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Updated: Feb 12, 2026

Author Spotlight: Investigating HR-Dependent Cardiac Function in Mouse Models Through a Novel Atrial-Pacing Approach
Published on: July 21, 2023
Novel drugs for heart rate control in heart failure
Agata Bielecka-Dabrowa1, Stephan von Haehling2, Jacek Rysz3
1Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Zeromskiego 113, 90-549, Lodz, Poland. agatbiel7@poczta.onet.pl.
Insights
Ivabradine effectively lowers heart rate in heart failure patients, improving outcomes in some trials. However, its benefit in heart failure with preserved ejection fraction (HFpEF) remains uncertain, necessitating further research.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Increased sympathetic activity and elevated heart rate (HR) are linked to poor cardiovascular outcomes, especially in heart failure (HF).
- Ivabradine selectively reduces HR without impacting myocardial contractility, blood pressure, or cardiac conduction.
Purpose of the Study:
- To evaluate the efficacy of ivabradine in improving cardiovascular outcomes in patients with heart failure.
- To investigate the role of HR reduction with ivabradine in heart failure with preserved ejection fraction (HFpEF).
Main Methods:
- Review of clinical trials (BEAUTIFUL, CARVIVA HF, SHIFT, INTENSIFY) in systolic heart failure.
- Analysis of a diabetes mouse model of HFpEF.
- Examination of the EDIFY trial results for HFpEF patients.
Main Results:
- Ivabradine demonstrated positive outcomes in prior trials for systolic dysfunction.
- A meta-analysis showed neutral results.
- In a HFpEF mouse model, ivabradine improved cardiac function and vascular stiffness.
- The EDIFY trial did not support ivabradine use in HFpEF patients.
Conclusions:
- While ivabradine shows promise for certain heart failure populations, its benefit in HFpEF is not established.
- Further clinical trials are warranted to clarify the role of ivabradine in diverse heart failure phenotypes.
Abstract:
In patients with heart failure, increased sympathetic activity is associated with a positive chronotropic stimulation leading to accelerated resting heart rate. Elevated heart rate (HR) is a risk factor for cardiovascular events, both in the general population and in patients with heart failure. Ivabradine is a pure HR-lowering agent, and it does not affect myocardial contractility, blood pressure, intracardiac conduction, or ventricular repolarization. In clinical trials such as BEAUTIFUL, CARVIVA HF, SHIFT, and INTENSIFY in patients with systolic left ventricular dysfunction, heart rate reduction with ivabradine brought positive outcomes. However, the results of the recent meta-analysis are rather neutral. In a diabetes mouse model of heart failure with preserved ejection fraction (HFpEF), selective heart rate reduction by If inhibition improved vascular stiffness, left ventricular (LV) contractility, and diastolic function. However, EDIFY (Effect of ivabradine in patients with heart rate with preserved ejection fraction) trial show that the use of ivabradine in patients with HFpEF is not supported. The further clinical trials investigating the use of ivabradine in heart failure should be carried out.
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