Preventive effects of statin therapy in coronary artery diseases: Current controversy

Abstract

S tatins inhibit hepatic biosynthesis of cholesterol where they prevent mevalonate formation, and inhibit 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) (1-2). Through the last decades, research targets the protective cardiovascular effects of statins (3-4). Statins have desired roles preventing primary and secondary all-cause death and major cardiovascular events of coronary artery disease (CAD) (5). Protecting against atherosclerotic cardiovascular disease, statin therapy is effective with modification of risk factors (6).The favorable pleiotropic effects occur through increasing expression of atheroprotection genes, inhibiting inflammatory markers, protecting endothelium, enhancing plaques stability, inhibiting platelets aggregation, increasing nitric oxide bioavailability, decreasing circulating oxidative stress and inflammatory biomarkers, and inhibiting thrombogenesis (2,7).Variable recommendations of statins in high-risk CAD patients exist. Many guidelines recommend low-density lipoprotein-cholesterol (LDL-C) goal at 70 mg/dl (8-9), but the guideline of American College of Cardiology/ American Heart Association (ACC/AHA) supports high-intensity statins and repeated lipid measures (10).A debate exists about prescribing patterns, eligible patients, high-intensity doses (11-13), combined lipid-lowering therapy, improved outcomes following coronary surgery or intervention (14-15). Therefore, our review of the contemporary literature concerns contemporary status and debates of statin therapy in CAD patients. Our methods of constituting this narrative review include searching MEDLINE with a limit of publication dates between January and December 2017, using search terms of (statins) and (coronary artery disease) which yield 319 trials, of which 104 studies were relevant to the aim of our review. Impact of Statins on BiomarkersThe current research proceeds to investigate the role of statins in repairing, stabilization, and regression of coronary artery lesions, which form a cornerstone in inhibition of cardiac events ( 16). However, the mechanisms rather than lowering LDL-C to produce beneficial cardiovascular pleiotropic effects, remain multifactorial and unclear.