Electrophysiological effects of left ventricular hypertrophy. Effect of calcium and potassium channel blockade

P R Kowey1, T D Friechling, J Sewter

  • 1Cardiovascular Research Laboratory, Medical College of Pennsylvania, Philadelphia.

Circulation
|June 1, 1991
PubMed

Insights

Left ventricular hypertrophy (LVH) increases vulnerability to ventricular fibrillation by altering electrical recovery. Blocking potassium channels, but not calcium channels, protects against this arrhythmia.

Area of Science:

  • Cardiology
  • Electrophysiology
  • Pharmacology

Background:

  • Left ventricular hypertrophy (LVH) can lead to cardiac arrhythmias.
  • The arrhythmogenic effects of LVH require detailed electrophysiological investigation.

Purpose of the Study:

  • To define the arrhythmogenic effects of LVH in an intact heart model.
  • To assess the impact of calcium and potassium channel blockade on LVH-induced arrhythmias.

Main Methods:

  • Electrophysiological assessment in a feline aortic-banding model of LVH.
  • Measurement of conduction times, excitability, refractoriness, and action potential duration.
  • Evaluation of ventricular fibrillation (VF) vulnerability and thresholds.

Main Results:

  • LVH cats exhibited increased vulnerability to VF, spontaneous VF, and lower VF thresholds compared to controls.
  • LVH caused greater dispersion of effective refractory period and action potential duration.
  • Risotilide (potassium channel blocker) reduced dispersion and ventricular vulnerability; verapamil (calcium channel blocker) had no significant effect.

Conclusions:

  • LVH significantly increases ventricular vulnerability to fibrillation by promoting dispersion of refractoriness and repolarization.
  • Voltage-dependent potassium channel blockade mitigates LVH-induced arrhythmogenesis.
  • Slow inward calcium channel blockade does not protect against LVH-related ventricular fibrillation.
Abstract

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