Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel

To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD). We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospecti...

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Veröffentlicht in:	European heart journal Jg. 38; H. 32; S. 2459
Hauptverfasser:	Ference, Brian A, Ginsberg, Henry N, Graham, Ian, Ray, Kausik K, Packard, Chris J, Bruckert, Eric, Hegele, Robert A, Krauss, Ronald M, Raal, Frederick J, Schunkert, Heribert, Watts, Gerald F, Borén, Jan, Fazio, Sergio, Horton, Jay D, Masana, Luis, Nicholls, Stephen J, Nordestgaard, Børge G, van de Sluis, Bart, Taskinen, Marja-Riitta, Tokgözoglu, Lale, Landmesser, Ulf, Laufs, Ulrich, Wiklund, Olov, Stock, Jane K, Chapman, M John, Catapano, Alberico L
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	England 21.08.2017
Schlagworte:	Anticholesteremic Agents - therapeutic use Atherosclerosis - etiology Atherosclerosis - prevention & control Cholesterol, HDL - metabolism Cholesterol, LDL - metabolism Consensus Epidemiologic Methods Ezetimibe - therapeutic use Genetic Predisposition to Disease - genetics Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use Hyperlipidemias - prevention & control Lipoproteins, LDL - physiology PCSK9 Inhibitors Low-density lipoprotein Recommendations Atherosclerosis Ezetimibe Clinical trials Cardiovascular disease PCSK9 Mendelian randomization Statin Causality
ISSN:	1522-9645, 1522-9645
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Abstract	To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD). We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects. Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.
AbstractList	To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD). We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects. Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD. To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD).AIMSTo appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD).We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects.METHODS AND RESULTSWe assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects.Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.CONCLUSIONConsistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.
Author	Masana, Luis Packard, Chris J Krauss, Ronald M Ginsberg, Henry N Stock, Jane K Taskinen, Marja-Riitta Bruckert, Eric Landmesser, Ulf Graham, Ian Borén, Jan Fazio, Sergio Schunkert, Heribert Tokgözoglu, Lale Ray, Kausik K Horton, Jay D Catapano, Alberico L Watts, Gerald F Raal, Frederick J Nordestgaard, Børge G Hegele, Robert A Nicholls, Stephen J Wiklund, Olov van de Sluis, Bart Laufs, Ulrich Chapman, M John Ference, Brian A
Author_xml	– sequence: 1 givenname: Brian A surname: Ference fullname: Ference, Brian A organization: Division of Translational Research and Clinical Epidemiology, Division of Cardiovascular Medicine, Wayne State University School of Medicine, Detroit, MI 48202, USA – sequence: 2 givenname: Henry N surname: Ginsberg fullname: Ginsberg, Henry N organization: Irving Institute for Clinical and Translational Research, Columbia University, New York, NY, USA – sequence: 3 givenname: Ian surname: Graham fullname: Graham, Ian organization: Trinity College Dublin, Ireland – sequence: 4 givenname: Kausik K surname: Ray fullname: Ray, Kausik K organization: Department of Primary Care and Public Health, Imperial Centre for Cardiovascular Disease Prevention, Imperial College, London, UK – sequence: 5 givenname: Chris J surname: Packard fullname: Packard, Chris J organization: College of Medical, Veterinary, and Life Sciences, University of Glasgow, Glasgow, UK – sequence: 6 givenname: Eric surname: Bruckert fullname: Bruckert, Eric organization: INSERM UMRS1166, Department of Endocrinology-Metabolism, ICAN - Institute of CardioMetabolism and Nutrition, AP-HP, Hôpital de la Pitié, Paris, France – sequence: 7 givenname: Robert A surname: Hegele fullname: Hegele, Robert A organization: Department of Medicine, Robarts Research Institute, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada – sequence: 8 givenname: Ronald M surname: Krauss fullname: Krauss, Ronald M organization: Department of Atherosclerosis Research, Children's Hospital Oakland Research Institute, Oakland, CA 94609, USA – sequence: 9 givenname: Frederick J surname: Raal fullname: Raal, Frederick J organization: Faculty of Health Sciences, University of Witwatersrand, Johannesburg, South Africa – sequence: 10 givenname: Heribert surname: Schunkert fullname: Schunkert, Heribert organization: Deutsches Zentrum für Herz und Kreislauferkrankungen (DZHK), Partner Site Munich Heart Alliance, Munich 81377, Germany – sequence: 11 givenname: Gerald F surname: Watts fullname: Watts, Gerald F organization: Lipid Disorders Clinic, Centre for Cardiovascular Medicine, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia, Australia – sequence: 12 givenname: Jan surname: Borén fullname: Borén, Jan organization: Department of Molecular and Clinical Medicine, Wallenberg Laboratory, Sahlgrenska University Hospital, University of Gothenburg, Gothenburg, Sweden – sequence: 13 givenname: Sergio surname: Fazio fullname: Fazio, Sergio organization: Department of Medicine, Center for Preventive Cardiology of the Knight Cardiovascular Institute, Oregon Health and Science University, Portland, OR, USA – sequence: 14 givenname: Jay D surname: Horton fullname: Horton, Jay D organization: Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA – sequence: 15 givenname: Luis surname: Masana fullname: Masana, Luis organization: Research Unit of Lipids and Atherosclerosis, University Rovira i Virgili, C. Sant Llorenç 21, Reus 43201, Spain – sequence: 16 givenname: Stephen J surname: Nicholls fullname: Nicholls, Stephen J organization: South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia – sequence: 17 givenname: Børge G surname: Nordestgaard fullname: Nordestgaard, Børge G organization: The Copenhagen City Heart Study, Frederiksberg Hospital, Copenhagen University Hospital, Denmark – sequence: 18 givenname: Bart surname: van de Sluis fullname: van de Sluis, Bart organization: Department of Pediatrics, Molecular Genetics Section, University of Groningen, University Medical Center Groningen, Antonius Deusinglaan 1, Groningen AV 9713, The Netherlands – sequence: 19 givenname: Marja-Riitta surname: Taskinen fullname: Taskinen, Marja-Riitta organization: Helsinki University Central Hospital and Research Programs' Unit, Diabetes and Obesity, Heart and Lung Centre, University of Helsinki, Helsinki, Finland – sequence: 20 givenname: Lale surname: Tokgözoglu fullname: Tokgözoglu, Lale organization: Hacettepe University, Ankara, Turkey – sequence: 21 givenname: Ulf surname: Landmesser fullname: Landmesser, Ulf organization: Department of Cardiology, Charité-Universitätsmedizin Berlin (CBF), Hindenburgdamm 30, Berlin 12203, Germany – sequence: 22 givenname: Ulrich surname: Laufs fullname: Laufs, Ulrich organization: Klinik für Innere Medizin III, Kardiologie, Angiologie und Internistische Intensivmedizin, Universitätsklinikum des Saarlandes, Homburg, Saar, Germany – sequence: 23 givenname: Olov surname: Wiklund fullname: Wiklund, Olov organization: Department of Cardiology, Sahlgrenska University Hospital, Gothenburg, Sweden – sequence: 24 givenname: Jane K surname: Stock fullname: Stock, Jane K organization: European Atherosclerosis Society, Gothenburg, Sweden – sequence: 25 givenname: M John surname: Chapman fullname: Chapman, M John organization: INSERM, Dyslipidemia and Atherosclerosis Research, and University of Pierre and Marie Curie, Pitié-Sâlpetrière University Hospital, Paris, France – sequence: 26 givenname: Alberico L surname: Catapano fullname: Catapano, Alberico L organization: Department of Pharmacological and Biomolecular Sciences, University of Milan and IRCCS Multimedica, Milan, Italy
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/28444290$$D View this record in MEDLINE/PubMed
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Keywords	Low-density lipoprotein Recommendations Atherosclerosis Ezetimibe Clinical trials Cardiovascular disease PCSK9 Mendelian randomization Statin Causality
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References	28675189 - J R Coll Physicians Edinb. 2017 Jun;47(2):153-155. doi: 10.4997/JRCPE.2017.212.
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Snippet	To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD). We assessed whether... To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD).AIMSTo appraise the...
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SubjectTerms	Anticholesteremic Agents - therapeutic use Atherosclerosis - etiology Atherosclerosis - prevention & control Cholesterol, HDL - metabolism Cholesterol, LDL - metabolism Consensus Epidemiologic Methods Ezetimibe - therapeutic use Genetic Predisposition to Disease - genetics Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use Hyperlipidemias - prevention & control Lipoproteins, LDL - physiology PCSK9 Inhibitors
Title	Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel
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