Smoking induces lipoprotein-associated phospholipase A(2) in cardiovascular disease free adults: The ATTICA Study

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dc.contributor.authorTselepis, A. D.en
dc.contributor.authorPanagiotakos, D. B.en
dc.contributor.authorPitsavos, C.en
dc.contributor.authorTellis, C. C.en
dc.contributor.authorChrysohoou, C.en
dc.contributor.authorStefanadis, C.en
dc.date.accessioned2015-11-24T16:47:27Z
dc.date.available2015-11-24T16:47:27Z
dc.identifier.issn0021-9150-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/9186
dc.rightsDefault Licence-
dc.subjectatherosclerosisen
dc.subjectcardiovascular diseaseen
dc.subjectinflammationen
dc.subjectlp-pla(2)en
dc.subjectsmokingen
dc.subjectplatelet-activating-factoren
dc.subjectfactor-acetylhydrolase activityen
dc.subjectcigarette-smokingen
dc.subjecthuman plasmaen
dc.subjectsecondhand smokeen
dc.subjectblood-plasmaen
dc.subjectrisk-factorsen
dc.subjectdense ldlen
dc.subjectpaf-ahen
dc.subjectinflammationen
dc.titleSmoking induces lipoprotein-associated phospholipase A(2) in cardiovascular disease free adults: The ATTICA Studyen
heal.abstractObjectives: We studied the association of lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) mass and activity with various lifestyle, clinical and biochemical characteristics in cardiovascular disease (CVD) free adults. Background: Lipoprotein-associated phospholipase A(2) is a novel biomarker of inflammation and risk for CVD. The Lp-PLA(2) mass and activity are primarily influenced by the plasma levels of low-density lipoprotein (LDL), however, the influence of various lifestyle characteristics on Lp-PLA(2) have not been adequately studied. Methods and results: In a random sub-sample of 186 subjects, 64 men (52 +/- 13 years) and 122 women (48 +/- 13 years) from the ATTICA Study (Greece), LP-PLA(2) activity and mass in total plasma as well as the enzyme activity and mass associated with high-density lipoprotein (HDL-Lp-PLA(2)) were determined using established methods. Several socio-demographic, lifestyle, clinical and biochemical parameters were assessed in all participants. Multiple linear regression analysis revealed that among the lifestyle characteristics, total plasma Lp-PLA(2) activity and mass were positively and independently associated with current smoking (p = 0.02 and p = 0.05, respectively), as well as with exposure to second-hand smoke (p = 0.02 and p = 0.01, respectively). Furthermore, HDL-Lp-PLA(2) activity and mass were inversely and independently associated with current smoking (p = 0.04 and p = 0.09, respectively). Conclusions: Smoking is associated with and might even induce an increase in proatherogenic total plasma Lp-PLA(2), but attenuates antiatherogenic HDL-Lp-PLA(2). These results further support the role of smoking as an important avoidable cause of CVD. (C) 2009 Elsevier Ireland Ltd. All rights reserved.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.primaryDOI 10.1016/j.atherosclerosis.2009.02.016-
heal.identifier.secondary<Go to ISI>://000270002000049-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0021915009001439/1-s2.0-S0021915009001439-main.pdf?_tid=3bf49dc78a0db9dfb8b07ae5006969d4&acdnat=1333112226_2b43b2a8e83fd64b217007232e3daec5-
heal.journalNameAtherosclerosisen
heal.journalTypepeer reviewed-
heal.languageen-
heal.publicationDate2009-
heal.publisherElsevier Irelanden
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείαςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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