Statins

Statins are the cornerstone of pharmacological cardiovascular preventive therapy to reduce atherosclerotic cardiovascular disease (ASCVD) risk. Statins reduce cholesterol biosynthesis by competitively inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Decreased hepatic cholesterol production triggers an increased expression of hepatic low-density lipoprotein (LDL) receptors that transfer LDL particles into the hepatocyte and reduce LDL cholesterol (LDL-C) in the blood. Randomized controlled trials have shown that statin therapy results in a 22% proportional reduction in major ASCVD events for each 38.7-mg/dL (1-mmol/L) reduction in LDL-C, regardless of baseline LDL-C concentration. Although statins have been proven to decrease cardiovascular events substantially, adherence to statins is suboptimal despite the favorable safety profile. The principal side effects reported on statin therapy are muscle symptoms, which may be accompanied by creatine kinase elevation. Sufficient time should be spent to discuss the risk/benefit ratio with the patient, and after a washout period, most patients can be rechallenged with either the same statin at a lower dose or switching to an alternative statin.