Ivabradine improves survival and attenuates cardiac remodeling in isoproterenol-induced myocardial injury

Fundam Clin Pharmacol. 2021 Aug;35(4):744-748. doi: 10.1111/fcp.12620. Epub 2020 Nov 7.

Abstract

This study investigated whether ivabradine, a selective If current inhibitor reducing heart rate (HR), is able to improve survival and prevent left ventricular (LV) remodeling in isoproterenol-induced heart damage. Wistar rats were treated for 6 weeks: controls (n = 10), ivabradine (10 mg/kg/day orally; n = 10), isoproterenol (5 mg/kg/day intraperitoneally; n = 40), and isoproterenol plus ivabradine (n = 40). Isoproterenol increased mortality, induced hypertrophy of both ventricles and LV fibrotic rebuilding, and reduced systolic blood pressure (SBP). Ivabradine significantly increased survival rate (by 120%) and prolonged average survival time (by 20%). Furthermore, ivabradine reduced LV weight and hydroxyproline content in soluble and insoluble collagen fraction, reduced HR and attenuated SBP decline. We conclude that ivabradine improved survival in isoproterenol-damaged hearts.

Keywords: heart hypertrophy; isoproterenol; ivabradine; mortality; remodeling; survival.

MeSH terms

  • Animals
  • Cardiotonic Agents / administration & dosage
  • Cardiotonic Agents / pharmacology*
  • Disease Models, Animal
  • Heart Failure / drug therapy
  • Isoproterenol
  • Ivabradine / administration & dosage
  • Ivabradine / pharmacology*
  • Male
  • Myocardial Infarction / physiopathology*
  • Rats
  • Rats, Wistar
  • Ventricular Function, Left / drug effects*
  • Ventricular Remodeling / drug effects*

Substances

  • Cardiotonic Agents
  • Ivabradine
  • Isoproterenol