Review Article: Impact of Ivabradine on Cardiovascular Morbidity

Abstract

Heart failure is a complex clinical syndrome with a high incidence all over the world. Although various types of pharmacological and device therapies are available, the control of increased heart rate (HR) is critical. The bradycardic agent, ivabradine (IVA), has been displayed to reduce HR by inhibiting the funny current (If). The underlying mechanism states that ivabradine can enter the hyperpolarization-activated cyclic nucleotide-gated (HCN) channels and bind to the intracellular side, subsequently inhibiting the If. This phenomenon can prolong the slow spontaneous phase in the diastolic depolarization, and thus, reduce HR. Many epidemiological studies reported a strong independent association between elevated heart rate and major cardiovascular risk factors including atherosclerosis, ventricular arrhythmias, and left ventricular dysfunction. The heart rate reduction with IVA is beneficial in patients with coronary artery disease CAD, chronic stable angina pectoris, and chronic heart failure (CHF), with acceptable tolerance and safety profile. The pharmacodynamic and pharmacokinetic properties of this drug make it an important agent in the management of patients with CAD and HF. The aim of this short review is to explore recent results with IVA a new medication that lowers heart rate by selectively inhibiting the If current, and to describe others future potential applications.