Ranolazine is used for refractory angina. Its novel antianginal mechanism involves:
- A Late sodium current (INa-L) inhibition, reducing intracellular sodium and calcium overload in ischemic cardiomyocytes ✓
- B L-type calcium channel blockade in coronary smooth muscle
- C Partial fatty acid oxidation (pFOX) inhibition to shift myocardial metabolism toward glucose
- D Beta1-selective adrenoreceptor blockade in the heart
Explanation
Ranolazine inhibits the late phase of the inward sodium current (late INa), which is abnormally prolonged in ischemic myocardium. This late INa causes intracellular sodium accumulation, which in turn via the Na+/Ca2+ exchanger increases intracellular calcium, contributing to diastolic dysfunction and arrhythmias. By blocking late INa, ranolazine reduces calcium overload, improves diastolic relaxation, and relieves angina without affecting heart rate or blood pressure. Option C (partial fatty acid oxidation inhibition) was the originally proposed mechanism but later shown to be secondary; option A is the primary established mechanism.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.