Author/Authors :
Kumudha Ramasubbu، نويسنده , , Jerry Estep، نويسنده , , Donna L. White، نويسنده , , Anita Deswal، نويسنده , , Douglas L. Mann، نويسنده ,
Abstract :
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.
Keywords :
CI , nitric oxide , heart failure , Left ventricular , HMG-CoA , Confidence interval , Hazard ratio , NO , endothelial nitric oxide synthase , EPC , Hf , NADPH , LV , NYHA , New York Heart Association , HR , LVEF , left ventricular ejection fraction , eNOS , LVEDD , endothelial progenitor cell , left ventricular end-diastolic dimension , nicotinamide adenine dinucleotide phosphate , 3-hydroxy-3-methylglutaryl coenzyme A , CoQ10 , coenzyme Q10 , PI3K/Akt , phosphatidylinositol-3 kinase-Akt