A patient with stable angina continues to have anginal episodes despite maximum beta-blocker therapy. Ivabradine is added. The molecular target of ivabradine is:

• A Voltage-gated L-type Ca2+ channels in cardiomyocytes and vascular smooth muscle
• B ATP-sensitive K+ (KATP) channels in ischemic myocardium
• C Beta-1 adrenergic receptors in the SA node and ventricular myocardium
• D HCN (hyperpolarization-activated cyclic nucleotide-gated) If channels in the SA node ✓

Explanation

Ivabradine is a selective inhibitor of the funny current (If) conducted through HCN channels in the SA node pacemaker cells. The If current is an inward mixed Na+/K+ current that activates upon hyperpolarization and is responsible for spontaneous diastolic depolarization (pacemaker potential). By blocking If, ivabradine slows the rate of diastolic depolarization, reducing heart rate without affecting myocardial contractility or blood pressure—unlike beta-blockers. Its rate-reducing effect is greater at higher heart rates (use-dependent block). It has no effect on ventricular conduction.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.