Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk

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dc.contributor.author Merhi, Mahmoud
dc.contributor.author Demirdjian, Sally
dc.contributor.author Hariri, Essa
dc.contributor.author Sabbah, Nada
dc.contributor.author Youhanna, Sonia
dc.contributor.author Ghassibe-Sabbagh, Michella
dc.contributor.author Naoum, Joseph
dc.contributor.author Haber, Marc
dc.contributor.author Kanbar, Roy en_US
dc.contributor.author Zalloua, Pierre en_US
dc.contributor.author Khazen, Georges en_US
dc.date.accessioned 2016-03-17T09:19:37Z
dc.date.available 2016-03-17T09:19:37Z
dc.date.copyright 2015
dc.date.issued 2016-03-17
dc.identifier.issn 1023-3830 en_US
dc.identifier.uri http://hdl.handle.net/10725/3347
dc.description.abstract Background The role of inflammation in coronary artery disease (CAD) pathogenesis is well recognized. Moreover, smoking inhalation increases the activity of inflammatory mediators through an increase in leukotriene synthesis essential in atherosclerosis pathogenesis. Aim The aim of this study is to investigate the effect of “selected” genetic variants within the leukotriene (LT) pathway and other variants on the development of CAD. Methods CAD was detected by cardiac catheterization. Logistic regression was performed to investigate the association of smoking and selected susceptibility variants in the LT pathway including ALOX5AP, LTA4H, LTC4S, PON1, and LTA as well as CYP1A1 on CAD risk while controlling for age, gender, BMI, family history, diabetes, hyperlipidemia, and hypertension. Results rs4769874 (ALOX5AP), rs854560 (PON1), and rs4646903 (CYP1A1 MspI polymorphism) are significantly associated with an increased risk of CAD with respective odds ratios of 1.53703, 1.67710, and 1.35520; the genetic variant rs9579646 (ALOX5AP) is significantly associated with a decreased risk of CAD (OR 0.76163). Moreover, a significant smoking-gene interaction is determined with CYP1A1 MspI polymorphism rs4646903 and is associated with a decreased risk of CAD in current smokers (OR 0.52137). Conclusion This study provides further evidence that genetic variation of the LT pathway, PON1, and CYP1A1 can modulate the atherogenic processes and eventually increase the risk of CAD in our study population. Moreover, it also shows the effect of smoking-gene interaction on CAD risk, where the CYP1A1 MspI polymorphism revealed a decreased risk in current smokers. en_US
dc.language.iso en en_US
dc.title Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk en_US
dc.type Article en_US
dc.description.version Published en_US
dc.author.school SAS en_US
dc.author.idnumber 201005298 en_US
dc.author.idnumber 200300001
dc.author.idnumber 201105253
dc.author.woa N/A en_US
dc.author.department Computer Science and Mathematics en_US
dc.description.embargo N/A en_US
dc.relation.journal Inflammation Research en_US
dc.journal.volume 64 en_US
dc.journal.issue 6 en_US
dc.article.pages 415-422 en_US
dc.keywords CAD en_US
dc.keywords Inflammation en_US
dc.keywords Leukotriene en_US
dc.keywords Smoking-gene en_US
dc.keywords Interaction en_US
dc.identifier.doi http://dx.doi.org/10.1007/s00011-015-0821-1 en_US
dc.identifier.ctation Merhi, M., Demirdjian, S., Hariri, E., Sabbah, N., Youhanna, S., Ghassibe-Sabbagh, M., ... & Chammas, E. (2015). Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk. Inflammation Research, 64(6), 415-422. en_US
dc.author.email roy.kanbar@lau.edu.lb
dc.author.email pierre.zalloua@lau.edu.lb
dc.author.email GKhazen@lau.edu.lb
dc.identifier.url http://link.springer.com/article/10.1007/s00011-015-0821-1
dc.orcid.id https://orcid.org/0000-0001-5450-6443
dc.orcid.id https://orcid.org/0000-0002-8494-5081 en_US

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