Promoter polymorphism in the CD14 gene and concentration of soluble CD14 in patients with in-stent restenosis after elective coronary stenting.

Abstract:

BACKGROUND:Activated monocytes/macrophages, neutrophils, endothelial cells and smooth muscle cells participate in the restenosis processes. Monocytes/macrophages and neutrophils are activated by lipopolysaccharide (LPS) via CD14. Endothelial cells and smooth muscle cells are also stimulated by soluble CD14 (sCD14)-LPS complexes. METHODS:We tested the hypothesis that C(-260)-->T polymorphism of the CD14 gene and sCD14 might be predictors for in-stent restenosis. We analyzed 129 consecutive patients who underwent elective coronary stenting. The restenosis was defined as > or =50% diameter stenosis at follow-up angiography. RESULTS:The prevalence of the T/T genotype and the concentration of sCD14 were significantly higher in the restenosis group than in the no-restenosis group. This CD14 polymorphism also affected the levels of sCD14, therefore, we divided the patients into four groups. The loss index was 24.8% in C/C or C/T and < or =50th percentile of sCD14, 35.9% in T/T and < or =50th percentile of sCD14, 44.2% in C/C or C/T and >50th percentile of sCD14, and 49.1% in T/T and >50th percentile of sCD14 (P=0.02). The restenosis rate was 10.0%, 26.7%, 26.2% and 50.0% in each group, respectively (P=0.003). In the multivariate analysis, T/T and >50th percentile of sCD14 was the independent predictor for in-stent restenosis. CONCLUSIONS:This study showed that the T/T genotype with a high level of sCD14 is an independent predictor of in-stent restenosis. The activation of monocytes/macrophages, endothelial cells and smooth muscle cells mediated by CD14 and/or sCD14 may play an important role in the restenosis processes.

journal_name

Int J Cardiol

authors

Shimada K,Miyauchi K,Mokuno H,Watanabe Y,Iwama Y,Shigekiyo M,Matsumoto M,Okazaki S,Tanimoto K,Kurata T,Sato H,Daida H

doi

10.1016/j.ijcard.2003.05.007

subject

Has Abstract

pub_date

2004-03-01 00:00:00

pages

87-92

issue

1

eissn

0167-5273

issn

1874-1754

pii

S0167527303003085

journal_volume

94

pub_type

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