Ivabradine reduces heart rate in chronic heart failure. Its mechanism is unique because:
- A It blocks beta-1 adrenoceptors selectively in the sinoatrial node
- B It prolongs the QT interval by blocking IKr potassium channels
- C It blocks the funny current (If) — hyperpolarization-activated cyclic nucleotide-gated channels — in sinoatrial node cells ✓
- D It inhibits L-type calcium channels in nodal tissue, reducing diastolic depolarization slope
Explanation
Ivabradine selectively blocks the If (funny current) channel — an HCN (hyperpolarization-activated cyclic nucleotide-gated) channel — in sinoatrial node pacemaker cells, slowing the rate of spontaneous depolarization without affecting contractility or blood pressure. Unlike beta-blockers, it does not reduce myocardial oxygen consumption beyond heart rate reduction, and unlike calcium channel blockers, it has no vasodilatory effect. It is used in heart failure (EF <35%) when beta-blockers are insufficient or not tolerated.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.