Factor VIII, von Willebrand factor and the risk of major ischaemic heart disease in the Caerphilly Heart Study
Factor VIII, von Willebrand factor and the risk of major ischaemic heart disease in the Caerphilly Heart Study
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DOI：
10.1111/j.1365-2141.1999.01317.x
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发表时间：
1999-04-01
影响因子：
6.5
通讯作者：
Ford, RP
中科院分区：
文献类型：
--
作者：
Rumley, A;Lowe, GDO;Ford, RP
在卡氏心脏研究的第二阶段，对1997年49-65岁男性的/血管性血友病因子(VWF)复合体(因子活性FVIIIc(一期法)、VWF抗原VWF Ag(酶联免疫吸附试验)和VWF活性(VWF ACT)三项测定)与主要缺血性心脏病事件的关系进行了研究。使用Logistic回归分析将这些变量与129名男性在平均61个月的随访期内发生的心肌梗死或IHD死亡相关。所有这三项测量都高度相关(r=0.63-0.77)，在单变量分析(相对危险度最高的五分之一与最低的五分之一的相对优势为1.68-1.9；P=0.028-0.006)以及调整了主要的缺氧性心脏病危险因素和基线缺氧性心脏病的多变量分析中，每一项都与发生的主要缺氧性心脏病显著相关。经VWF Ag调整后，FVIIIc和VWF ACT与IHD事件均无明显关联。因此，我们认为，因子VIII/VWF复合体的这三种测量结果与IHD事件之间的关联可能至少有三种解释：VWF Ag是动脉内皮细胞紊乱的标志；VWF ACT促进血小板黏附/聚集，从而促进动脉血栓形成的血小板成分；FVIIIc促进纤维蛋白形成，从而促进动脉血栓形成的纤维蛋白成分。
The relationships of three measurements of the factor VIII/von Willebrand factor (VWF) complex (factor VIII activity, FVIIIc (one-stage assay); VWF antigen, VWF Ag (ELISA); and VWF activity, VWF act, measured by a recently-developed ELISA) to major ischaemic heart disease (IHD) events were studied in 1997 men aged 49-65 years, in the second phase of the Caerphilly Heart Study. These variables were related using logistic regression analysis to myocardial infarction or IHD death, which occurred in 129 men during an average follow-up period of 61 months. All three measurements were highly correlated (r=0.63-0.77), and each was significantly associated with incident major IHD on univariate analyses (relative odds in highest fifth compared to lowest fifth, 1.68-1.90; P=0.028-0.006) and on multivariate analyses adjusting for major IHD risk factors and for baseline IHD. Neither FVIIIc nor VWF act was significantly related to incident IHD following adjustment for VWF Ag. We therefore suggest that the associations between these three measurements of the factor VIII/VWF complex and incident IHD might have at least three explanations: VWF Ag is a marker of arterial endothelial disturbance; VWF act promotes platelet adhesion/aggregation and hence the platelet component of arterial thrombosis; and FVIIIc promotes fibrin formation and hence the fibrin component of arterial thrombosis.