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Editor's Correspondence |

Mechanism of Action of Ranolazine—Reply

David Nash, MD
Arch Intern Med. 2006;166(12):1325-1326. doi:10.1001/archinte.166.12.1326-a.
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I wish to thank Graboys and Lown for their supportive letter. I regret that I overlooked their original publication on the topic of medical therapy of myocardial ischemia from 1981. Their remarks in relation to their recent data are also supportive of my original thesis of the benefits of medical therapy. I especially agree with their comment that costly invasive procedures are often performed without proven mortality benefit. While there have been improvements in angioplasty techniques and results, the medical therapies are also advancing even as we discuss the pros and cons. Drugs to raise high-density lipoprotein cholesterol levels, therapy to provide ApoA-I Milano, and other therapies are in active investigation. The future of medical therapy for chronic stable angina appears bright, and it is an approach whose time has come. The letter of Marx and Sweeny is also appreciated. As they note, current research supports the concept that ranolazine achieves its effect by improving dysfunctional sodium channels, and therapeutic benefit is supported by the clinical trials listed in their letter. The antianginal and anti-ischemic effects of ranolazine therapy are achieved without significant hemodynamic effects. This is yet another example of how medical therapies are continuing to advance for treatment of chronic stable angina.

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