Steeds R, Adams M, Smith P, Channer K, Samani N J
Department of Cardiology, University of Leicester, United Kingdom.
Thromb Haemost. 1998 May;79(5):980-4.
An insertion (I)/deletion (D) polymorphism in the tissue plasminogen activator (TPA) gene locus has recently been reported to be associated with the risk of myocardial infarction (MI) with increased risk in II/ID subjects compared with DD subjects. To investigate this further, we analysed 529 acute MI cases and 525 population-based control subjects recruited in two centers (Leicester and Sheffield, UK). We found no difference between cases and controls in TPA I/D allele frequencies (cases I = 0.574, controls I = 0.582, p = 0.74) or genotype distribution (cases II 33%, ID 48%, DD 19%; controls II 34%, ID 49%, DD 17%, p = 0.88). Compared with the DD genotype, the age, sex and centre adjusted odds ratios for MI for II genotype was 0.95 (95% confidence interval, 0.64-1.40, p = 0.85) and that for ID genotype was 0.89 (0.62-1.27, p = 0.56). There was no significant effect modification by smoking status, body mass index or cholesterol level. There was no difference in the reported frequency of positive family history of coronary heart disease or mean age at MI in the different genotype groups. We conclude that in our populations the TPA I/D polymorphism is not a major independent risk factor for myocardial infarction.
组织纤溶酶原激活物（TPA）基因位点的插入（I）/缺失（D）多态性最近被报道与心肌梗死（MI）风险相关，与DD型受试者相比，II/ID型受试者的风险增加。为进一步研究这一问题，我们分析了在两个中心（英国莱斯特和谢菲尔德）招募的529例急性心肌梗死病例和525例基于人群的对照受试者。我们发现病例组和对照组在TPA I/D等位基因频率（病例组I = 0.574，对照组I = 0.582，p = 0.74）或基因型分布（病例组II 33%，ID 48%，DD 19%；对照组II 34%，ID 49%，DD 17%，p = 0.88）上没有差异。与DD基因型相比，II基因型心肌梗死的年龄、性别和中心校正比值比为0.95（95%置信区间，0.64 - 1.40，p = 0.85），ID基因型为0.89（0.62 - 1.27，p = 0.56）。吸烟状况、体重指数或胆固醇水平没有显著的效应修饰作用。不同基因型组中冠心病阳性家族史的报告频率或心肌梗死的平均年龄没有差异。我们得出结论，在我们的人群中，TPA I/D多态性不是心肌梗死的主要独立危险因素。
