That Myalgia of Yours Is Not From Statin Intolerance

Peter P. Toth, MD, PHD


J Am Coll Cardiol. 2021;78(12):1223-1226. 

In This Article

Abstract and Introduction


Statins reduce the burden of atherogenic lipoprotein burden in serum and attenuate inflammation, endothelial cell dysfunction, and oxidative tone within arterial walls. The beneficial impact of statins on cardiovascular (CV) outcomes is among the most highly investigated issues in all of modern medicine. Statins reduce risk of myocardial infarction (MI), ischemic stroke, hospitalization for unstable angina, need for revascularization, CV mortality, and all-cause mortality.[1] Despite this extraordinary spectrum of CV benefit, 50% of patients stop their statin after 6 months, and only 20% of high-risk patients remain adherent to them after 5 years.[2,3]

The principal reasons for premature statin discontinuation are such statin-associated muscle symptoms (SAMS) as myalgia, cramping, or fatigue.[4] Statin intolerance is succinctly defined as the inability to tolerate a dose of a statin necessary to provide an appropriate risk-stratified reduction in low-density lipoprotein cholesterol. Premature statin discontinuation is associated with a significant increase in risk for MI, stroke, and death compared with patients who remain adherent.[5–7] Any form of negative press adversely affects rates of statin adherence.[8] Statin intolerance occurs more frequently among women, persons who identify as members of non-White racial and ethnic groups, older patients, and persons with lower socioeconomic status.[3] Lower rates of statin adherence contribute to the health care disparities experienced by these groups and may also be a reason why CV mortality is increasing.[9]