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Are functional and genetic components of platelets linked to coronary artery disease: A case-control study.

机译：血小板与冠状动脉疾病相关的功能和遗传成分：病例对照研究。

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摘要

Coronary artery disease (CAD) is a multifactorial disease process involving behavioral, inflammatory, clinical, thrombotic, and genetic components. Previous epidemiologic studies focused on identifying behavioral and demographic risk factors of CAD, but none focused on platelets. Current platelet literature lacks the known effects of platelet function and platelet receptor polymorphisms on CAD. This case-control analysis addressed these issues by analyzing data collected for a previous study. Cases were individuals who had undergone CABG and thus had been diagnosed with CAD, while the controls were volunteers presumed to be CAD free. The platelet function variables analyzed included fibrinogen Von Willebrand Factor activity (VWF), shear-induced platelet aggregation (SIPA), sCD40L, and mean platelet volume; and the platelet polymorphisms studied included PIA, alpha2 807, Ko, Kozak, and VNTR. Univariate analysis found fibrinogen, VWF, SIPA, and PIA to be independent risk factors of CAD. Logistic regression was used to build a predictive model for CAD using the platelet function and platelet polymorphism data adjusted for age, sex, race, and current smoking status. A model containing only platelet polymorphisms and their respective receptor densities, found polymorphisms within GPIbalpha to be associated with CAD, yielding an 86% (95% C.I. 0.97--3.55) increased risk with the presence of at least 1 polymorphism in Ko, Kozak, or VNTR. Another model included both platelet function and platelet polymorphism data. Fibrinogen, the receptor density of GPIbalpha, and the polymorphism in GPIa-IIa (alpha2 807) were all associated with CAD with odds ratios of 1.10, 1.04, and 2.30 for fibrinogen (10mg/dl increase), GPIbalpha receptors (1 MFI increase), and GPIa-IIa, respectively. In addition, risk estimates and 99% confidence intervals adjusted for race were calculated to determine if the presence of a platelet receptor polymorphism was associated with CAD. The results were as follows: PIA (1.64, 0.74--3.65); alpha2 807 (1.35, 0.77--2.37); Ko (1.71, 0.70--4.16); Kozak (1.17, 0.54--2.52); and VNTR (1.24, 0.52--2.91). Although not statistically significant, all platelet polymorphisms were associated with an increased risk for CAD. These exploratory findings indicate that platelets do appear to have a role in atherosclerosis and that anti-platelet drugs targeting GPI-IIa and GPIbalpha may be better treatment candidates for individuals with CAD.
机译：冠状动脉疾病（CAD）是一种多因素疾病过程，涉及行为，炎症，临床，血栓形成和遗传因素。以前的流行病学研究集中于确定CAD的行为和人口统计学危险因素，但没有一个集中于血小板。当前的血小板文献缺乏血小板功能和血小板受体多态性对CAD的已知作用。这种病例对照分析通过分析为先前研究收集的数据解决了这些问题。病例是经历过CABG并因此被诊断出患有CAD的个体，而对照组是被假定为无CAD的志愿者。分析的血小板功能变量包括纤维蛋白原冯·威勒布兰德因子活性（VWF），剪切诱导的血小板聚集（SIPA），sCD40L和平均血小板体积。研究的血小板多态性包括PIA，alpha2 807，Ko，Kozak和VNTR。单因素分析发现纤维蛋白原，VWF，SIPA和PIA是CAD的独立危险因素。使用血小板功能和针对年龄，性别，种族和当前吸烟状况进行调整的血小板多态性数据，使用Logistic回归建立CAD的预测模型。在仅包含血小板多态性及其各自受体密度的模型中，发现GPIbalpha中的多态性与CAD相关联，在Ko，Kozak，Kozak和Kosak的至少1种多态性的存在下，风险增加了86％（95％CI 0.97--3.55）。或VNTR。另一个模型包括血小板功能和血小板多态性数据。纤维蛋白原，GPIbalpha的受体密度和GPIa-IIa（alpha2 807）的多态性均与CAD相关，纤维蛋白原的比值比分别为1.10、1.04和2.30（增加10mg / dl），GPIbalpha受体（增加1 MFI） ，和GPIa-IIa。此外，计算了风险估计值和针对种族调整的99％置信区间，以确定血小板受体多态性的存在是否与CAD相关。结果如下：PIA（1.64，0.74--3.65）; alpha2 807（1.35，0.77--2.37）; Ko（1.71，0.70--4.16）; Kozak（1.17，0.54--2.52）;和VNTR（1.24，0.52--2.91）。尽管无统计学意义，但所有血小板多态性均与CAD风险增加相关。这些探索性发现表明，血小板似乎确实在动脉粥样硬化中起作用，并且针对GPI-IIa和GPIbalpha的抗血小板药物可能是CAD患者更好的候选治疗药物。

著录项

  • 作者

    Wood, Jennifer Jean.;

  • 作者单位

    The University of Texas School of Public Health.;

  • 授予单位 The University of Texas School of Public Health.;
  • 学科 Health Sciences Public Health.; Biology Genetics.; Biology Biostatistics.
  • 学位 Ph.D.
  • 年度 2004
  • 页码 83 p.
  • 总页数 83
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 预防医学、卫生学;遗传学;生物数学方法;
  • 关键词

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