Статья

Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement

Florian KronenbergInstitute of Genetic Epidemiology, Medical University of Innsbruck , Innsbruck , AustriaSamia MoraCenter for Lipid Metabolomics, Division of Preventive Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School , Boston, MA 02115 , USAErik S.G. StroesDepartment of Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam , Amsterdam , the NetherlandsBrian A. FerenceCentre for Naturally Randomized Trials, University of Cambridge , Cambridge , UKBenoît J. ArsenaultCentre de Recherche de l’Institut Universitaire de Cardiologie et de Pneumologie de Québec, and Department of Medicine, Faculty of Medicine, Université Laval , Québec City, QC , CanadaLars BerglundDepartment of Internal Medicine, School of Medicine, University of California-Davis , Davis, Sacramento, CA , USAMarc R. DweckBritish Heart Foundation Centre for Cardiovascular Science, Edinburgh Heart Centre, University of Edinburgh , Chancellors Building, Little France Crescent, Edinburgh EH16 4SB , UKMarlys L. KoschinskyRobarts Research Institute, Schulich School of Medicine and Dentistry, Western University , London, Ontario , CanadaGilles LambertInserm, UMR 1188 Diabète Athérothrombose Thérapies Réunion Océan Indien (DéTROI), Université de La Réunion , 97400 Saint-Denis de La Reunion , FranceFrançois MachDepartment of Cardiology, Geneva University Hospital , Geneva , SwitzerlandCatherine J. McNealDivision of Cardiology, Department of Internal Medicine, Baylor Scott & White Health , 2301 S. 31st St. , USAPatrick M. MoriartyUniversity of Kansas Medical Center , Kansas City, KS , USAPradeep NatarajanCardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, and Program in Medical and Population Genetics and Cardiovascular Disease Initiative, Broad Institute of Harvard and MIT , Cambridge, MA , USABørge G. NordestgaardDepartment of Clinical Biochemistry and the Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital , Herlev , DenmarkKlaus G. ParhoferMedizinische Klinik und Poliklinik IV, Ludwigs- Maximilians University Klinikum , Munich , GermanySalim S. ViraniSection of Cardiovascular Research, Baylor College of Medicine & Michael E. DeBakey Veterans Affairs Medical Center , Houston, TX , USAArnold von EckardsteinInstitute of Clinical Chemistry, University Hospital Zurich, University of Zurich , Zurich , SwitzerlandGerald F. WattsMedical School, University of Western Australia, and Department of Cardiology, Lipid Disorders Clinic, Royal Perth Hospital , Perth , AustraliaJane K. StockEuropean Atherosclerosis Society , Mässans Gata 10, SE-412 51 Gothenburg , SwedenKausik K. RayImperial Centre for Cardiovascular Disease Prevention, Department of Primary Care and Public Health, School of Public Health, Imperial College London , London , UKLâle TokgözoğluDepartment of Cardiology, Hacettepe University Faculty of Medicine , Ankara , TurkeyAlberico L. CatapanoDepartment of Pharmacological and Biomolecular Sciences, University of Milano , Milano , Italy

2022en

ABI

Аннотация

This 2022 European Atherosclerosis Society lipoprotein(a) [Lp(a)] consensus statement updates evidence for the role of Lp(a) in atherosclerotic cardiovascular disease (ASCVD) and aortic valve stenosis, provides clinical guidance for testing and treating elevated Lp(a) levels, and considers its inclusion in global risk estimation. Epidemiologic and genetic studies involving hundreds of thousands of individuals strongly support a causal and continuous association between Lp(a) concentration and cardiovascular outcomes in different ethnicities; elevated Lp(a) is a risk factor even at very low levels of low-density lipoprotein cholesterol. High Lp(a) is associated with both microcalcification and macrocalcification of the aortic valve. Current findings do not support Lp(a) as a risk factor for venous thrombotic events and impaired fibrinolysis. Very low Lp(a) levels may associate with increased risk of diabetes mellitus meriting further study. Lp(a) has pro-inflammatory and pro-atherosclerotic properties, which may partly relate to the oxidized phospholipids carried by Lp(a). This panel recommends testing Lp(a) concentration at least once in adults; cascade testing has potential value in familial hypercholesterolaemia, or with family or personal history of (very) high Lp(a) or premature ASCVD. Without specific Lp(a)-lowering therapies, early intensive risk factor management is recommended, targeted according to global cardiovascular risk and Lp(a) level. Lipoprotein apheresis is an option for very high Lp(a) with progressive cardiovascular disease despite optimal management of risk factors. In conclusion, this statement reinforces evidence for Lp(a) as a causal risk factor for cardiovascular outcomes. Trials of specific Lp(a)-lowering treatments are critical to confirm clinical benefit for cardiovascular disease and aortic valve stenosis.

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Идентификаторы

DOI: 10.1093/eurheartj/ehac361

Цитирования и источники

Цитирований: 3Использованных источников: 0

Показатели — AkademScholar