Ranolazine exerts anti-anginal effects without significant hemodynamic changes. Its primary mechanism targets which ion channel abnormality in ischemic myocardium?

• A T-type calcium channel blockade in coronary arterial smooth muscle
• B IKr (hERG) channel activation prolonging repolarization and reducing calcium entry
• C KATP channel opening causing coronary vasodilation without systemic vasodilation
• D Late inward sodium current (late INa) inhibition, reducing sodium and calcium overload in ischemic myocytes ✓

Explanation

In myocardial ischemia, the normally brief late inward sodium current (late INa) becomes pathologically prolonged, causing intracellular Na+ accumulation. This triggers reverse-mode Na+/Ca2+ exchange, leading to calcium overload, impaired relaxation, increased wall tension, and oxygen demand. Ranolazine selectively inhibits the late INa (without significantly affecting the peak INa or standard cardiac channels at therapeutic concentrations), reducing sodium and secondary calcium overload. It improves diastolic function and reduces ischemia without affecting heart rate or blood pressure — making it suitable as add-on therapy when beta-blockers, nitrates, or CCBs are insufficient.

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

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