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首页> 外文期刊>Platelets >Platelet glycoprotein IIIa Leu33Pro gene polymorphism and coronary artery disease: A meta-analysis of cohort studies
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Platelet glycoprotein IIIa Leu33Pro gene polymorphism and coronary artery disease: A meta-analysis of cohort studies

机译：血小板糖蛋白IIIa Leu33Pro基因多态性与冠状动脉疾病：一项队列研究的荟萃分析

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Great interest has been focused in the last year on genetic predictors of cardiovascular risk. Glycoprotein IIb/IIIa (GP IIb/IIIa), fibrinogen receptor, is the final common pathway for aggregation and a key point for atherothrombosis. A single nucleotide polymorphism of IIIa subunit (Leu33Pro-PlA(1)/PlA(2) allele) has been suggested to increase aggregation and adhesion, however, contrasting reports have been reported so far on its effects on coronary artery disease (CAD). Aim of the current study was to perform a large meta-analysis including cohorts of patients undergoing coronary angiography in order to evaluate whether this polymorphism is associated with coronary artery disease. Literature archives (Pubmed, EMBASE, Cochrane) and main scientific sessions abstracts were scanned for data of consecutive cohorts of patients undergoing coronary angiography, where PlA genotype was assessed. Primary endpoint was the prevalence of CAD. Secondary endpoint was severity of CAD defined as prevalence of multivessel disease (>= 2 vessels). Data from seven studies were extracted, including a final number of 6700 patients. Among them 1893 (28.3%) carried the PlA(2) polymorphism, 163 of them in homozygosis. Angiographically defined CAD was present in 3573 (74.3%) PlA(1)/PlA(1) patients and in 1430 (75.5%) PlA(2) carriers. PlA(2) polymorphism was not associated with an increased prevalence of coronary artery disease, (OR [95% CI] = 1.07 [0.95-1.21], p = 0.28, pheterogeneity = 0.39). Similar results were obtained for multivessel disease (OR [95% CI] = 1.07 [0.95-1.20], p = 0.27, p(heterogeneity) = 0.12). Meta-regression analysis demonstrated a significant inverse relationship between the risk of CAD among the PlA 2 carriers and ageing (r = -0.044, (-0.09, -0.0008), p = 0.046). Present meta-analysis demonstrates that 33Leu -> Pro substitution of GPIIIa does not influence the prevalence and extent of angiographically defined coronary artery disease in general population, although apparently playing a role among younger patients.
机译：去年，人们对心血管风险的遗传预测因子表现出极大的兴趣。糖蛋白IIb / IIIa（GP IIb / IIIa）是纤维蛋白原受体，是聚集的最终常见途径，是动脉粥样硬化形成的关键点。 IIIa亚基（Leu33Pro-PlA（1）/ PlA（2）等位基因）的单核苷酸多态性已被建议增加聚集和粘附，但是，迄今为止，已有报道报道了其对冠状动脉疾病（CAD）的影响。当前研究的目的是进行大型荟萃分析，包括接受冠状动脉造影的患者队列，以评估这种多态性是否与冠状动脉疾病有关。扫描文献档案（Pubmed，EMBASE，Cochrane）和主要的科学摘要，以获取进行冠脉造影的患者连续队列数据，并评估PlA基因型。主要终点是CAD的患病率。次要终点为CAD的严重程度，定义为多支血管病变的患病率（> = 2支血管）。提取了来自七项研究的数据，包括最终的6700名患者。其中1893（28.3％）位携带PlA（2）多态性，其中163位处于纯合状态。血管造影定义的CAD存在于3573（74.3％）PlA（1）/ PlA（1）患者和1430（75.5％）PlA（2）携带者中。 PlA（2）多态性与冠状动脉疾病的患病率增加无关（OR [95％CI] = 1.07 [0.95-1.21]，p = 0.28，色母性= 0.39）。对于多支血管疾病也获得了相似的结果（OR [95％CI] = 1.07 [0.95-1.20]，p = 0.27，p（异质性）= 0.12）。荟萃回归分析显示，PlA 2携带者的CAD风险与衰老之间存在显着的负相关关系（r = -0.044，（-0.09，-0.0008），p = 0.046）。目前的荟萃分析表明，GPIIIa的33Leu-> Pro替代品不会影响一般人群中由血管造影确定的冠状动脉疾病的发生率和程度，尽管显然在年轻患者中发挥了作用。

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