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The article by Nash¹ titled "The Case for Medical Treatment in Chronic Stable Coronary Artery Disease" in the December 12/26, 2005 issue of the ARCHIVES cited a mechanism for ranolazine that is not consistent with current data regarding the antianginal effects of ranolazine therapy.

Several mechanisms have been previously proposed.^2-3 Although ranolazine was shown to have partial fatty acid oxidase inhibitor activity in preclinical investigations,^2-3 it occurs at concentrations far above those achieved in recent clinical trials demonstrating therapeutic benefit and is probably not the primary mechanism for clinical efficacy.^3-5

Current research supports an alternative explanation of the mechanism: that ranolazine achieves its effect by improving dysfunctional sodium channels.

The proposed ranolazine mechanism of action is the inhibition of pathologic increases in late Na⁺ current induced during myocardial ischemia. Because of Na⁺/Ca²⁺ coupling, this would be expected to reduce ischemia-induced calcium overload, thereby improving related diastolic function (ie, . . . [Full Text of this Article]

AUTHOR INFORMATION
Celeste Marx, PharmD; Michael Sweeney, MD

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