophy and in none of eight normotensive dogs surviving to 3 h. Entrainment and several observations during induction were consistent with reentrant ventricular tachycardia. To exclude hypertension alone as an etiology of tachycardia, five normotensive dogs without inducible monomorphic tachycardia remained unchanged during hypertension produced with low doses of phenylephrine or descending aortic occlusion.
Thus, the electrophysiologic response to ischemia is altered in hypertrophied myocardium, which predisposes to rapid sustained monomorphic ventricular tachycardia.
☆ This work was performed during the tenure of an Established Investigator Award of the American Heart Association, Dallas, Texas. In addition, the work was supported by Grant HL20827 from the National Institutes of Health, Bethesda, Maryland and by funds from the Veterans Administration Medical Center, Iowa City, Iowa and the Iowa Affiliate of the American Heart Association, Des Moines, Iowa.
- Received August 22, 1988.
- Revision received April 26, 1989.
- Accepted May 10, 1989.