Therapeutic Use and Molecular Aspects of Ivabradine in Cardiac Remodeling: A Review

Cardiac remodeling can cause ventricular dysfunction and progress to heart failure, a cardiovascular disease that claims many lives globally. Ivabradine, a funny channel (I-f) inhibitor, is used in patients with chronic heart failure as an adjunct to other heart failure medications. This review aims to gather updated information regarding the therapeutic use and mechanism of action of ivabradine in heart failure. The drug reduces elevated resting heart rate, which is linked to increased morbidity and mortality in patients with heart failure. Its use is associated with improved cardiac function, structure, and quality of life in the patients. Ivabradine exerts several pleiotropic effects, including an antiremodeling property, which are independent of its principal heart-rate-reducing effects. Its suppressive effects on cardiac remodeling have been demonstrated in animal models of cardiac remodeling and heart failure. It reduces myocardial fibrosis, apoptosis, inflammation, and oxidative stress as well as increases autophagy in the animals. It also modulates myocardial calcium homeostasis, neurohumoral systems, and energy metabolism. However, its role in improving heart failure remains unclear. Therefore, elucidating its molecular mechanisms is imperative and would aid in the design of future studies.

Automated summary

Cardiac remodeling can lead to ventricular dysfunction and progress to heart failure, a life-threatening cardiovascular disease. Ivabradine, an I-f inhibitor, is used as an adjunct to other heart failure medications in patients with chronic heart failure. This review aims to provide updated information on the therapeutic use and mechanism of action of ivabradine in heart failure. The drug reduces resting heart rate and has beneficial effects on cardiac function, structure, and quality of life, but its molecular mechanisms and role in improving heart failure are not yet fully understood.