Ivabradine is used in heart failure patients in sinus rhythm with HR ≥70 bpm. Its mechanism — inhibition of the 'funny current' (If) — specifically targets which ion channel, and what property makes it rate-dependent in effect?
- A Voltage-gated sodium channels; faster inactivation at higher heart rates
- B L-type calcium channels; use-dependent block increasing with rate
- C HCN (hyperpolarization-activated cyclic nucleotide-gated) channels; drug enters the channel more at higher rates as more channels open ✓
- D IKr (hERG) channels; tachycardia-dependent block prolonging QT
Explanation
Ivabradine selectively inhibits the HCN (If) channel — the pacemaker 'funny current' — in sinoatrial node cells. It is rate-dependent because the drug enters the channel from the intracellular side only when the channel is in the open state (during hyperpolarization). At higher heart rates, channels spend more time open, allowing greater drug access — this is termed 'use-dependent' or 'open-channel block,' meaning ivabradine reduces heart rate more effectively at baseline tachycardia than at normal rates. This selectivity for SA node with no effect on myocardial contractility or conduction through the AV node distinguishes it from beta-blockers.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.