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C-Reactive Protein Concentrations Are Very High and More Stable over Time Than the Traditional Vascular Risk Factors Total Cholesterol and Systolic Blood Pressure in an Australian Aboriginal Cohort

¹ Menzies School of Health Research, John Mathews Building, Royal Darwin Hospital, Darwin, NT, Australia;² Institute of Advanced Studies, Charles Darwin University, Darwin, NT, Australia;³ The University of Melbourne, Department of Medicine, St Vincent’s Hospital, Fitzroy, VIC, Australia;⁴ Onemda VicHealth Koori Health Unit, Centre for Health and Society, School of Population Health, The University of Melbourne, Parkville, VIC, Australia.

^aAddress correspondence to this author at: Onemda VicHealth Koori Health Unit, Centre for Health and Society, School of Population Health, The University of Melbourne, Parkville, VIC 3010, Australia. Fax +61-3-8344 0824; e-mail rowleyk{at}unimelb.edu.au.

Background: Stability of circulating high-sensitivity C-reactive protein (hsCRP) concentrations has implications for its utility in assessing cardiovascular disease (CVD) risk. We sought to determine hsCRP reproducibility in an indigenous Australian cohort with a view to use hsCRP as a marker of future CVD in community-based risk-factor screenings.

Methods: Seventy people living in a community on the northern coast of Australia participated in 2 risk-factor screenings over a median (interquartile range) follow-up time of 829 (814–1001) days. hsCRP was measured by high-sensitivity nephelometry.

Results: Geometric mean hsCRP concentrations at baseline and follow-up were 4.5 and 5.1 mg/L, respectively (P = 0.220), and Pearson product-moment correlation was 0.775. The proportion of people at high CVD risk (hsCRP >3.0 mg/L) at baseline was 67.1% and remained consistently high (68.6%) at follow-up. Linear regression analysis for follow-up hsCRP as a function of baseline hsCRP, sex, and differences in total and regional body fatness showed that baseline hsCRP was the single predictor in the model, accounting for 63.9% of the total variance in follow-up hsCRP (P_model < 0.001). Prevalence agreement (95% CI) between baseline and follow-up for the hsCRP >3.0 mg/L category was 84% (73%–92%) (P_McNemar = not significant), and coefficient was fair (0.64, compared with 0.31 for systolic blood pressure 140 mmHg and 0.43 for total cholesterol 5.5 mmol/L).

Conclusions: hsCRP concentrations remained consistently reproducible over time across a wide concentration range in an Aboriginal cohort. Correlations between concentrations over time were better than for other traditional CVD risk factors. hsCRP concentration has potential as a marker of future CVD risk.