Heywood D M, Carter A M, Catto A J, Bamford J M, Grant P J
Division of Medicine, School of Medicine, University of Leeds, UK.
Stroke. 1997 Apr;28(4):816-21. doi: 10.1161/01.str.28.4.816.
FVII:C has been shown to be an independent risk factor for myocardial infarction and is related to environmental and genetic factors. This study sought to investigate FVII:C levels and factor VII (FVII) gene polymorphisms in relation to stroke and disease outcome.
To examine the association of FVII:C and the Msp I and promoter insertion polymorphisms of the FVII gene in acute stroke, 317 patients and 198 age-matched control subjects were studied.
FVII:C levels were significantly lower in patients at onset than 3 months later (119% versus 135%, respectively; P < .0005). Levels were significantly lower in patients at onset than in control subjects (124% [95% confidence interval, 120% to 129%] versus 141% [95% confidence interval, 135% to 148%], respectively; P < .0005) but were not significantly different at 3 months (135% [95% confidence interval, 128% to 141%] versus 141% [95% confidence interval, 135% to 148%], respectively). We found no difference in genotype distribution for either polymorphism between patients and control subjects, no difference in FVII:C level or genotype distribution between pathological types of stroke, and no relationship with poststroke mortality. Both polymorphisms were significantly associated with FVII:C levels in patients and control subjects. In a multiple regression model for patients, Msp I genotype, cholesterol, and smoking remained as independent predictors of FVII:C levels, accounting for 32% of interindividual variation.
These results suggest that neither FVII:C levels nor FVII gene polymorphisms are associated with cerebrovascular disease. There were no genotype-specific correlations of environmental factors with FVII:C, but there was evidence of an acute-phase or consumptive fall in FVII:C levels at the time of stroke, whereas levels increased to those similar for healthy age-matched control subjects by 3 months, when the acute phase had presumably subsided.
已有研究表明，FVII:C是心肌梗死的独立危险因素，且与环境和遗传因素相关。本研究旨在探讨FVII:C水平及凝血因子VII（FVII）基因多态性与中风及疾病转归的关系。
为研究急性中风患者中FVII:C以及FVII基因的Msp I和启动子插入多态性之间的关联，我们对317例患者和198例年龄匹配的对照者进行了研究。
发病时患者的FVII:C水平显著低于发病3个月后（分别为119%和135%；P <.0005）。发病时患者的FVII:C水平显著低于对照者（分别为124% [95%置信区间，120%至129%]和141% [95%置信区间，135%至148%]；P <.0005），但在3个月时两者无显著差异（分别为135% [95%置信区间，128%至141%]和141% [95%置信区间，135%至148%]）。我们发现患者与对照者在任何一种多态性的基因型分布上均无差异，中风不同病理类型之间的FVII:C水平或基因型分布也无差异，且与中风后死亡率无关。两种多态性在患者和对照者中均与FVII:C水平显著相关。在患者的多元回归模型中，Msp I基因型、胆固醇和吸烟仍是FVII:C水平的独立预测因素，可解释个体间变异的32%。
这些结果表明，FVII:C水平和FVII基因多态性均与脑血管疾病无关。环境因素与FVII:C之间不存在基因型特异性关联，但有证据表明中风时FVII:C水平出现急性期下降或消耗性降低，而在3个月时，当急性期可能已消退时，其水平升高至与年龄匹配的健康对照者相似。
