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OBJECTIVE: To evaluate the association between vascular inflammation as measured by subacute C-reactive protein (CRP; 1-10 mg/l) and all-cause mortality and the association between change in CRP status (normal 3 mg/l) and all-cause mortality. METHODS: Probabilistic record linkage was used to match hospital episode data, laboratory reports and mortality statistics in a large urban population. Survival was evaluated using Cox proportional hazards regression models. RESULTS: 22 962 patients had their first CRP measurement in the subacute range (1-10 mg/l). Analysis grouped by each additional unit increase in CRP across the subacute range was associated with a 7.3% (95% CI 5.4% to 9.2%) increase in the hazard ratio (HR) of death over 4 years, after controlling for confounding factors (p3 mg/l), the HR increased 6.7-fold (p<0.001) relative to cases whose CRP remained normal. By comparison, among those subjects whose CRP was reduced from elevated to normal, the hazard ratio halved to 3.5 (p = 0.018). In an underpowered analysis of time to cardiovascular events, an identical pattern of risk emerged. CONCLUSIONS: CRP level predicted all-cause mortality, and additional inclusion of prior change in CRP level and current CRP level more so. Increasing vascular inflammation, as measured by CRP, increases the likelihood of death.
Currie et al. (Wed,) studied this question.