Abstract

Statins are the most prescribed and effective drugs to treat cardiovascular diseases (CVD). Nevertheless, these drugs can be responsible for skeletal muscle toxicity which leads to reduced compliance. The discontinuation of therapy increases the incidence of CVD. Thus, it is essential to assess the risk. In fact, many studies have been performed at preclinical and clinical level to investigate pathophysiological mechanisms and clinical implications of statin myotoxicity. Consequently, new toxicological aspects and new biomarkers have arisen. Indeed, these drugs may affect gene transcription and ion transport and contribute to muscle function impairment. Identifying a marker of toxicity is important to prevent or to cure statin induced myopathy while assuring the right therapy for hypercholesterolemia and counteracting CVD. In this review we focused on the mechanisms of muscle damage discovered in preclinical and clinical studies and highlighted the pathological situations in which statin therapy should be avoided. In this context, preventive or substitutive therapies should also be evaluated.

Highlights

  • This study provides a summary of the causes responsible for statin-induced myopathy

  • Ion channels and in particular the ClC-1 chloride channel appears to be a susceptible target for statin action

  • Since these channels are important for skeletal muscle excitability and contraction their alteration can contribute to myopathy

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Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Statins represent the first line therapy in the prevention and treatment of metabolic syndrome [3] and cardiovascular diseases (CVD), that are the primary causes of mortality in the world Their beneficial role is linked to the reduction of low-density lipoprotein (LDL) cholesterol in blood, resulting from the inhibition of cholesterol synthesis. SAMS are not common to all statins since different factors may contribute to this condition (genetic, pharmacodynamic, pharmacokinetics, presence of comorbidity, polypharmacy) These recommendations can assist the clinicians in improving adherence to therapy and the possibility that patients experiencing SAMS may receive the best cholesterol lowering therapy as to minimize CVD risk

The Causes of Statin-Induced Myopathy
Ion Channels as Biomarkers of Statin-Induced Muscle Symptoms of Myopathy
Translational Studies
Higher Risk with Statin Therapy
Management of the Risk of Myopathy with Statin Therapy
Findings
Summary and Conclusions
Full Text
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