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Ranexa for Treating Angina

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Updated November 12, 2011

Written or reviewed by a board-certified physician. See About.com's Medical Review Board.

Ranexa (ranolazine) is a relatively new drug, with a unique mechanism of action, used for the treatment of angina.

Originally it was believed that Ranexa caused the heart muscle to switch from using fatty acids to glucose for energy production, which would reduce the amount of oxygen the heart muscle needed to function. More recently, it appears that the principle effect of Ranexa is actually to block what is called the "late sodium channel" in heart cells, which are suffering from ischemia, or lack of oxygen associated with atherosclerosis, in the coronary arteries. Blocking this sodium channel improves the metabolism in ischemic heart cells, reducing damage to the heart muscle, and also reducing angina symptoms.

Ranexa has been shown to significantly improve the amount of time patients with stable angina are able to exercise before developing symptoms.

Initially, a chief concern about Ranexa was that it can prolong the "QT interval" on the ECG (a measurement of electrical activity within the heart) -- and some drugs that do that can increase the risk of developing dangerous heart arrhythmias. However, careful studies have shown this risk to be minimal or nonexistent with Ranexa. In fact, Ranexa now has been shown to actually reduce the risk of developing ventricular arrhythmias and atrial fibrillation.

The most common side effects of Ranexa have been headache, constipation and nausea.

Ranexa was originally recommended as a second or third choice drug in treating patients with angina, but in November, 2008 it was approved by the FDA as a first-line agent.

Sources:

Chaitman, BR. Ranolazine for the treatment of chronic angina and potential use in other cardiovascular conditions. Circulation 2006; 113:2462.

Morrow DA, Scirica BM, Karwatowska-Prokopczuk E, et al. Effects of ranolazine on recurrent cardiovascular events in patients with non-ST-elevation acute coronary syndromes. The MERLIN-TIMI 36 randomized trial. JAMA 2007; 297:1775-1783.

Belardinelli L, Shryock JC, Fraser H. The mechanism of ranolazine action to reduce ischemia-induced diastolic dysfunction. Eur Heart J Suppl (February 2006) 8 (suppl A): A10-A13. doi: 10.1093/eurheartj/sui091.

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