Statins reduce cholesterol biosynthesis in the liver and increasethe clearance of LDL-cholesterol (LDL-C). These lipid-lowering agents prevent theformation of cholesterol precursor mevalonate and inhibiting3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA),resulting in depletion of Mevalonate, limiting the production of isoprenoid anddecreasing the formation of Rho and Ras proteins involved in intracellularsignaling pathways 1, 2.Through the last three decades an extensiveresearch in literature focused on pleiotropic protective effects of statins,particularly in patients with coronary artery disease (CAD) and stroke, whichare independent of LDL-C lowering effect 3, 4.Statinscan exert their favorable pleiotropic effects through increasing expression ofatheroprotective genes, inhibition of pro-inflammatory mediators, endothelialprotective effects, enhancing the stability of atherosclerotic plaques,inhibiting vascular smooth muscle proliferation, decreasing plateletaggregation, increasing nitric oxide bioavailability, reducing adhesionmolecules, decreasing circulating biomarkers of oxidative stress andinflammation, inhibiting thrombogenic response 5, 6.In clinical practice, statins have a potentialprotective role in primary and secondary prevention of all-cause mortality andmajor coronary events as compared to control 7. For primary preventionof atherosclerotic cardiovascular disease (ASCVD) events and mortality, statintherapy is demonstrated one of the most effective interventions and risk-factormodifications 8.
Therecommendations for secondary prevention in high risk patients with CAD aredifferent between guidelines. Many guidelines recommend LCL-C goal of <70mg/dL 9, 10, while the use of high-intensity statins for secondary preventionin acute coronary syndrome (ACS)patients with repeated measurement of lipid profiles is recommended by the mostrecent 2013 American College of Cardiology/American Heart Association ACC/AHAguideline on cholesterol management 11.Despite the known great cardiovascular effects of statins beyondcholesterol lowering, a debate still surrounding its clinical use including:guideline-based eligibility of statin therapy and prescription ofhigh-intensity statins 12, 13, effects of statin monotherapy versuscombination with other lipid-lowering agents 14, utilization of statinsbefore and after coronary artery revascularization 15, and residual risk ofsecondary coronary artery events 16. Therefore, the aim of this reviewarticle is to highlight the current targets and debates of scientific researchconcerning the role of statin therapy in patients with CAD.