Statin-associated muscle symptoms: impact on statin therapy: European Atherosclerosis Society Consensus Panel Statement on Assessment, Aetiology and Management

TY - JOUR

T1 - Statin-associated muscle symptoms: impact on statin therapy

T2 - European Atherosclerosis Society Consensus Panel Statement on Assessment, Aetiology and Management

AU - Stroes, Erik S

AU - Thompson, Paul D

AU - Corsini, Alberto

AU - Vladutiu, Georgirene D

AU - Raal, Frederick J

AU - Ray, Kausik K

AU - Roden, Michael

AU - Stein, Evan

AU - Tokgözoğlu, Lale

AU - Nordestgaard, Børge G

AU - Bruckert, Eric

AU - De Backer, Guy

AU - Krauss, Ronald M

AU - Laufs, Ulrich

AU - Santos, Raul D

AU - Hegele, Robert A

AU - Hovingh, G Kees

AU - Leiter, Lawrence A

AU - Mach, Francois

AU - März, Winfried

AU - Newman, Connie B

AU - Wiklund, Olov

AU - Jacobson, Terry A

AU - Catapano, Alberico L

AU - Chapman, M John

AU - Ginsberg, Henry N

AU - European Atherosclerosis Society Consensus Panel

N1 - © The Author 2015. Published by Oxford University Press on behalf of the European Society of Cardiology.

PY - 2015/5/1

Y1 - 2015/5/1

N2 - Statin-associated muscle symptoms (SAMS) are one of the principal reasons for statin non-adherence and/or discontinuation, contributing to adverse cardiovascular outcomes. This European Atherosclerosis Society (EAS) Consensus Panel overviews current understanding of the pathophysiology of statin-associated myopathy, and provides guidance for diagnosis and management of SAMS. Statin-associated myopathy, with significant elevation of serum creatine kinase (CK), is a rare but serious side effect of statins, affecting 1 per 1000 to 1 per 10 000 people on standard statin doses. Statin-associated muscle symptoms cover a broader range of clinical presentations, usually with normal or minimally elevated CK levels, with a prevalence of 7-29% in registries and observational studies. Preclinical studies show that statins decrease mitochondrial function, attenuate energy production, and alter muscle protein degradation, thereby providing a potential link between statins and muscle symptoms; controlled mechanistic and genetic studies in humans are necessary to further understanding. The Panel proposes to identify SAMS by symptoms typical of statin myalgia (i.e. muscle pain or aching) and their temporal association with discontinuation and response to repetitive statin re-challenge. In people with SAMS, the Panel recommends the use of a maximally tolerated statin dose combined with non-statin lipid-lowering therapies to attain recommended low-density lipoprotein cholesterol targets. The Panel recommends a structured work-up to identify individuals with clinically relevant SAMS generally to at least three different statins, so that they can be offered therapeutic regimens to satisfactorily address their cardiovascular risk. Further research into the underlying pathophysiological mechanisms may offer future therapeutic potential.

AB - Statin-associated muscle symptoms (SAMS) are one of the principal reasons for statin non-adherence and/or discontinuation, contributing to adverse cardiovascular outcomes. This European Atherosclerosis Society (EAS) Consensus Panel overviews current understanding of the pathophysiology of statin-associated myopathy, and provides guidance for diagnosis and management of SAMS. Statin-associated myopathy, with significant elevation of serum creatine kinase (CK), is a rare but serious side effect of statins, affecting 1 per 1000 to 1 per 10 000 people on standard statin doses. Statin-associated muscle symptoms cover a broader range of clinical presentations, usually with normal or minimally elevated CK levels, with a prevalence of 7-29% in registries and observational studies. Preclinical studies show that statins decrease mitochondrial function, attenuate energy production, and alter muscle protein degradation, thereby providing a potential link between statins and muscle symptoms; controlled mechanistic and genetic studies in humans are necessary to further understanding. The Panel proposes to identify SAMS by symptoms typical of statin myalgia (i.e. muscle pain or aching) and their temporal association with discontinuation and response to repetitive statin re-challenge. In people with SAMS, the Panel recommends the use of a maximally tolerated statin dose combined with non-statin lipid-lowering therapies to attain recommended low-density lipoprotein cholesterol targets. The Panel recommends a structured work-up to identify individuals with clinically relevant SAMS generally to at least three different statins, so that they can be offered therapeutic regimens to satisfactorily address their cardiovascular risk. Further research into the underlying pathophysiological mechanisms may offer future therapeutic potential.

KW - Cholesterol Ester Transfer Proteins

KW - Complementary Therapies

KW - Consensus

KW - Creatine Kinase

KW - Diet

KW - Genetic Predisposition to Disease

KW - Humans

KW - Hydroxymethylglutaryl-CoA Reductase Inhibitors

KW - Hypolipidemic Agents

KW - Mitochondria, Muscle

KW - Mitochondrial Diseases

KW - Muscular Diseases

KW - Proprotein Convertases

KW - Risk Factors

KW - Serine Endopeptidases

U2 - 10.1093/eurheartj/ehv043

DO - 10.1093/eurheartj/ehv043

M3 - Review

C2 - 25694464

SN - 0195-668X

VL - 36

SP - 1012-22b

JO - European Heart Journal

JF - European Heart Journal

IS - 17

ER -