Abstract
Ranolazine, an inhibitor of the late current of the cardiac action potential (late INa), is a well established clinical treatment for chronic angina. The late INa in cardiac myocytes also plays an important role in the pathophysiology of acute myocardial ischemia and reperfusion, and thus is a potential therapeutic target to ameliorate consequences of myocardial infarction. In experimental animal models, ranolazine has been shown to reduce myocardial infarct size, improve left ventricular function, decrease ischemia/reperfusion-induced arrhythmias and improve outcome in heart failure. Here we focus specifically on data from in vivo animal studies of myocardial ischemia and reperfusion.
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Acknowledgements
RAK has previously been a speaker for and consultant to CV Therapeutics, Inc. and Gilead, Inc. These two companies have provided research support for some of the studies.
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Hale, S.L., Kloner, R.A. Ranolazine Treatment for Myocardial Infarction? Effects on the Development of Necrosis, Left Ventricular Function and Arrhythmias in Experimental Models. Cardiovasc Drugs Ther 28, 469–475 (2014). https://doi.org/10.1007/s10557-014-6548-3
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DOI: https://doi.org/10.1007/s10557-014-6548-3