von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects - The Hoorn study

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 investig ated the association of vWf and CRP with cardiovascular and all-cause morta lity among diabetic and nondiabetic subjects. An age-, sex-, and glucose to lerance-stratified sample (n=631) of a population-based cohort aged 50 to 7 5 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, respecti vely, a 3- and 2-fold increase in cardiovascular mortality after adjustment for age, sex, and glucose tolerance status. Analyses in nondiabetic and di abetic subjects separately gave similar results. After further adjustment f or hypertension, levels of HDL cholesterol and triglyceride, smoking habits , ischemic heart disease, and peripheral arterial disease, the relative ris ks (RRs) were 3.0 (95% CI 1.2 to 7.9) for vWf and 1.4 (95% CI 0.6 to 3.5) f or CRP. When both vWf and CRP were included in the latter multivariate anal ysis, 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 mortal ity 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 level s of vWf are independently associated with cardiovascular and all-cause mor tality in both diabetic and nondiabetic subjects. The association between i ncreased levels of CRP and cardiovascular mortality was partly explained by other risk factors. Mutual adjustment of vWf and CRP did not markedly chan ge the results, favoring the hypothesis that vWf and CRP predict mortality through different pathways.