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    Genetic variation in PEAR1, cardiovascular outcomes and effects of aspirin in a healthy elderly population

    80128.pdf (11.39Mb)
    Access Status
    Open access
    Authors
    Lewis, J.P.
    Riaz, M.
    Xie, S.
    Polekhina, G.
    Wolfe, R.
    Nelson, M.
    Tonkin, A.M.
    Reid, Christopher
    Murray, A.M.
    McNeil, J.J.
    Shuldiner, A.R.
    Lacaze, P.
    Date
    2020
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Lewis, J.P. and Riaz, M. and Xie, S. and Polekhina, G. and Wolfe, R. and Nelson, M. and Tonkin, A.M. et al. 2020. Genetic variation in PEAR1, cardiovascular outcomes and effects of aspirin in a healthy elderly population. Clinical Pharmacology and Therapeutics. 108 (6): pp. 1289-1298.
    Source Title
    Clinical Pharmacology and Therapeutics
    DOI
    10.1002/cpt.1959
    ISSN
    0009-9236
    Faculty
    Faculty of Health Sciences
    School
    School of Public Health
    Funding and Sponsorship
    http://purl.org/au-research/grants/nhmrc/334047
    http://purl.org/au-research/grants/nhmrc/1127060
    Remarks

    This is the peer reviewed version of the following article: Lewis, J.P. and Riaz, M. and Xie, S. and Polekhina, G. and Wolfe, R. and Nelson, M. and Tonkin, A.M. et al. 2020. Genetic variation in PEAR1, cardiovascular outcomes and effects of aspirin in a healthy elderly population. Clinical Pharmacology and Therapeutics, which has been published in final form at https://doi.org/10.1002/cpt.1959. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.

    URI
    http://hdl.handle.net/20.500.11937/80046
    Collection
    • Curtin Research Publications
    Abstract

    This article is protected by copyright. All rights reserved. The platelet endothelial aggregation receptor-1 (PEAR1) rs12041331 variant has been identified as a genetic determinant of platelet aggregation in response to antiplatelet therapies, including aspirin. However, association with atherothrombotic cardiovascular events is less clear, with limited evidence from large trials. Here, we tested association of rs12041331 with cardiovascular events and aspirin use in a randomized trial population of healthy older individuals. We undertook post-hoc analysis of N=13,547 participants of the ASPirin in Reducing Events in the Elderly (ASPREE) trial, median age 74 years. Participants had no previous diagnosis of atherothrombotic cardiovascular disease at enrolment, and were randomized to either 100 mg daily low-dose aspirin or placebo for median 4.7 years follow-up. We used Cox proportional hazard regression to model the relationship between rs12041331 and the ASPREE primary cardiovascular disease endpoint (CVD), and composites of major adverse cardiovascular events (MACE) and ischaemic stroke (STROKE); and bleeding events; major hemorrhage (MHEM) and intracranial bleeding (ICB). We performed whole-population analysis using additive and dominant inheritance models, then stratified by treatment group. Interaction effects between genotypes and treatment group were examined. We observed no statistically significant association (P<0.05) in the population, or by treatment group, between rs12041331 and cardiovascular or bleeding events in either model. We also found no significant interaction effects between rs12041331-A and treatment group, for CVD (P=0.65), MACE (P=0.32), STROKE (P=0.56), MHEM (P=0.59) or ICB (P=0.56). The genetic variant PEAR1 rs12041331 is not associated with cardiovascular events in response to low-dose aspirin in a healthy elderly population.

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