Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement
File(s) ehac361.pdf (11.38 MB)
Published version
Author(s)
Type
Journal Article
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.
Date Issued
2022-10-14
Date Acceptance
2022-06-21
Citation
European Heart Journal, 2022, 43 (39), pp.3925-3946
ISSN
0195-668X
Publisher
Oxford University Press
Start Page
3925
End Page
3946
Journal / Book Title
European Heart Journal
Volume
43
Issue
39
Copyright Statement
© The Author(s) 2022. Published by Oxford University Press on behalf of European Society of Cardiology. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
License URL
Identifier
https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000868350400007&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
PII: 6670882
Subjects
Aortic stenosis
Cardiac & Cardiovascular Systems
Cardiovascular risk
Cardiovascular System & Cardiology
Clinical guidance
Consensus
ELEVATED LIPOPROTEIN(A)
GENOME-WIDE ASSOCIATION
INSULIN-RESISTANCE
ISCHEMIC-STROKE
Life Sciences & Biomedicine
Lipoprotein(a)
LP(A) LEVELS
Model of care
OXIDIZED PHOSPHOLIPIDS
PCSK9 INHIBITION
RISK-FACTOR
Science & Technology
STAGE RENAL-DISEASE
SUBTILISIN/KEXIN TYPE 9
Testing
Treatment
Publication Status
Published
Coverage Spatial
England
Date Publish Online
2022-08-18
