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      Association between Thrombomodulin Polymorphisms and Coronary Artery Disease Risk: A Meta-Analysis

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          Abstract

          Background

          The associations between the thrombomodulin (TM) polymorphisms and coronary artery disease (CAD) risk remain controversial. The aim of this study was to evaluate the association of TM polymorphisms with CAD susceptibility using a meta-analysis approach.

          Material/Methods

          All eligible studies were identified through a search of PubMed, EMBASE, and China National Knowledge Infrastructure (CNKI) before February 2014. The associations between the TM polymorphisms and CAD risk was assessed by odds ratios (ORs) and 95% confidence intervals (CIs).

          Results

          A total of 14 case-control studies, including 5493 cases and 8297 controls, were eventually collected. There was a significant association between TM -33G/A polymorphism and CAD risk (OR=1.61; 95% CI, 1.35–1.92; I 2 =15%). The TM Ala455Val polymorphism was also associated with a significantly increased CAD risk (OR=1.14; 95% CI, 1.05–1.24; I 2 =0%). These results remained statistically significant when the adjusted ORs were combined.

          Conclusions

          Our results suggest that TM-33G/A and Ala455Val polymorphisms are risk factors for CAD.

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          Most cited references20

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          Structure and function of thrombomodulin: a natural anticoagulant.

          P Majerus, W Dittman (1990)
          Article 0 comments Cited 23 times – based on 0 reviews     Review now
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            Thrombomodulin Ala455Val polymorphism and risk of coronary heart disease.

            Haejun Ahn, E Boerwinkle, A Folsom … (2001)
            Thrombomodulin (TM) is expressed on the endothelial surface and plays an important role in vasoprotection. A common polymorphism of TM at amino acid position 455 with an alanine (A) to valine (V) transition was previously reported to be associated cross-sectionally with acute myocardial infarction. Whether this single nucleotide polymorphism predicts risk of developing coronary heart disease (CHD) is unclear. Within a large cohort study, we identified 467 incident CHD cases during an average of 5 years of follow-up. We determined TM-455 genotypes on 376 CHD cases (23% black, 77% white) and a reference sample of 461. The AA genotype was significantly more prevalent in noncases than in cases (P:=0.016). The prevalences of the AA genotype in noncase blacks and whites were 93% and 67%, respectively. The AA genotype frequency was significantly reduced in black cases versus noncases (P:=0.018). It was also lower in white cases than in noncases, but the difference was not statistically significant (P:=0.066). Weighted proportional hazards regression analysis after adjustment for age, sex, and other CHD risk factors showed that having the V allele increased risk of CHD by 6.1-fold (risk ratio 6.1, 95% CI 1.7 to 22.9) in blacks but did not significantly increase the risk in whites. The TM A455V polymorphism predicts risk of developing CHD in blacks.
            Article 0 comments Cited 13 times – based on 0 reviews     Review now
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              Interaction between soluble thrombomodulin and intercellular adhesion molecule-1 in predicting risk of coronary heart disease.

              Eric Boerwinkle, Harinder Juneja, William Wu … (2003)
              Results from previous ARIC (Atherosclerosis Risk In Communities) analyses indicate that soluble intercellular adhesive molecule-1 (sICAM) and soluble thrombomodulin (sTM) levels are associated with risk of coronary heart disease (CHD) in an opposite direction. A high sICAM level increases the risk of CHD, whereas a high level of sTM has a lower risk of CHD. It was unclear whether there was an interaction between sTM and sICAM. Using a nested case-cohort design, we measured sTM and sICAM in 317 incident CHD cases and 726 non-cases from the ARIC participants. Consistent with our previous reports, sICAM values in the upper versus the lower tertile increased the risk of CHD event by approximately 2-fold (95% confidence interval [CI], 1.46 to 2.87) whereas sTM values in the lower versus the upper tertile increased CHD risk by approximately 4-fold (95% CI, 2.80 to 5.74). Interaction between these 2 parameters was determined by weighted Cox proportional hazard regression. A significant interaction (P=0.038) was noted. Combinatorial analysis shows a significant increase in CHD risk ratio (RR) (4.66, 95% CI, 1.89 to 11.46) of the lower sTM/upper sICAM group versus the upper sTM/lower sICAM group. Individuals whose sTM values were in the upper tertile had a RR below 1, even when sICAM were in the upper tertile. The RR of lower tertile sTM was increased by sICAM in a tertile-dependent manner. Weighted Cox proportional hazard analysis shows a significant interaction between sTM and sICAM in predicting risk of CHD event. Combinatorial analysis reveals that an upper tertile sICAM had a significant increase in the risk of a CHD event only when sTM was in the lower tertile.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Med Sci Monit
                Journal ID (iso-abbrev): Med. Sci. Monit
                Journal ID (publisher-id): Medical Science Monitor
                Title: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research
                Publisher: International Scientific Literature, Inc.
                ISSN (Print): 1234-1010
                ISSN (Electronic): 1643-3750
                Publication date Collection: 2014
                Publication date (Electronic): 10 August 2014
                Volume: 20
                Pages: 1407-1414
                Affiliations
                Emergency Center, Ji’nan Sixth People’s Hospital, Zhangqiu, Shandong Province, China
                Author notes
                Corresponding Author: Siliang Zheng, e-mail: zhengsl0531@ 123456163.com
                [A]

                Study Design

                [B]

                Data Collection

                [C]

                Statistical Analysis

                [D]

                Data Interpretation

                [E]

                Manuscript Preparation

                [F]

                Literature Search

                [G]

                Funds Collection

                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: 890717
                DOI: 10.12659/MSM.890717
                PMC ID: 4138070
                PubMed ID: 25108690
                SO-VID: 69b5df8c-68a8-4035-8fa2-42ce1a30fc34
                Copyright © © Med Sci Monit, 2014
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License

                History
                Date received : 18 March 2014
                Date accepted : 03 April 2014
                Categories
                Subject: Review Articles

                Keywords: coronary artery disease,genetics,meta-analysis,thrombomodulin
                Data availability:
                Keywords: coronary artery disease, genetics, meta-analysis, thrombomodulin

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