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

Erik S Stroes; Paul D Thompson; Alberto Corsini; Georgirene D Vladutiu; Frederick J Raal; Kausik K Ray; Michael Roden; Evan Stein; Lale Tokgözoğlu; Børge G Nordestgaard; Eric Bruckert; Guy De Backer; Ronald M Krauss; Ulrich Laufs; Raul D Santos; Robert A Hegele; G Kees Hovingh; Lawrence A Leiter; Francois Mach; Winfried März; Connie B Newman; Olov Wiklund; Terry A Jacobson; Alberico L Catapano; M John Chapman; Henry N Ginsberg; European Atherosclerosis Society Consensus Panel

doi:10.1093/eurheartj/ehv043

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

Erik S Stroes, Paul D Thompson, Alberto Corsini, Georgirene D Vladutiu, Frederick J Raal, Kausik K Ray, Michael Roden, Evan Stein, Lale Tokgözoğlu, Børge G Nordestgaard, Eric Bruckert, Guy De Backer, Ronald M Krauss, Ulrich Laufs, Raul D Santos, Robert A Hegele, G Kees Hovingh, Lawrence A Leiter, Francois Mach, Winfried MärzConnie B Newman, Olov Wiklund, Terry A Jacobson, Alberico L Catapano, M John Chapman, Henry N Ginsberg, European Atherosclerosis Society Consensus Panel

Department of Clinical Medicine

724 Citations (Scopus)

Abstract

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.

Original language	English
Journal	European Heart Journal
Volume	36
Issue number	17
Pages (from-to)	1012-22b
Number of pages	13
ISSN	0195-668X
DOIs	https://doi.org/10.1093/eurheartj/ehv043
Publication status	Published - 1 May 2015

Keywords

Cholesterol Ester Transfer Proteins
Complementary Therapies
Consensus
Creatine Kinase
Diet
Genetic Predisposition to Disease
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Hypolipidemic Agents
Mitochondria, Muscle
Mitochondrial Diseases
Muscular Diseases
Proprotein Convertases
Risk Factors
Serine Endopeptidases

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10.1093/eurheartj/ehv043

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Stroes, E. S., Thompson, P. D., Corsini, A., Vladutiu, G. D., Raal, F. J., Ray, K. K., Roden, M., Stein, E., Tokgözoğlu, L., Nordestgaard, B. G., Bruckert, E., De Backer, G., Krauss, R. M., Laufs, U., Santos, R. D., Hegele, R. A., Hovingh, G. K., Leiter, L. A., Mach, F., ... European Atherosclerosis Society Consensus Panel (2015). Statin-associated muscle symptoms: impact on statin therapy: European Atherosclerosis Society Consensus Panel Statement on Assessment, Aetiology and Management. European Heart Journal, 36(17), 1012-22b. https://doi.org/10.1093/eurheartj/ehv043

Stroes, ES, Thompson, PD, Corsini, A, Vladutiu, GD, Raal, FJ, Ray, KK, Roden, M, Stein, E, Tokgözoğlu, L, Nordestgaard, BG, Bruckert, E, De Backer, G, Krauss, RM, Laufs, U, Santos, RD, Hegele, RA, Hovingh, GK, Leiter, LA, Mach, F, März, W, Newman, CB, Wiklund, O, Jacobson, TA, Catapano, AL, Chapman, MJ, Ginsberg, HN & European Atherosclerosis Society Consensus Panel 2015, 'Statin-associated muscle symptoms: impact on statin therapy: European Atherosclerosis Society Consensus Panel Statement on Assessment, Aetiology and Management', European Heart Journal, vol. 36, no. 17, pp. 1012-22b. https://doi.org/10.1093/eurheartj/ehv043

@article{53465cd70ddb4898a03b132778848dca,

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

abstract = "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.",

keywords = "Cholesterol Ester Transfer Proteins, Complementary Therapies, Consensus, Creatine Kinase, Diet, Genetic Predisposition to Disease, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hypolipidemic Agents, Mitochondria, Muscle, Mitochondrial Diseases, Muscular Diseases, Proprotein Convertases, Risk Factors, Serine Endopeptidases",

author = "Stroes, {Erik S} and Thompson, {Paul D} and Alberto Corsini and Vladutiu, {Georgirene D} and Raal, {Frederick J} and Ray, {Kausik K} and Michael Roden and Evan Stein and Lale Tokg{\"o}zoğlu and Nordestgaard, {B{\o}rge G} and Eric Bruckert and {De Backer}, Guy and Krauss, {Ronald M} and Ulrich Laufs and Santos, {Raul D} and Hegele, {Robert A} and Hovingh, {G Kees} and Leiter, {Lawrence A} and Francois Mach and Winfried M{\"a}rz and Newman, {Connie B} and Olov Wiklund and Jacobson, {Terry A} and Catapano, {Alberico L} and Chapman, {M John} and Ginsberg, {Henry N} and {European Atherosclerosis Society Consensus Panel}",

note = "{\textcopyright} The Author 2015. Published by Oxford University Press on behalf of the European Society of Cardiology.",

year = "2015",

month = may,

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doi = "10.1093/eurheartj/ehv043",

language = "English",

volume = "36",

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journal = "European Heart Journal",

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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 -

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

Abstract

Keywords

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