Chronic hypertension and left ventricular hypertrophy facilitate induction of sustained ventricular tachycardia in dogs 3 hours after left circumflex coronary artery occlusion
JB Martins,
W Kim,
and
ML Marcus
Department of Internal Medicine, University of Iowa Hospitals, Iowa City.
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 less than 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.
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