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Related Concept Videos

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Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
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Updated: May 23, 2025

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
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Heart Rate Reduction Is Associated With Reverse Left Ventricular Remodeling and Mechanism-Specific Molecular

Natasha L Altman1, Edward A Gill1, Rami Kahwash2

  • 1Division of Cardiology (N.L.A., E.A.G., L.K.M., J.A.W., A.K.-F., W.A.M., I.A.C., E.R.J., D.S., S.L.E., M.R.G.T., S.L.G., L.M., T.A.M., P.M.B., D.P.K., M.R.B.), University of Colorado Anschutz Medical Campus, Aurora.

Circulation. Heart Failure
|March 7, 2025
PubMed
Summary

Lowering heart rate (HR) with ivabradine in nonischemic dilated cardiomyopathy significantly improves left ventricular ejection fraction (LVEF) and induces unique molecular changes. This HR reduction is crucial for reverse remodeling, especially when beta-blockers are insufficient.

Keywords:
cardiomyopathy, dilatedgene expressionheart failureheart rateivabradineneuregulin-1ventricular remodeling

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Area of Science:

  • Cardiovascular Medicine
  • Molecular Cardiology
  • Pharmacology

Background:

  • Heart rate (HR) influences heart failure outcomes through mechanisms potentially involving left ventricular remodeling.
  • The specific molecular phenotype associated with HR changes in human ventricular myocardium remains unclear.

Purpose of the Study:

  • To investigate the effects of HR lowering on left ventricular remodeling and gene expression in patients with nonischemic dilated cardiomyopathy.
  • To determine if inhibiting the HCN4 channel with ivabradine can induce reverse remodeling and alter the molecular phenotype.

Main Methods:

  • A randomized, double-blind study involving 22 patients with nonischemic dilated cardiomyopathy refractory to beta-blockade.
  • Patients received either ivabradine (HCN4 channel inhibitor) or placebo for 24 weeks, alongside beta-blockers.
  • Left ventricular ejection fraction (LVEF) was measured, and myocardial gene expression was analyzed from endomyocardial biopsies.

Main Results:

  • Patients with decreased HR (treated with ivabradine) showed a significant increase in LVEF (29.4% to 44.2%, P=0.0003).
  • The 'Unchanged HR' group (placebo or ivabradine) showed no significant LVEF improvement (26.6% to 29.2%, P=0.28).
  • Gene expression analysis revealed 151 differentially expressed genes in the decreased HR group, with unique cardioprotective profiles, distinct from beta-blocker response groups.

Conclusions:

  • HR lowering, achieved via HCN4 channel inhibition with ivabradine, is associated with substantial left ventricular reverse remodeling in nonischemic dilated cardiomyopathy.
  • Failure to lower HR can lead to nonresponse to beta-blocker therapy for reverse remodeling.
  • HR reduction through ivabradine induces a unique molecular signature in the myocardium, suggesting novel therapeutic pathways.