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.
Specific inhibition of HCN channels slows rhythm differently in atria, ventricle and outflow tract and stabilizes conduction in the anoxic-reoxygenated embryonic heart model
