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(Circulation. 1995;91:426-430.)
© 1995 American Heart Association, Inc.
Articles |
Effect of Left Ventricular Hypertrophy and Its Regression on Ventricular Electrophysiology and Vulnerability to Inducible Arrhythmia in the Feline Heart
Presented in part at the 13th Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology, May 1992, Chicago, Ill.
From the Cardiovascular Division, the Lankenau Hospital and Medical Research Center, Wynnewood, Pa, and Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pa.
Correspondence to Seth J. Rials MD, PhD, Lankenau Medical Office Building East, 100 Lancaster Ave, Suite 556, Wynnewood, PA 19096.
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.
Key Words: hypertrophy • arrhythmia • ventricles • electrophysiology
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