Effects of ivabradine on endothelial function, aortic properties and ventricular-arterial coupling in chronic

Ivano Bonadei1, Edoardo Sciatti1, Enrico Vizzardi1

  • 1Cardiology Unit, University and ASST Spedali Civili, Brescia, Italy.

Cardiovascular Therapeutics
|February 21, 2018
PubMed

Insights

Ivabradine improves ventricular-arterial coupling (VAC), aortic stiffness, and endothelial function in chronic heart failure (CHF) patients. This heart failure treatment enhances cardiovascular health by optimizing heart rate control.

Area of Science:

  • Cardiology
  • Pharmacology
  • Vascular Medicine

Background:

  • Elevated heart rate (HR) is a significant prognostic indicator in chronic heart failure (CHF).
  • Ivabradine is known to reduce adverse cardiovascular events and improve cardiac remodeling in CHF patients.
  • The impact of ivabradine on ventricular-arterial coupling (VAC), aortic stiffness, and endothelial function requires further elucidation.

Purpose of the Study:

  • To evaluate the short-term effects of ivabradine on ventricular-arterial coupling (VAC).
  • To assess the impact of ivabradine on aortic stiffness and endothelial function in stable CHF patients.
  • To determine if ivabradine improves cardiovascular parameters beyond heart rate reduction in CHF.

Main Methods:

  • A cohort of 30 stable CHF patients (LVEF ≤ 35%, NYHA class II, HR ≥ 70 bpm) on optimized therapy were studied.
  • Transthoracic echocardiography assessed aortic elastic properties (aortic distensibility, aortic stiffness index, systolic aortic strain) and VAC.
  • Peripheral arterial tonometry measured endothelial function; ivabradine (5 mg bid) was added, with follow-up assessments after 4 months.

Main Results:

  • Baseline assessment revealed impaired VAC in 73% and endothelial dysfunction in 63% of patients.
  • After 4 months of ivabradine therapy, significant improvements were observed in VAC (P=.021), aortic elasticity parameters (P≤.033), and endothelial function (P<.001).
  • At follow-up, the prevalence of impaired VAC decreased to 40% (P=.018) and endothelial dysfunction to 33% (P=.038).

Conclusions:

  • Adding ivabradine to optimized medical therapy in CHF patients significantly improves endothelial function.
  • Ivabradine positively impacts aortic properties and ventricular-arterial coupling in this patient cohort.
  • These findings suggest that ivabradine offers multifaceted cardiovascular benefits in managing chronic heart failure.
Abstract

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