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

European heart journal, 2022-10, Vol.43 (39), p.3925-3946 [Peer Reviewed Journal]

Distributed under a Creative Commons Attribution 4.0 International License ;The Author(s) 2022. Published by Oxford University Press on behalf of European Society of Cardiology. 2022 ;ISSN: 0195-668X ;EISSN: 1522-9645 ;DOI: 10.1093/eurheartj/ehac361 ;PMID: 36036785

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  • Title:
    Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement
  • Author: Kronenberg, Florian ; Mora, Samia ; Stroes, Erik S G ; Ference, Brian A ; Arsenault, Benoit J ; Berglund, Lars ; Dweck, Marc R ; Koschinsky, Marlys ; Lambert, Gilles ; Mach, François ; McNeal, Catherine J ; Moriarty, Patrick M ; Natarajan, Pradeep ; Nordestgaard, Børge G ; Parhofer, Klaus G ; Virani, Salim S ; von Eckardstein, Arnold ; Watts, Gerald F ; Stock, Jane K ; Ray, Kausik K ; Tokgözoğlu, Lale S ; Catapano, Alberico L
  • Subjects: Life Sciences ; Special
  • Is Part Of: European heart journal, 2022-10, Vol.43 (39), p.3925-3946
  • Description: Abstract 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.
  • Publisher: US: Oxford University Press (OUP)
  • Language: English
  • Identifier: ISSN: 0195-668X
    EISSN: 1522-9645
    DOI: 10.1093/eurheartj/ehac361
    PMID: 36036785
  • Source: GFMER Free Medical Journals
    Alma/SFX Local Collection
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