Mette Hjortdal Sørensen1, Oke Gerke2, Jesper Eugen-Olsen3, Henrik Munkholm4, Jess Lambrechtsen5, Niels Peter Rønnow Sand6, Hans Mickley7, Lars Melholt Rasmussen8, Michael Hecht Olsen9, Axel Diederichsen10. 1. Department of Cardiology, Odense University Hospital, Sdr. Boulevard 29, 5000 Odense C, Denmark; Centre for Individualized Medicine in Arterial Diseases (CIMA), Odense University Hospital, Sdr. Boulevard 29, 5000 Odense C, Denmark. Electronic address: mettehjortdal@gmail.com. 2. Department of Nuclear Medicine, Odense University Hospital, Sdr. Boulevard 29, 5000 Odense, Denmark; Centre of Health Economics Research, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark. 3. Clinical Research Centre, Copenhagen University Hospital, Kettegård Allé 30, 2650 Hvidovre, Denmark. 4. Department of Cardiology, Vejle Hospital, Kabbeltoft 25, 7100 Vejle, Denmark. 5. Department of Cardiology, Svendborg Hospital, Valdemarsgade 53, 5700 Svendborg, Denmark. 6. Department of Cardiology, Centre Sydvestjylland, Finsensgade 35, 6700 Esbjerg, Denmark; Institute of Regional Health Services Research, University of Southern Denmark, Winsløwparken 19, 3., 5000 Odense C, Denmark. 7. Department of Cardiology, Odense University Hospital, Sdr. Boulevard 29, 5000 Odense C, Denmark. 8. Centre for Individualized Medicine in Arterial Diseases (CIMA), Odense University Hospital, Sdr. Boulevard 29, 5000 Odense C, Denmark; Department of Clinical Biochemistry and Pharmacology, Odense University Hospital, Sdr. Boulevard 29, 5000 Odense C, Denmark. 9. Centre for Individualized Medicine in Arterial Diseases (CIMA), Odense University Hospital, Sdr. Boulevard 29, 5000 Odense C, Denmark; The Cardiovascular and Metabolic Preventive Clinic, Department of Endocrinology, Odense University Hospital, Sdr. Boulevard 29, 5000 Odense C, Denmark. 10. Department of Cardiology, Odense University Hospital, Sdr. Boulevard 29, 5000 Odense C, Denmark; Centre for Individualized Medicine in Arterial Diseases (CIMA), Odense University Hospital, Sdr. Boulevard 29, 5000 Odense C, Denmark.
Abstract
OBJECTIVE: The main objective of this study was to investigate the association between two markers of low-grade inflammation; soluble urokinase plasminogen activator receptor (suPAR) and high-sensitive C-reactive protein (hs-CRP); and coronary artery calcification (CAC) score detected by cardiac computed tomography (CT) scan. DESIGN: A cross sectional study of 1126 randomly sampled middle-aged men and women. METHODS: CAC score was measured by a non-contrast cardiac CT scan and total 10-year cardiovascular mortality risk was estimated using the Systematic Coronary Risk Evaluation (SCORE). Plasma samples were analysed for suPAR and hs-CRP. The association of suPAR and hs-CRP to CAC was evaluated by logistic regression analyses adjusting for categorised SCORE. The additive effect of suPAR to SCORE was evaluated by comparing area under curve (AUC) and net reclassification improvement (NRI). RESULTS: The odds of being in a higher CAC category, i.e. having more severe CAC, increased 16% (odds ratio (OR) 1.16, p = 0.02) when plasma suPAR concentration increased 1 ng/ml, and this was more pronounced in women (OR 1.30, p = 0.01) than in men (OR 1.15, p = 0.05). In comparison, hs-CRP was not associated with CAC category (OR 1.00, p = 0.90). When adding suPAR to categorised SCORE, AUC increased from 0.66 to 0.70 (p = 0.04) in women and from 0.65 to 0.68 (p = 0.03) in men. NRI was significant in men (NRI 19.3%, 95% CI 6.1-32.6, p = 0.004) as well as in women (NRI 20.8%, 95%CI 1.0-40.7, p = 0.04), without significant gender difference. CONCLUSIONS: suPAR, but not hs-CRP, appeared to be associated with CAC score independently of SCORE. The association was strongest in women.
OBJECTIVE: The main objective of this study was to investigate the association between two markers of low-grade inflammation; soluble urokinase plasminogen activator receptor (suPAR) and high-sensitive C-reactive protein (hs-CRP); and coronary artery calcification (CAC) score detected by cardiac computed tomography (CT) scan. DESIGN: A cross sectional study of 1126 randomly sampled middle-aged men and women. METHODS: CAC score was measured by a non-contrast cardiac CT scan and total 10-year cardiovascular mortality risk was estimated using the Systematic Coronary Risk Evaluation (SCORE). Plasma samples were analysed for suPAR and hs-CRP. The association of suPAR and hs-CRP to CAC was evaluated by logistic regression analyses adjusting for categorised SCORE. The additive effect of suPAR to SCORE was evaluated by comparing area under curve (AUC) and net reclassification improvement (NRI). RESULTS: The odds of being in a higher CAC category, i.e. having more severe CAC, increased 16% (odds ratio (OR) 1.16, p = 0.02) when plasma suPAR concentration increased 1 ng/ml, and this was more pronounced in women (OR 1.30, p = 0.01) than in men (OR 1.15, p = 0.05). In comparison, hs-CRP was not associated with CAC category (OR 1.00, p = 0.90). When adding suPAR to categorised SCORE, AUC increased from 0.66 to 0.70 (p = 0.04) in women and from 0.65 to 0.68 (p = 0.03) in men. NRI was significant in men (NRI 19.3%, 95% CI 6.1-32.6, p = 0.004) as well as in women (NRI 20.8%, 95%CI 1.0-40.7, p = 0.04), without significant gender difference. CONCLUSIONS:suPAR, but not hs-CRP, appeared to be associated with CAC score independently of SCORE. The association was strongest in women.
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