Ivabradine is added to therapy in a 70-year-old patient with stable heart failure (LVEF 30%) who is already on maximum-dose carvedilol. The unique electrophysiological mechanism of ivabradine that distinguishes it from beta-blockers is:
- A It inhibits the funny current (If, HCN channels) in the SA node, selectively reducing heart rate without affecting contractility or AV conduction ✓
- B It blocks L-type calcium channels in the sinoatrial node, reducing the rate of depolarisation
- C It prolongs the action potential duration by blocking the delayed rectifier potassium current
- D It activates M2 muscarinic receptors on the SA node, mimicking enhanced vagal tone
Explanation
Ivabradine selectively inhibits the hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels responsible for the funny current (If) in the sinoatrial node. This current governs the slope of spontaneous diastolic depolarisation in pacemaker cells. Ivabradine reduces heart rate in a rate-dependent manner without affecting myocardial contractility, blood pressure, or AV/ventricular conduction — making it suitable as an add-on when heart rate remains >70 bpm despite maximised beta-blockade. L-type calcium channel blockade characterises verapamil, not ivabradine.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.