Aspirin and lipoprotein(a) in primary prevention.
Journal
Current opinion in lipidology
ISSN: 1473-6535
Titre abrégé: Curr Opin Lipidol
Pays: England
ID NLM: 9010000
Informations de publication
Date de publication:
01 10 2023
01 10 2023
Historique:
medline:
12
9
2023
pubmed:
1
8
2023
entrez:
1
8
2023
Statut:
ppublish
Résumé
Lipoprotein(a) [Lp(a)] is causally associated with cardiovascular diseases, and elevated levels are highly prevalent. However, there is a lack of available therapies to address Lp(a)-mediated risk. Though aspirin has progressively fallen out of favor for primary prevention, individuals with high Lp(a) may represent a high-risk group that derives a net benefit. Aspirin has been demonstrated to have a clear benefit in secondary prevention of cardiovascular disease, but recent primary prevention trials have at best demonstrated a small benefit. However, individuals with elevated Lp(a) may be of high risk enough to benefit, particularly given interactions between Lp(a) and the fibrinolytic system / platelets, and the lack of available targeted medical therapies. In secondary analyses of the Women's Health Study (WHS) and the Aspirin in Reducing Events in the Elderly (ASPREE) trial, aspirin use was associated with a significant reduction in cardiovascular events in carriers of genetic polymorphisms associated with elevated Lp(a) levels. Further studies are needed, however, as these studies focused on narrower subsets of the overall population and genetic markers. Individuals with elevated Lp(a) may benefit from aspirin therapy in primary prevention, but further study with plasma Lp(a) levels, broader populations, and randomization of aspirin are needed.
Identifiants
pubmed: 37527183
doi: 10.1097/MOL.0000000000000891
pii: 00041433-990000000-00042
doi:
Substances chimiques
Aspirin
R16CO5Y76E
Lipoprotein(a)
0
Types de publication
Review
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
214-220Informations de copyright
Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.
Références
Bhatia HS, Wilkinson MJ. Lipoprotein(a): evidence for role as a causal risk factor in cardiovascular disease and emerging therapies. J Clin Med 2022; 11:6040.
Varvel S, McConnell JP, Tsimikas S. Prevalence of elevated Lp(a) mass levels and patient thresholds in 532 359 patients in the United States. Arterioscler Thromb Vasc Biol 2016; 36:2239–2245.
Enkhmaa B, Berglund L. Nongenetic influences on lipoprotein(a) concentrations. Atherosclerosis 2022; 349:53–62.
Willeit P, Ridker PM, Nestel PJ, et al. Baseline and on-statin treatment lipoprotein(a) levels for prediction of cardiovascular events: individual patient-data meta-analysis of statin outcome trials. The Lancet 2018; 392:1311–1320.
Bittner VA, Szarek M, Aylward PE, et al. Effect of alirocumab on lipoprotein(a) and cardiovascular risk after acute coronary syndrome. J Am Coll Cardiol 2020; 75:133–144.
O’Donoghue ML, Fazio S, Giugliano RP, et al. Lipoprotein(a), PCSK9 inhibition, and cardiovascular risk. Circulation 2019; 139:1483–1492.
Tsimikas S, Moriarty PM, Stroes ES. Emerging RNA therapeutics to lower blood levels of Lp(a): JACC focus seminar 2/4. J Am Coll Cardiol 2021; 77:1576–1589.
Antithrombotic Trialists’ (ATT) Collaboration. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials. The Lancet 2009; 373:1849–1860.
Gaziano JM, Brotons C, Coppolecchia R, et al. Use of aspirin to reduce risk of initial vascular events in patients at moderate risk of cardiovascular disease (ARRIVE): a randomised, double-blind, placebo-controlled trial. The Lancet 2018; 392:1036–1046.
Bowman L, Mafham M, et al. Group ASC. Effects of aspirin for primary prevention in persons with diabetes mellitus. N Engl J Med 2018; 379:1529–1539.
McNeil JJ, Wolfe R, Woods RL, et al. Effect of aspirin on cardiovascular events and bleeding in the healthy elderly. N Engl J Med 2018; 379:1509–1518.
Zheng SL, Roddick AJ. Association of aspirin use for primary prevention with cardiovascular events and bleeding events: a systematic review and meta-analysis. JAMA 2019; 321:277–287.
Force UPST. Aspirin use to prevent cardiovascular disease: US preventive services task force recommendation statement. JAMA 2022; 327:1577–1584.
Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA guideline on the primary prevention of cardiovascular disease: a report of the American college of cardiology/American heart association task force on clinical practice guidelines. J Am Coll Cardiol 2019; 74:e177–e232.
Palabrica TM, Liu AC, Aronovitz MJ, et al. Antifibrinolytic activity of apolipoprotein(a) in vivo: human apolipoprotein(a) transgenic mice are resistant to tissue plasminogen activator-mediated thrombolysis. Nat Med 1995; 1:256–259.
Helgadottir A, Gretarsdottir S, Thorleifsson G, et al. Apolipoprotein(a) genetic sequence variants associated with systemic atherosclerosis and coronary atherosclerotic burden but not with venous thromboembolism. J Am Coll Cardiol 2012; 60:722–729.
Kamstrup PR, Tybjærg-Hansen A, Nordestgaard BG. Genetic evidence that lipoprotein(a) associates with atherosclerotic stenosis rather than venous thrombosis. Arterioscler Thromb Vasc Biol 2012; 32:1732–1741.
Rand ML, Sangrar W, Hancock MA, et al. Apolipoprotein(a) enhances platelet responses to the thrombin receptor-activating peptide SFLLRN. Arterioscler Thromb Vasc Biol 1998; 18:1393–1399.
Martínez C, Rivera J, Loyau S, et al. Binding of recombinant apolipoprotein(a) to human platelets and effect on platelet aggregation. Thromb Haemost 2001; 85:686–693.
Podrez EA, Byzova TV, Febbraio M, et al. Platelet CD36 links hyperlipidemia, oxidant stress and a prothrombotic phenotype. Nat Med 2007; 13:1086–1095.
Zhu P, Tang XF, Song Y, et al. Association of lipoprotein(a) with platelet aggregation and thrombogenicity in patients undergoing percutaneous coronary intervention. Platelets 2020; 1–6.
Dou H, Kotini A, Liu W, et al. Oxidized phospholipids promote NETosis and arterial thrombosis in LNK(SH2B3) deficiency. Circulation 2021; 144:1940–1954.
Gries A, Gries M, Wurm H, et al. Lipoprotein(a) inhibits collagen-induced aggregation of thrombocytes. Arterioscler Thromb Vasc Biol 1996; 16:648–655.
Barre DE. Lipoprotein (a) reduces platelet aggregation via apo(a)-mediated decreases in thromboxane A(2)production. Platelets 1998; 9:93–96.
Barre DE. Apolipoprotein (a) mediates the lipoprotein (a)-induced biphasic shift in human platelet cyclic AMP. Thromb Res 2003; 112:321–324.
Barre DE. Apoprotein (A) antagonises THE GPIIB/IIIA receptor on collagen and adp-stimulated human platelets. Front Biosci 2004; 9:404–410.
Barre DE. Arginyl-glycyl-aspartyl (RGD) epitope of human apolipoprotein (a) inhibits platelet aggregation by antagonizing the IIb subunit of the fibrinogen (GPIIb/IIIa) receptor. Thromb Res 2007; 119:601–607.
Zhu P, Tang XF, Song Y, et al. Association of lipoprotein(a) with platelet aggregation and thrombogenicity in patients undergoing percutaneous coronary intervention. Platelets 2021; 32:684–689.
Cui K, Yin D, Zhu C, et al. How do lipoprotein(a) concentrations affect clinical outcomes for patients with stable coronary artery disease who underwent different dual antiplatelet therapy after percutaneous coronary intervention? J Am Heart Assoc 2022; 11:e023578.
Chasman DI, Shiffman D, Zee RY, et al. Polymorphism in the apolipoprotein(a) gene, plasma lipoprotein(a), cardiovascular disease, and low-dose aspirin therapy. Atherosclerosis 2009; 203:371–376.
Shiffman D, Chasman DI, Ballantyne CM, et al. Coronary heart disease risk, aspirin use, and apolipoprotein(a) 4399Met allele in the Atherosclerosis Risk in Communities (ARIC) study. Thromb Haemost 2009; 102:179–180.
Lacaze P, Bakshi A, Riaz M, et al. Aspirin for primary prevention of cardiovascular events in relation to lipoprotein(a) genotypes. J Am Coll Cardiol 2022; 80:1287–1298.