von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects - The Hoorn study
von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects - The Hoorn study
复制标题
DOI：
10.1161/01.atv.19.12.3071
复制
发表时间：
1999-12-01
影响因子：
8.7
通讯作者：
Stehouwer, CDA
中科院分区：
文献类型：
--
作者：
Jager, A;van Hinsbergh, VWM;Stehouwer, CDA
在选定的人群中，von Willebrand因子(VWF)和C反应蛋白(CRP)水平的升高可以预测心血管死亡率。目前还不确定VWF和CRP是否预测普通人群的死亡率，以及VWF和CRP是否通过类似的途径预测死亡率。这项研究调查了糖尿病和非糖尿病受试者中VWF和CRP与心血管疾病和全因死亡率的关系。前瞻性地对年龄、性别和糖耐量分层样本(n=631)进行了为期5年的前瞻性跟踪调查。经过5年的随访，58名受试者死亡(24人死于心血管疾病)。在调整了年龄、性别和糖耐量状态后，上三分位数的vWF(>；1.56IU/mL)和C-反应蛋白(>；2.84 mg/L)水平分别与心血管死亡率增加3倍和2倍相关。对非糖尿病和糖尿病受试者的分析分别得出了类似的结果。在进一步调整高血压、高密度脂蛋白胆固醇和甘油三酯水平、吸烟习惯、缺血性心脏病和外周动脉疾病后，VWF和CRP的相对危险度(RR)分别为3.0(95%CI 1.2~7.9)和1.4(95%CI 0.6~3.5)。当VWF和CRP同时包括在后一个多因素分析中时，RRS为3.0(95%CI)。VWF为1.1~7.9)，CRP为1.3(95%CI为0.5~3.4)。VWF与心血管死亡风险之间的关联与血型无关(O型与非O型)，而且，在不同血型的受试者中也是相似的。重复对全因死亡率的分析，对CRP得出类似的结果。对于VWF，在调整所有其他危险因素后，RR为2.0(95%可信区间1.1~3.5)。在糖尿病和非糖尿病受试者中，VWF水平的升高与心血管疾病和各种原因的死亡率独立相关。C反应蛋白水平升高与心血管死亡率之间的关联部分由其他危险因素解释。VWF和CRP的相互调整没有明显改变结果，支持VWF和CRP通过不同的途径预测死亡率的假设。
Increased levels of von Willebrand factor (vWf) and C-reactive protein (CRP) predict cardiovascular mortality in selected populations. It is uncertain whether vWf and CRP predict mortality in a general population and whether vWf and CRP predict mortality through similar pathways. This study investigated the association of vWf and CRP with cardiovascular and all-cause mortality among diabetic and nondiabetic subjects. An age-, sex-, and glucose tolerance-stratified sample (n=631) of a population-based cohort aged 50 to 75 years was followed prospectively for 5 years. After 5 years of follow-up, 58 subjects had died (24 of cardiovascular causes). vWf (>1.56 IU/mL) and CRP (>2.84 mg/L) levels in the upper tertile were associated with, respectively, a 3- and 2-fold increase in cardiovascular mortality after adjustment for age, sex, and glucose tolerance status. Analyses in nondiabetic and diabetic subjects separately gave similar results. After further adjustment for hypertension, levels of HDL cholesterol and triglyceride, smoking habits, ischemic heart disease, and peripheral arterial disease, the relative risks (RRs) were 3.0 (95% CI 1.2 to 7.9) for vWf and 1.4 (95% CI 0.6 to 3.5) for CRP. When both vWf and CRP were included in the latter multivariate analysis, the RRs were 3.0 (95% CI. 1.1 to 7.9) for vWf and 1.3 (95% CI 0.5 to 3.4) for CRP. The association between vWf and risk of cardiovascular mortality was independent of blood group (O versus non-O) and, moreover, similar among subjects with different blood groups. Repeating the analyses for all-cause mortality gave similar results for CRP. For vWf, the RR was 2.0 (95% CI 1.1 to 3.5) after adjustment for all other risk factors. Increased levels of vWf are independently associated with cardiovascular and all-cause mortality in both diabetic and nondiabetic subjects. The association between increased levels of CRP and cardiovascular mortality was partly explained by other risk factors. Mutual adjustment of vWf and CRP did not markedly change the results, favoring the hypothesis that vWf and CRP predict mortality through different pathways.