Key result
Ivabradine administration in a rat model of heart failure dose-dependently reduced heart rate and improved intrinsic myocardial function.
Why the study?
Does ivabradine improve cardiac function in a rat model of heart failure?
Does ivabradine improve cardiac function in a rat model of heart failure?
Answers are grounded in this paper and cite their sources.
In a rat model of heart failure, pure heart rate reduction with ivabradine improves intrinsic myocardial function, suggesting a beneficial effect of heart rate slowing on cardiac remodeling.
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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Mulder et al. (2006) studied Heart failure. Ivabradine was evaluated on Heart rate and cardiac function. Ivabradine administration in a rat model of heart failure dose-dependently reduced heart rate and improved intrinsic myocardial function.
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