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J Am Coll Cardiol, 2008; 51:415-426, doi:10.1016/j.jacc.2007.10.009 © 2008 by the American College of Cardiology Foundation |

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* Section of Cardiology and the Winters Center for Heart Failure Research, Department of Medicine, Baylor College of Medicine and The Texas Heart Institute at St. Lukes Episcopal Hospital, Houston, Texas
Houston Center for Quality of Care and Utilization Studies, Houston, Texas
Section of Cardiology, Michael E. DeBakey VA Medical Center, Houston, Texas.
Manuscript received July 2, 2007; revised manuscript received October 1, 2007, accepted October 2, 2007.
* Reprint requests and correspondence: Dr. Douglas L. Mann, Section of Cardiology, 1709 Dryden Road, BCM602, F.C. 9.83, Houston, Texas 77030. (Email: dmann{at}bcm.tmc.edu).
Over the past 2 decades our understanding of the pathologic mechanisms that lead to heart failure (HF) has evolved from simplistic hemodynamic models to more complex models that have implicated neurohormonal activation and adverse cardiac remodeling as important mechanisms of disease progression. 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have become a standard part of the armamentarium in the prevention and treatment of coronary artery disease. Apart from their lipid-lowering capabilities, statins seem to have non–lipid-lowering effects that impact neurohormonal activation and cardiac remodeling. This review will examine the potential benefits of statins in HF patients with ischemic and nonischemic cardiomyopathy as well as potential concerns regarding the use of statins in these patients.
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