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Hyperpolarization-activated cyclic nucleotide-gated channel inhibitor in myocardial infarction: Potential benefits

Adivitch Sripusanapan1,2,3, Panat Yanpiset1,2,3, Sirawit Sriwichaiin1,2,3

  • 1Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.

Acta Physiologica (Oxford, England)
|January 17, 2024
PubMed

Insights

Ivabradine offers cardioprotection after myocardial infarction (MI) beyond just slowing heart rate. This review explores its mechanisms, including mitochondrial protection and improved autophagy, for treating heart failure survivors.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Molecular Biology

Background:

  • Myocardial infarction (MI) leads to cardiomyocyte loss, cardiac remodeling, and chronic heart failure, contributing significantly to global mortality.
  • Ivabradine, a heart rate-lowering drug, targets hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in cardiac pacemaker cells.
  • Ectopic expression of HCN channels in non-pacemaker cardiomyocytes post-MI suggests potential alternative roles for ivabradine.

Purpose of the Study:

  • To review and discuss the cardioprotective mechanisms of ivabradine in the context of myocardial infarction that are independent of heart rate reduction.
  • To explore the molecular pathways through which ivabradine exerts beneficial effects in post-MI hearts.

Main Methods:

  • Literature review of studies investigating ivabradine's effects in myocardial infarction models.
  • Analysis of research focusing on molecular mechanisms beyond heart rate modulation.
  • Synthesis of evidence regarding ivabradine's impact on cellular processes like mitochondrial function, autophagy, calcium cycling, electrophysiology, and matrix metalloproteinases.

Main Results:

  • Accumulating evidence suggests ivabradine possesses cardioprotective properties independent of its heart rate-lowering effect.
  • These effects include prevention of reactive oxygen species-induced mitochondrial damage, enhancement of the autophagy system, and modulation of intracellular calcium cycling.
  • Ivabradine also modifies ventricular electrophysiology and regulates matrix metalloproteinases, contributing to its protective role post-MI.

Conclusions:

  • Ivabradine demonstrates significant cardioprotective potential in myocardial infarction through multiple molecular mechanisms.
  • These non-heart rate-lowering effects offer novel therapeutic strategies for managing heart failure following MI.
  • Further research into these mechanisms could optimize ivabradine's clinical application in cardiovascular disease.

Keywords:
cardiac electrophysiologyischemiaivabradinemyocardial infarctionreperfusion

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