CV's ranolazine shortens QT interval in LQT3

6 April 2008

USA-based CV Therapeutics' ranolazine significantly (p<0.001) shortened the QT interval of patients with a hereditary form of long QT syndrome called LQT3, which is caused by a genetic mutation in the late sodium channel and can be associated with heart rhythm problems, including sudden death. Ranolazine also shortened cardiac relaxation time in the study, data from which were presented at the American College of Cardiology's 57th Annual Scientific Session in Chicago.

In December 2007, the US Food and Drug Administration approved new language for the product labeling of Ranexa (ranolazine extended-release tablets) which describes the ability of the compound to inhibit the late sodium current at therapeutic levels. Published data on ranolazine's mechanism of action suggests that, during ischemic episodes, excess sodium can flow into cardiac cells through sodium channels, CV noted. This excess sodium can lead to calcium overload which, in turn, can result in impaired heart relaxation. Late sodium current inhibition has been shown to improve mechanical and electrical dysfunctions of cardiac cells under these circumstances.

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