Setor K Kunutsor1, Jose Luis Flores-Guerrero2, Lyanne M Kieneker2, Tom Nilsen3, Clara Hidden3, Erling Sundrehagen3, Samuel Seidu4, Robin P F Dullaart2, Stephan J L Bakker2. 1. National Institute for Health Research Bristol Biomedical Research Centre, University Hospitals Bristol NHS Foundation Trust and University of Bristol, Bristol, UK; Translational Health Sciences, Bristol Medical School, Musculoskeletal Research Unit, University of Bristol, Learning & Research Building (Level 1), Southmead Hospital, Bristol, BS10 5NB, UK. Electronic address: skk31@cantab.net. 2. Department of Internal Medicine, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands. 3. Gentian, Moss, Norway. 4. Leicester Diabetes Centre, Leicester General Hospital, Gwendolen Road, Leicester, LE5 4WP, UK; Diabetes Research Centre, University of Leicester, Leicester General Hospital, Gwendolen Road, Leicester, LE5 4WP, UK.
Abstract
BACKGROUND AND AIMS: We aimed to assess the association of circulating calprotectin, an inflammation-associated protein, with cardiovascular disease (CVD) risk and determine whether it improves risk prediction. METHODS: Plasma calprotectin measurements were made at baseline in 5290 participants in the PREVEND prospective study. Hazard ratios (95% confidence intervals [CI]) for CVD were calculated. RESULTS: After a median follow-up of 8.3 years, 339 first CVD events were recorded. Calprotectin concentration was correlated with several conventional risk factors as well as with high-sensitivity C-reactive protein (hsCRP) (r = 0.42). Calprotectin was log-linearly associated with CVD risk. The risk for CVD adjusted for conventional cardiovascular risk factors was 1.26 (95% CI, 1.13-1.41) per 1 standard deviation higher baseline loge calprotectin, and was 1.24 (95% CI, 1.11-1.39) following further adjustment for triglycerides, body mass index, and other potential confounders. The association remained present after further adjustment for hsCRP 1.15 (95% CI, 1.02-1.30). Comparing extreme quartiles of plasma calprotectin levels, the corresponding adjusted HRs for CVD were 1.96 (1.37-2.82), 1.89 (1.31-2.72), and 1.56 (1.07-2.29). The association of calprotectin with CVD risk did not vary importantly in several relevant clinical subgroups. Adding calprotectin to the Framingham CVD Risk Score was associated with a C-index change (0.0016; p=0.42) difference in -2 log likelihood (p=0.038), IDI (0.0080; p < 0.001), and NRI (4.03%; p=0.024). CONCLUSIONS: There is a log-linear association of calprotectin concentration with risk of CVD, which may be partly dependent on hsCRP. Adding calprotectin to conventional risk factors improves CVD risk assessment using measures of reclassification and -2 log likelihood.
BACKGROUND AND AIMS: We aimed to assess the association of circulating calprotectin, an inflammation-associated protein, with cardiovascular disease (CVD) risk and determine whether it improves risk prediction. METHODS: Plasma calprotectin measurements were made at baseline in 5290 participants in the PREVEND prospective study. Hazard ratios (95% confidence intervals [CI]) for CVD were calculated. RESULTS: After a median follow-up of 8.3 years, 339 first CVD events were recorded. Calprotectin concentration was correlated with several conventional risk factors as well as with high-sensitivity C-reactive protein (hsCRP) (r = 0.42). Calprotectin was log-linearly associated with CVD risk. The risk for CVD adjusted for conventional cardiovascular risk factors was 1.26 (95% CI, 1.13-1.41) per 1 standard deviation higher baseline loge calprotectin, and was 1.24 (95% CI, 1.11-1.39) following further adjustment for triglycerides, body mass index, and other potential confounders. The association remained present after further adjustment for hsCRP 1.15 (95% CI, 1.02-1.30). Comparing extreme quartiles of plasma calprotectin levels, the corresponding adjusted HRs for CVD were 1.96 (1.37-2.82), 1.89 (1.31-2.72), and 1.56 (1.07-2.29). The association of calprotectin with CVD risk did not vary importantly in several relevant clinical subgroups. Adding calprotectin to the Framingham CVD Risk Score was associated with a C-index change (0.0016; p=0.42) difference in -2 log likelihood (p=0.038), IDI (0.0080; p < 0.001), and NRI (4.03%; p=0.024). CONCLUSIONS: There is a log-linear association of calprotectin concentration with risk of CVD, which may be partly dependent on hsCRP. Adding calprotectin to conventional risk factors improves CVD risk assessment using measures of reclassification and -2 log likelihood.
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