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Interleukin 10: A new risk marker for the development of restenosis after percutaneous coronary intervention

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Author: Monraats, P.S. · Kurreeman, F.A.S. · Pons, D. · Sewgobind, V.D.K.D. · Vries, F.R. de · Zwinderman, A.H. · Maat, M.P.M. de · Doevendans, P.A. · Winter, R.J. de · Tio, R.A. · Waltenberger, J. · Huizinga, T.W.J. · Eefting, D. · Quax, P.H.A. · Frants, R.R. · Laarse, A. van der · Wall, E.E. van der · Jukema, J.W.
Type:article
Date:2007
Institution: TNO Kwaliteit van Leven
Source:Genes and Immunity, 1, 8, 44-50
Identifier: 239819
doi: doi:10.1038/sj.gene.6364343
Keywords: Health · Biomedical Research · alanine · clopidogrel · cysteine · glycine · interleukin 10 · ticlopidine · adult · aged · article · cardiovascular risk · confidence interval · controlled study · coronary artery bypass graft · disease marker · DNA flanking region · DNA microarray · drug eluting stent · female · gene linkage disequilibrium · gene locus · genetic association · genetic polymorphism · genetic predisposition · genetic risk · genetic variability · genotype · heart infarction · human · hypothesis · in-stent restenosis · major clinical study · male · pathogenesis · percutaneous coronary intervention · priority journal · risk factor · 3' Untranslated Regions · Aged · Angioplasty, Transluminal, Percutaneous Coronary · Coronary Restenosis · Female · Genetic Predisposition to Disease · Genotype · Humans · Inflammation · Interleukin-10 · Male · Middle Aged · Polymorphism, Genetic · Promoter Regions (Genetics) · Prospective Studies · Risk Factors · Treatment Outcome

Abstract

Genetic factors appear to be important in the process of restenosis after percutaneous coronary intervention (PCI), as well as in inflammation, a pivotal factor in restenosis. An important mediator in the inflammatory response is interleukin (IL)-10. Our aim was to study whether genetic variants in IL-10 predispose to the risk of restenosis. The GENetic DEterminants of Restenosis (GENDER) study included 3104 patients treated with successful PCI. Target vessel revascularization (TVR) was chosen as primary end point. Genotyping of the -2849G/A, -1082G/A, -592C/A and +4259A/G polymorphisms of the IL-10 gene was performed by MassArray platform. After adjusting for clinical variables, three polymorphisms significantly increased the risk of restenosis (-2849AA: relative risk (RR), 1.7, 95% confidence interval (CI), 1.2-2.5; -1082AA: RR, 1.4, 95% CI, 1.1-1.8 and +4259GG: RR, 2.0, 95% CI, 1.4-2.8). To further exclude possible involvement of neighboring genes due to LD in the IL-10 locus, additional polymorphisms were genotyped. The results reveal that association of the IL-10 gene with restenosis is independent of flanking genes. Our findings demonstrate that IL-10 is associated with restenosis and therefore support the hypothesis that anti-inflammatory genes also may be involved in developing restenosis. Furthermore, they may provide a new targeting gene for drug-eluting stents.