Ivabradine reduces heart rate in stable angina and chronic HFrEF. Its mechanism of action, different from β-blockers, is:
- A Inhibition of the L-type calcium current in SA nodal cells, slowing phase 4 depolarization
- B Activation of inwardly rectifying K+ (IKACh) channels in SA node, hyperpolarizing the resting potential
- C Blockade of I(Kr) channels in SA node, prolonging the action potential duration
- D Selective blockade of I(f) (funny current / HCN channel) in the SA node, reducing spontaneous depolarization rate without affecting contractility or conduction velocity ✓
Explanation
Ivabradine selectively and dose-dependently inhibits the hyperpolarization-activated cyclic nucleotide–gated (HCN) channels carrying the I(f) 'funny' current in the SA node, which is the primary pacemaker current responsible for phase 4 (diastolic) depolarization. By reducing I(f), ivabradine slows the heart rate without negative inotropy, without affecting blood pressure, and without affecting AV nodal conduction or ventricular repolarization — pharmacodynamically distinct from β-blockers and calcium channel blockers. It is used in HFrEF patients who remain symptomatic on maximally tolerated β-blockers with HR ≥70 bpm (SHIFT trial) and in stable angina with contraindications to β-blockers.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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