Ivabradine reduces heart rate in heart failure without affecting contractility because it selectively:
- A Blocks L-type calcium channels in sinoatrial node pacemaker cells
- B Activates cardiac M2 receptors, mimicking vagal bradycardia
- C Blocks beta-1 adrenergic receptors only in nodal tissue via tissue-selective distribution
- D Inhibits the 'funny current' (If) channels (HCN channels) in the sinoatrial node, slowing phase 4 spontaneous depolarization ✓
Explanation
Ivabradine inhibits the hyperpolarization-activated cyclic nucleotide-gated (HCN) channels responsible for the 'funny current' (If) in sinoatrial node cells. The If current is activated during hyperpolarization and carries Na+ and K+ inward during phase 4, controlling the slope of spontaneous depolarization that determines heart rate. By slowing phase 4, ivabradine reduces heart rate in a use-dependent manner (more effective at higher heart rates). It has no effect on myocardial contractility (L-type calcium channels, inotropy) or blood pressure, making it ideal for HFrEF patients with persistent tachycardia despite beta-blockers. SHIFT trial validated its mortality benefit.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.