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首页> 外文期刊>Journal of cardiovascular risk >Genetic polymorphism of platelet glycoprotein IIIa in patients with acute myocardial infarction and acute ischaemic stroke.
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Genetic polymorphism of platelet glycoprotein IIIa in patients with acute myocardial infarction and acute ischaemic stroke.

机译:急性心肌梗死和急性缺血性卒中患者血小板糖蛋白IIIa的遗传多态性。

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摘要

BACKGROUND: It has recently been suggested that the Leu33Pro polymorphism of the platelet glycoprotein IIIa affects the risk of coronary thrombosis. Finland is genetically isolated and has an incidence of cardiovascular disease among the highest in the world. Interestingly, the prevalence of ischaemic heart disease also varies in different parts of the country, being highest in eastern Finland. METHOD: We studied the Leu33Pro polymorphism using polymerase chain reaction in 133 patients with coronary artery disease, 234 patients with cerebrovascular disease and 326 control subjects originating from two areas of Finland. RESULTS: The frequencies of the Pro33 allele in the patients with acute myocardial infarction and cerebrovascular attack were 13% and 14%, respectively, and did not differ from the controls (13%). Among patients with acute myocardial infarction from the Helsinki area, the family history of premature coronary artery disease was more often positive in carriers of the Pro33 allele than in non-carriers, but after adjustment for multiple comparisons the difference was no longer significant. CONCLUSIONS: We could not confirm the original observation that the Pro33 allele constitutes an independent risk factor for coronary artery disease. Further studies are needed to clarify whether co-occurrence of Pro33 and some unrecognized inherited factor pose an additional risk of vascular disease.
机译:背景:最近有人提出,血小板糖蛋白IIIa的Leu33Pro多态性会影响冠状动脉血栓形成的风险。芬兰是基因分离的国家,心血管疾病的发病率居世界之首。有趣的是,缺血性心脏病的患病率在该国不同地区也有所不同,在芬兰东部最高。方法:我们使用聚合酶链反应研究了133名冠心病,234名脑血管病和326名来自芬兰两个地区的对照组的Leu33Pro多态性。结果:急性心肌梗死和脑血管发作患者的Pro33等位基因频率分别为13%和14%,与对照组(13%)没有差异。在来自赫尔辛基地区的急性心肌梗死患者中,Pro33等位基因携带者的早发冠心病家族史多于非携带者,但经过多次比较校正后,差异不再显着。结论:我们不能证实Pro33等位基因构成冠心病独立危险因素的原始观察结果。需要进一步的研究来阐明Pro33和某些无法识别的遗传因子的同时存在是否会增加血管疾病的风险。

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