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Heart rate reduction with ivabradine prevents the global phenotype of left ventricular remodeling

Claudio Ceconi1, Laura Comini, Silvia Suffredini

  • 1Department of Cardiology, University of Ferrara, Ferrara, Italy. claudio.ceconi@unife.it

American Journal of Physiology. Heart and Circulatory Physiology
|October 19, 2010
PubMed

Insights

Ivabradine effectively reduced heart rate (HR) in rats post-myocardial infarction. This intervention improved left ventricular (LV) remodeling, cardiac metabolism, and electrophysiology, preventing adverse structural changes.

Area of Science:

  • Cardiology
  • Pharmacology
  • Physiology

Background:

  • Left ventricular (LV) remodeling is a significant consequence of myocardial infarction (MI).
  • Chronic heart rate (HR) elevation post-MI contributes to adverse LV remodeling.
  • Ivabradine is a selective HR-reducing agent that targets the hyperpolarization-activated current (If).

Purpose of the Study:

  • To investigate the effects of chronic HR reduction using ivabradine on LV remodeling in a rat model of MI.
  • To assess the impact of ivabradine on cardiac structure, function, metabolism, and electrophysiology following MI.

Main Methods:

  • Wistar rats underwent coronary artery ligation to induce MI.
  • Post-MI rats were treated with ivabradine or vehicle for 90 days.
  • Cardiac function (LV volumes, LVEF), plasma biomarkers (ANP), cardiac hydroxyproline, electrophysiology (patch-clamp), and energy metabolism were assessed.

Main Results:

  • Ivabradine significantly reduced HR by 12% in MI rats.
  • Ivabradine improved LV volumes and increased LVEF by 15%.
  • Reductions in plasma ANP and cardiac hydroxyproline were observed, alongside improved cardiac energy metabolism (creatine phosphate, ATP, energy charge).

Conclusions:

  • Chronic HR reduction with ivabradine prevents adverse LV remodeling post-MI in rats.
  • Ivabradine optimizes cardiac energy consumption and mitigates electrophysiological and structural remodeling.
  • HR is a key determinant of cardiac remodeling, and its modulation offers a therapeutic strategy.

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