Effect of Left Ventricular Hypertrophy and Its Regression on Ventricular Electrophysiology and Vulnerability to Inducible Arrhythmia in the Feline Heart
- 15 January 1995
- journal article
- Published by Wolters Kluwer Health in Circulation
- Vol. 91 (2) , 426-430
- https://doi.org/10.1161/01.cir.91.2.426
Abstract
Background Left ventricular hypertrophy (LVH) is associated with an increased risk of death, susceptibility to ventricular arrhythmia, and multiple electrophysiological abnormalities. The purpose of the present study was to determine whether the susceptibility to arrhythmia and electrical abnormalities persists after regression of hypertrophy in an animal model of LVH. Methods and Results We placed constricting bands on the ascending aorta of cats (n=9) or performed sham operations (n=9). Serial cardiac echocardiography was performed to measure left ventricular wall thickness. After LVH had developed in the banded animals, the constricting bands were removed and serial echocardiograms were used to monitor for regression of hypertrophy. Electrophysiological studies were performed in cats that showed regression of LVH (Regress, n=5), those that showed no change in LV wall thickness (No Regress, n=4), and in the sham-operated animals (Sham). Cats with persistent LVH had a higher incidence of inducible polymorphic ventricular tachycardia (4 of 4) compared with Regress (1 of 5) or Sham (1 of 9) cats (P<.05) and had lower ventricular fibrillation thresholds (9±2 mA) than Regress (17±4 mA) or Sham (16±3 mA) cats (P<.05). Persistent LVH in the No Regress group was associated with prolongation of epicardial monophasic action potential duration (MAPD) in the left but not the right ventricle. Dispersion of refractoriness was greater in the No Regress group (P<.05 versus Regress or Sham). Regress cats were identical to Sham cats in having a low incidence of inducible polymorphic ventricular arrhythmia, high fibrillation threshold, and MAPD measurements (P=NS versus Sham). Conclusions LVH produces multiple electrophysiological abnormalities and increased vulnerability to inducible polymorphic ventricular arrhythmia in this model of LVH. Cats that show regression of hypertrophy have normal ventricular electrophysiology and have the same low vulnerability to inducible ventricular arrhythmia as Sham animals.Keywords
This publication has 20 references indexed in Scilit:
- The ionic mechanism of reperfusion-induced early afterdepolarizations in feline left ventricular hypertrophy.Journal of Clinical Investigation, 1993
- Canine left ventricular hypertrophy predisposes to ventricular tachycardia induction by phase 2 early afterdepolarizations after administration of BAY K 8644Journal of the American College of Cardiology, 1992
- Effect of gallopamil on electrophysiologic abnormalities and ventricular arrhythmias associated with left ventricular hypertrophy in the feline heartAmerican Heart Journal, 1992
- Triggered Activity As a Possible Mechanism for Arrhythmias in Ventricular HypertrophyPacing and Clinical Electrophysiology, 1991
- Prognostic Implications of Echocardiographically Determined Left Ventricular Mass in the Framingham Heart StudyNew England Journal of Medicine, 1990
- Chronic hypertension and left ventricular hypertrophy facilitate induction of sustained ventricular tachycardia in dogs 3 hours after left circumflex coronary artery occlusionJournal of the American College of Cardiology, 1989
- Ventricular Arrhythmias in Patients with Hypertensive Left Ventricular HypertrophyNew England Journal of Medicine, 1987
- A prognostic comparison of asymptomatic left ventricular hypertrophy and unrecognized myocardial infarction: The Framingham studyAmerican Heart Journal, 1986
- Manipulation of ascending aortic pressure and flow wave reflections with the Valsalva maneuver: relationship to input impedance.Circulation, 1981
- Aortic input impedance in normal man: relationship to pressure wave forms.Circulation, 1980