Objective To evaluate the association between vascular inflammation as measured by sub-acute C-reactive protein (CRP; 1 - 10mg/L) and all-cause mortality and the association between change in change in CRP status (normal, ≤3mg/L and elevated >3mg/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 (CPHM).
Results 22,982 cases had their first CRP measurement in the sub-acute range (1 - 10mg/L). Analysis grouped by each additional unit increase in CRP across the sub-acute range was associated with a 7.3% increase in the hazard ratio (HR) of death over four years, after controlling for confounding factors (p < 0.001). Repeated CRP observations around one year apart were recorded in 5,811 subjects. After controlling for confounding factors, in cases whose CRP changed from normal (≤ 3 mg/L) to elevated (> 3 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.
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