About: Secretory Phospholipase A(2)-IIA and Cardiovascular Disease     Goto   Sponge   NotDistinct   Permalink

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  • Objectives This study sought to investigate the role of secretory phospholipase A(2) (sPLA(2))-IIA in cardiovascular disease. Background Higher circulating levels of sPLA(2)-IIA mass or sPLA(2) enzyme activity have been associated with increased risk of cardiovascular events. However, it is not clear if this association is causal. A recent phase III clinical trial of an sPLA(2) inhibitor (varespladib) was stopped prematurely for lack of efficacy. Methods We conducted a Mendelian randomization meta-analysis of 19 general population studies (8,021 incident, 7,513 prevalent major vascular events [MVE] in 74,683 individuals) and 10 acute coronary syndrome (ACS) cohorts (2,520 recurrent MVE in 18,355 individuals) using rs11573156, a variant in PLA2G2A encoding the sPLA(2)-IIA isoenzyme, as an instrumental variable. Results PLA2G2A rs11573156 C allele associated with lower circulating sPLA(2)-IIA mass (38% to 44%) and sPLA(2) enzyme activity (3% to 23%) per C allele. The odds ratio (OR) for MVE per rs11573156 C allele was 1.02 (95% confidence interval [CI]: 0.98 to 1.06) in general populations and 0.96 (95% CI: 0.90 to 1.03) in ACS cohorts. In the general population studies, the OR derived from the genetic instrumental variable analysis for MVE for a 1-log unit lower sPLA(2)-IIA mass was 1.04 (95% CI: 0.96 to 1.13), and differed from the non-genetic observational estimate (OR: 0.69; 95% CI: 0.61 to 0.79). In the ACS cohorts, both the genetic instrumental variable and observational ORs showed a null association with MVE. Instrumental variable analysis failed to show associations between sPLA2 enzyme activity and MVE. Conclusions Reducing sPLA(2)-IIA mass is unlikely to be a useful therapeutic goal for preventing cardiovascular events. (C) 2013 by the American College of Cardiology Foundation
  • Objectives This study sought to investigate the role of secretory phospholipase A(2) (sPLA(2))-IIA in cardiovascular disease. Background Higher circulating levels of sPLA(2)-IIA mass or sPLA(2) enzyme activity have been associated with increased risk of cardiovascular events. However, it is not clear if this association is causal. A recent phase III clinical trial of an sPLA(2) inhibitor (varespladib) was stopped prematurely for lack of efficacy. Methods We conducted a Mendelian randomization meta-analysis of 19 general population studies (8,021 incident, 7,513 prevalent major vascular events [MVE] in 74,683 individuals) and 10 acute coronary syndrome (ACS) cohorts (2,520 recurrent MVE in 18,355 individuals) using rs11573156, a variant in PLA2G2A encoding the sPLA(2)-IIA isoenzyme, as an instrumental variable. Results PLA2G2A rs11573156 C allele associated with lower circulating sPLA(2)-IIA mass (38% to 44%) and sPLA(2) enzyme activity (3% to 23%) per C allele. The odds ratio (OR) for MVE per rs11573156 C allele was 1.02 (95% confidence interval [CI]: 0.98 to 1.06) in general populations and 0.96 (95% CI: 0.90 to 1.03) in ACS cohorts. In the general population studies, the OR derived from the genetic instrumental variable analysis for MVE for a 1-log unit lower sPLA(2)-IIA mass was 1.04 (95% CI: 0.96 to 1.13), and differed from the non-genetic observational estimate (OR: 0.69; 95% CI: 0.61 to 0.79). In the ACS cohorts, both the genetic instrumental variable and observational ORs showed a null association with MVE. Instrumental variable analysis failed to show associations between sPLA2 enzyme activity and MVE. Conclusions Reducing sPLA(2)-IIA mass is unlikely to be a useful therapeutic goal for preventing cardiovascular events. (C) 2013 by the American College of Cardiology Foundation (en)
Title
  • Secretory Phospholipase A(2)-IIA and Cardiovascular Disease
  • Secretory Phospholipase A(2)-IIA and Cardiovascular Disease (en)
skos:prefLabel
  • Secretory Phospholipase A(2)-IIA and Cardiovascular Disease
  • Secretory Phospholipase A(2)-IIA and Cardiovascular Disease (en)
skos:notation
  • RIV/00023001:_____/13:00058759!RIV14-MZ0-00023001
http://linked.open...avai/predkladatel
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  • N
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  • 21
http://linked.open...vai/riv/dodaniDat
http://linked.open...aciTvurceVysledku
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http://linked.open...iv/duvernostUdaju
http://linked.open...titaPredkladatele
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  • 104378
http://linked.open...ai/riv/idVysledku
  • RIV/00023001:_____/13:00058759
http://linked.open...riv/jazykVysledku
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  • Mendelian randomization; genetics; epidemiology; drug development; cardiovascular diseases (en)
http://linked.open.../riv/klicoveSlovo
http://linked.open...odStatuVydavatele
  • US - Spojené státy americké
http://linked.open...ontrolniKodProRIV
  • [BA2A64A52CE8]
http://linked.open...i/riv/nazevZdroje
  • Journal of the American College of Cardiology
http://linked.open...in/vavai/riv/obor
http://linked.open...ichTvurcuVysledku
http://linked.open...cetTvurcuVysledku
http://linked.open...UplatneniVysledku
http://linked.open...v/svazekPeriodika
  • 62
http://linked.open...iv/tvurceVysledku
  • Hubáček, Jaroslav
  • …
  • Asselbergs, Folkert W
  • Baldassarre, Damiano
  • Beutner, Frank
  • Boer, Jolanda MA
  • Breitling, Lutz P
  • Brenner, Hermann
  • Brunisholz, Kimberly D
  • Carruthers, Kathryn F
  • Cooper, Jackie A
  • Dallmeier, Dhayana
  • Danchin, Nicolas
  • Dehghan, Abbas
  • Exeter, Holly J
  • Folkersen, Lasse
  • Franco-Cereceda, Anders
  • Gansevoort, Ron T
  • Gertow, Karl
  • Goel, Anuj
  • Guardiola, Montse
  • Haase, Christiane L
  • Hofker, Marten H
  • Hofman, Albert
  • Holdt, Lesca M
  • Holmes, Michael V
  • Horne, Benjamin D
  • Hovingh, G. Kees
  • Kotti, Salma
  • Kuchenbaecker, Karoline B
  • Leach, Irene Mateo
  • Leusink, Maarten
  • Li, Mingyao
  • Mega, Jessica L
  • Navis, Gerjan J
  • Nelson, Christopher P
  • Palmen, Jutta
  • Panayiotou, Andrie G
  • Rothenbacher, Dietrich
  • Scholz, Markus
  • Simon, Tabassome
  • Staines-Urias, Eleonora
  • Stephens, Jeffrey W
  • Swerdlow, Daniel I
  • Tedgui, Alain
  • Thiery, Joachim
  • Tremoli, Elena
  • Trompet, Stella
  • Van Iperen, Erik PA
  • Veglia, Fabrizio
  • Verschuren, Jeffrey JW
  • de Faire, Ulf
  • van 't Hooft, Ferdinand
http://linked.open...ain/vavai/riv/wos
  • 000326939500010
issn
  • 0735-1097
number of pages
http://bibframe.org/vocab/doi
  • 10.1016/j.jacc.2013.06.044
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