Ranolazine is an antianginal drug approved as add-on therapy when beta-blockers and nitrates are insufficient. Its mechanism is:
- A Partial fatty acid oxidation inhibitor shifting metabolism to glucose utilization
- B Direct mitochondrial K-ATP channel opener reducing cellular energy demand
- C Inhibition of late inward sodium current (late I-Na) reducing calcium overload in ischemic myocytes ✓
- D Selective sinus node If channel blocker reducing heart rate-related oxygen demand
Explanation
Ranolazine inhibits the late inward sodium current (late I-Na) that persists during myocardial ischemia. This prevents sodium overload which would otherwise drive the Na/Ca exchanger in reverse, causing cytosolic calcium accumulation, diastolic dysfunction, and angina. By reducing intracellular Na⁺ and consequently Ca²⁺ overload, ranolazine improves diastolic relaxation and reduces ischemic injury without significantly affecting heart rate or blood pressure.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.