No association between thrombospondin-4 A387P polymorphism and acute coronary syndrome in Chinese Han population

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• 作者：Guoping He ; Lei Gao ; Jizheng Ma ; Guoying Yang ; Hengfang Wu ; Xiangjian Chen ; Zhiping Bian ; Di Yang ; Jinan Zhang
• 关键词：thrombospondin ; polymorphism ; acute coronary syndrome
• 刊名：Journal of Nanjing Medical University
• 出版年：2007
• 出版时间：March 2007
• 年：2007
• 卷：21
• 期：2
• 页码：77-81
• 全文大小：486 K

文摘

The thrombospondin-4 (TSP-4) gene G29926C (A387P) polymorphism was recently reported to be associated with an increased risk of MI (myocardial infarction) in American population. However, several subsequent studies produced controversial findings. The aim of this study was to explore the possible association between TSP-4 A387P polymorphism and ACS (acute coronary syndrome) in Chinese Han population.

Methods

A case-control study including 412 patients with ACS and 337 controls free from CAD (coronary artery disease) was conducted. TSP-4 A387P polymorphism was determined by PCR (polymerase chain reaction) and RFLP (restriction fragment length polymorphism) analysis.

Results

Slightly decreased frequency of GC genotype was observed in patients with ACS, compared with controls (5.3 % vs. 7.1 % ), but the difference did not reach statistical significance (P = 0.31). Similarly, the prevalence of C allele was 2.7 % and 3.6 % for ACS and control groups, respectively (P = 0.32). None of homozygote was detected for C allele. Further analyses in subjects subgrouped according to sex and age also showed no association of TSP-4 A387P polymorphism with ACS. Furthermore, after adjustment for conventional risk factors by multiple logistic regression analysis, the carrier prevalence of C allele did not differ significantly between ACS and control groups (OR = 0.85; 95 % CI: 0.45-1.59; P = 0.60).

Conclusion

The present study suggested that the TSP-4 A387P variant showed a low prevalence compared with western populations and failed to associate with an altered risk of ACS in Chinese Han population. The findings further supplement experimental data for TSP-4 gene study of coronary disease.