Ranolazine is used as an add-on anti-anginal agent. Its mechanism of action that reduces myocardial oxygen demand without affecting heart rate or blood pressure is:

• A Selective blockade of L-type calcium channels in vascular smooth muscle
• B Inhibition of late inward sodium current (late INa), reducing intracellular calcium overload ✓
• C Opening of ATP-sensitive potassium channels in myocardium
• D Inhibition of fatty acid oxidation, shifting substrate utilization toward glucose

Explanation

Ranolazine selectively inhibits the late (persistent) inward sodium current (late INa) in cardiomyocytes. During ischemia, late INa becomes abnormally enhanced, causing intracellular sodium accumulation, which reverses the sodium-calcium exchanger (NCX) and leads to calcium overload, diastolic dysfunction, and increased wall tension. By reducing late INa, ranolazine prevents this cascade, improving diastolic function and reducing oxygen demand without hemodynamic effects — making it suitable for patients with bradycardia or hypotension. It also has a partial metabolic shift effect but this is secondary.

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

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