Ivabradine induces an increase in ventricular fibrillation threshold during acute myocardial ischemia: an experimental study

J Cardiovasc Pharmacol. 2008 Dec;52(6):548-54. doi: 10.1097/FJC.0b013e3181913df4.

Abstract

Background: Tachycardia often facilitates ischemic ventricular fibrillation (VF).

Objective: This study assessed the impact of ivabradine (IVA), a selective inhibitor of the cardiac pacemaker If current, on ventricular fibrillation threshold (VFT) during acute myocardial ischemia.

Methods: The experiments were conducted on a total of 54 domestic pigs. Myocardial ischemia was induced in anesthetized pigs by total 1-minute coronary occlusion at baseline and then on 2 occasions after intravenous administration of saline or 0.5 mg/kg of IVA. VF was triggered by electrical stimuli of increasing intensity at a fixed rate. Heart rate (HR), VFT, monophasic action potential duration, and peak of the time derivative of left ventricular pressure (LV dP/dt max) were monitored on each occasion. The activity of mitochondrial succinodehydrogenase was measured on heart sections.

Results: Compared with controls, IVA induced a 31% reduction in HR, a 2.9-fold increase in VFT, and prevented ischemia-induced monophasic action potential duration shortening (+1 +/- 12 vs. -14 +/- 11 milliseconds) without affecting peak LV dP/dt. This beneficial effect on VFT was mainly due to HR reduction and was accompanied by a significant reduction in the hypoxic area (26% +/- 1% vs. 38% +/- 1%, P < 0.0001).

Conclusion: HR reduction and the decrease in myocardial damage induced by IVA protected against primary ischemic VF without altering myocardial contractility.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Action Potentials
  • Acute Disease
  • Animals
  • Anti-Arrhythmia Agents / pharmacology*
  • Benzazepines / pharmacology*
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Female
  • Heart Conduction System / drug effects*
  • Heart Conduction System / physiopathology
  • Heart Rate / drug effects
  • Ivabradine
  • Male
  • Mitochondria, Heart / drug effects
  • Mitochondria, Heart / enzymology
  • Myocardial Ischemia / complications
  • Myocardial Ischemia / drug therapy*
  • Myocardial Ischemia / physiopathology
  • Succinate Dehydrogenase / metabolism
  • Sus scrofa
  • Time Factors
  • Ventricular Fibrillation / etiology
  • Ventricular Fibrillation / physiopathology
  • Ventricular Fibrillation / prevention & control*
  • Ventricular Function, Left / drug effects
  • Ventricular Pressure / drug effects

Substances

  • Anti-Arrhythmia Agents
  • Benzazepines
  • Ivabradine
  • Succinate Dehydrogenase