Correlation of factor VIIa values with factor VII gene polymorphism, fasting and postprandial triglyceride levels, and subclinical carotid atherosclerosis
Correlation of factor VIIa values with factor VII gene polymorphism, fasting and postprandial triglyceride levels, and subclinical carotid atherosclerosis
复制标题
DOI：
10.1161/01.cir.98.25.2815
复制
发表时间：
1998-12-22
期刊：
影响因子：
37.8
通讯作者：
Wu, KK
中科院分区：
文献类型：
--
作者：
Ghaddar, HM;Folsom, AR;Wu, KK
背景-因子VII在凝血中起关键作用。据报道，因子VIIc水平是致死性冠心病（CHD）的危险因素。凝血因子VIIc和VIIag水平与血浆甘油三酯（TG）水平呈正相关，并受VII基因多态性的影响。本研究的目的是确定这些协会是否与激活因子VII（因子VIIa）。方法和结果空腹和3.5小时餐后样本从216例亚临床动脉粥样硬化和341匹配的对照组从ARIC队列中选择的因子VIIa，VIIc，VIIag和TG的水平进行了测定，因子VII密码子353基因多态性。Arg/Arg基因型的凝血因子VIIa水平高于Arg/Gln+Gln/Gln基因型，其差异与凝血因子VIIag、VIIc的差异雅阁。然而，因子VIIa差异在统计学上不显着。因子VIIa值与空腹或餐后3.5小时TG水平无关，也与亚临床atherosclerosis. Conclusions因子VIIa水平，如因子VIIag和VIIc水平，受因子VII基因密码子353多态性的影响。然而，与因子VIIag或VIIc不同，因子VIIa不受TG水平的影响;这些都与亚临床动脉粥样硬化无关。
Background-Factor VII plays a pivotal role in coagulation. Factor VIIc levels were reported to be a risk factor for fatal coronary heart disease (CHD). Factor VIIc and VIIag levels were noted to be positively associated with plasma triglyceride (TG) levels and influenced by a VII gene polymorphism. The purpose of this study is to determine whether these associations are related to activated factor VII (factor VIIa).Methods and Results-Fasting and 3.5-hour postprandial samples from 216 cases with subclinical atherosclerosis and 341 matched controls selected from the ARIC cohort were assayed for levels of factors VIIa, VIIc, and VIIag and TG, and factor VII codon 353 gene polymorphism. The level of factor VIIa was higher in Arg/Arg than in Arg/Gln+Gln/Gln genotypes, and the difference was in accord with that of factors VIIag and VIIc. However, the factor VIIa difference was statistically insignificant. Factor VIIa values were not correlated with fasting or 3.5-hour postprandial TG levels, nor were they associated with subclinical atherosclerosis.Conclusions-Factor VIIa levels, like factor VIIag and VIIc levels, are influenced by factor VII gene codon 353 polymorphism. However, unlike factor VIIag or VIIc, factor VIIa is not influenced by TG levels; none of these is associated with subclinical atherosclerosis.