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Review Article

Pharmacology of Ivabradine and the Effect on Chronic Heart Failure

Author(s): Yue Zhou, Jian Wang, Zhuo Meng, Shuang Zhou, Jiayu Peng, Sun Chen, Qingjie Wang* and Kun Sun*

Volume 19, Issue 21, 2019

Page: [1878 - 1901] Pages: 24

DOI: 10.2174/1568026619666190809093144

Price: $65

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Abstract

Chronic Heart Failure (CHF) is a complex clinical syndrome with a high incidence worldwide. Although various types of pharmacological and device therapies are available for CHF, the prognosis is not ideal, for which, the control of increased Heart Rate (HR) is critical. Recently, a bradycardic agent, ivabradine, is found 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. The clinical trials demonstrated the significant effects of the drug on reducing HR and improving the symptoms of CHF with fewer adverse effects. This review primarily introduces the chemical features and pharmacological characteristics of ivabradine and the mechanism of treating CHF. Also, some expected therapeutic effects on different diseases were also concluded. However, ivabradine, as a typical If channel inhibitor, necessitates additional research to verify its pharmacological functions.

Keywords: Chronic heart failure, Funny current, If channel inhibitor, Ivabradine, Hyperpolarization-activated cyclic nucleotide- gated, Heart rate, Pharmacology.

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