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Updated: Jul 20, 2026

A Pacing-Controlled Procedure for the Assessment of Heart Rate-Dependent Diastolic Functions in Murine Heart Failure Models
Published on: July 21, 2023
Heart rate slowing for myocardial dysfunction/heart failure
Paul Mulder1, Christian Thuillez
1INSERM U644, Faculté de Médecine et de Pharmacie, Rouen, France.
Insights
Reducing heart rate in heart failure patients using ivabradine improved cardiac function. This effect persisted after treatment withdrawal, suggesting intrinsic myocardial improvements from pure heart rate reduction.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Heart failure prevalence is increasing, with elevated heart rate contributing to cardiac dysfunction.
- The impact of isolated heart rate reduction on heart failure progression remains unclear.
Purpose of the Study:
- To investigate the effects of pure heart rate reduction on cardiac function in a rat model of heart failure.
- To determine if chronic heart rate reduction improves intrinsic myocardial function.
Main Methods:
- Utilized a rat model of heart failure.
- Administered ivabradine, an I(f) channel blocker, to reduce heart rate without altering blood pressure.
- Evaluated cardiac function and myocardial tissue characteristics after chronic ivabradine treatment.
Main Results:
- Ivabradine dose-dependently reduced heart rate, improving cardiac function.
- Improved cardiac function persisted after ivabradine withdrawal, indicating enhanced intrinsic myocardial function.
- Potential mechanisms include improved oxygen supply-demand ratio and reduced myocardial collagen accumulation.
Conclusions:
- Pure, chronic heart rate reduction can be beneficial in managing heart failure.
- Ivabradine's effects suggest a therapeutic potential for isolated heart rate lowering in heart failure.
Abstract:
Heart failure is a major health problem, and is one of the few cardiovascular diseases that increased its prevalence over the last decade. Increased heart rate, generally observed in patients with heart failure, is involved in the deterioration of cardiac pump function. However, the effects of 'pure' heart rate reduction on the progression of heart failure are unknown. In a rat model of heart failure, ivabradine, a blocker of I(f) channels reduces dose-dependently heart rate without modification of blood pressure. This heart rate reduction is associated with an improvement in cardiac function. After chronic administration, this improvement of cardiac function persists after ivabradine withdrawal, revealing an improvement in intrinsic myocardial function. This beneficial effect could be explained by direct effects of heart rate reduction induced by ivabradine, i.e. improved myocardial oxygen supply to demand ratio, and/or myocardial tissular effects induced by chronic decrease in heart rate such, i.e. decreased extracellular collagen accumulation, increased myocardial microcirculation. In conclusion, 'pure' chronic heart rate reduction can be beneficial in heart failure.
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