Abstract

STATIN INDUCED MYOPATHY: MECHANISMS, CLINICAL CHALLENGES AND ROLE OF LIPOPROTEIN (A) IN CARDIOVASCULAR RISK

*Ananda Krishnan

Abstract

Statins are the cornerstone of lipid-lowering therapy and play a crucial role in reducing cardiovascular morbidity and mortality. However, their use is frequently limited by statin-associated muscle symptoms (SAMS), ranging from mild myalgia to severe conditions such as rhabdomyolysis and immunemediated necrotizing myopathy. Although relatively uncommon, statin-induced myopathy significantly affects treatment adherence and may compromise cardiovascular risk reduction. The pathogenesis is multifactorial, involving disruption of the mevalonate pathway, mitochondrial dysfunction, oxidative stress, and genetic susceptibility. Management strategies include dose adjustment, switching statins, intermittent dosing, and the use of non-statin therapies. In addition, lipoprotein(a) [Lp(a)] has emerged as an independent contributor to residual cardiovascular risk, particularly in statin-intolerant patients, as its levels are minimally affected by statins. A personalized approach integrating clinical evaluation and alternative therapeutic options is essential for optimizing outcomes. Emerging therapies and advances in pharmacogenomics offer promising directions for improving the management of dyslipidemia.

Keywords: Statin-induced myopathy, Statin-associated muscle symptoms (SAMS), Statin intolerance, Lipoprotein(a), Cardiovascular risk, Dyslipidemia, HMG-CoA reductase inhibitors, Mitochondrial dysfunction, Pharmacogenomics, (SLCO1B1) polymorphism.