Statin-Associated Myopathy: Emphasis on Mechanisms and Targeted Therapy

Hyperlipidemia is a major risk factor for cardiovascular morbidity and mortality. Statins are the first-choice therapy for dyslipidemias and are considered the cornerstone of atherosclerotic cardiovascular disease (ASCVD) in both primary and secondary prevention. Despite the statin-therapy-mediated...

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Autores principales:	Pierandrea Vinci, Emiliano Panizon, Letizia Maria Tosoni, Carla Cerrato, Federica Pellicori, Filippo Mearelli, Chiara Biasinutto, Nicola Fiotti, Filippo Giorgio Di Girolamo, Gianni Biolo
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	statin myopathy SAMS mechanisms SAMS management Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/6644b63cca86472a83c48e43d239b7bf
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spelling	oai:doaj.org-article:6644b63cca86472a83c48e43d239b7bf2021-11-11T17:09:03ZStatin-Associated Myopathy: Emphasis on Mechanisms and Targeted Therapy10.3390/ijms2221116871422-00671661-6596https://doaj.org/article/6644b63cca86472a83c48e43d239b7bf2021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11687https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Hyperlipidemia is a major risk factor for cardiovascular morbidity and mortality. Statins are the first-choice therapy for dyslipidemias and are considered the cornerstone of atherosclerotic cardiovascular disease (ASCVD) in both primary and secondary prevention. Despite the statin-therapy-mediated positive effects on cardiovascular events, patient compliance is often poor. Statin-associated muscle symptoms (SAMS) are the most common side effect associated with treatment discontinuation. SAMS, which range from mild-to-moderate muscle pain, weakness, or fatigue to potentially life-threatening rhabdomyolysis, are reported by 10% to 25% of patients receiving statin therapy. There are many risk factors associated with patient features and hypolipidemic agents that seem to increase the risk of developing SAMS. Due to the lack of a “gold standard”, the diagnostic test for SAMS is based on a clinical criteria score, which is independent of creatine kinase (CK) elevation. Mechanisms that underlie the pathogenesis of SAMS remain almost unclear, though a high number of risk factors may increase the probability of myotoxicity induced by statin therapy. Some of these, related to pharmacokinetic properties of statins and to concomitant therapies or patient characteristics, may affect statin bioavailability and increase vulnerability to high-dose statins.Pierandrea VinciEmiliano PanizonLetizia Maria TosoniCarla CerratoFederica PellicoriFilippo MearelliChiara BiasinuttoNicola FiottiFilippo Giorgio Di GirolamoGianni BioloMDPI AGarticlestatin myopathySAMS mechanismsSAMS managementBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11687, p 11687 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	statin myopathy SAMS mechanisms SAMS management Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	statin myopathy SAMS mechanisms SAMS management Biology (General) QH301-705.5 Chemistry QD1-999 Pierandrea Vinci Emiliano Panizon Letizia Maria Tosoni Carla Cerrato Federica Pellicori Filippo Mearelli Chiara Biasinutto Nicola Fiotti Filippo Giorgio Di Girolamo Gianni Biolo Statin-Associated Myopathy: Emphasis on Mechanisms and Targeted Therapy
description	Hyperlipidemia is a major risk factor for cardiovascular morbidity and mortality. Statins are the first-choice therapy for dyslipidemias and are considered the cornerstone of atherosclerotic cardiovascular disease (ASCVD) in both primary and secondary prevention. Despite the statin-therapy-mediated positive effects on cardiovascular events, patient compliance is often poor. Statin-associated muscle symptoms (SAMS) are the most common side effect associated with treatment discontinuation. SAMS, which range from mild-to-moderate muscle pain, weakness, or fatigue to potentially life-threatening rhabdomyolysis, are reported by 10% to 25% of patients receiving statin therapy. There are many risk factors associated with patient features and hypolipidemic agents that seem to increase the risk of developing SAMS. Due to the lack of a “gold standard”, the diagnostic test for SAMS is based on a clinical criteria score, which is independent of creatine kinase (CK) elevation. Mechanisms that underlie the pathogenesis of SAMS remain almost unclear, though a high number of risk factors may increase the probability of myotoxicity induced by statin therapy. Some of these, related to pharmacokinetic properties of statins and to concomitant therapies or patient characteristics, may affect statin bioavailability and increase vulnerability to high-dose statins.
format	article
author	Pierandrea Vinci Emiliano Panizon Letizia Maria Tosoni Carla Cerrato Federica Pellicori Filippo Mearelli Chiara Biasinutto Nicola Fiotti Filippo Giorgio Di Girolamo Gianni Biolo
author_facet	Pierandrea Vinci Emiliano Panizon Letizia Maria Tosoni Carla Cerrato Federica Pellicori Filippo Mearelli Chiara Biasinutto Nicola Fiotti Filippo Giorgio Di Girolamo Gianni Biolo
author_sort	Pierandrea Vinci
title	Statin-Associated Myopathy: Emphasis on Mechanisms and Targeted Therapy
title_short	Statin-Associated Myopathy: Emphasis on Mechanisms and Targeted Therapy
title_full	Statin-Associated Myopathy: Emphasis on Mechanisms and Targeted Therapy
title_fullStr	Statin-Associated Myopathy: Emphasis on Mechanisms and Targeted Therapy
title_full_unstemmed	Statin-Associated Myopathy: Emphasis on Mechanisms and Targeted Therapy
title_sort	statin-associated myopathy: emphasis on mechanisms and targeted therapy
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/6644b63cca86472a83c48e43d239b7bf
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Statin-Associated Myopathy: Emphasis on Mechanisms and Targeted Therapy

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