Søren Zöga Diederichsen1, Mette Hjortdal Grønhøj2, Hans Mickley3, Oke Gerke4, Flemming Hald Steffensen5, Jess Lambrechtsen6, Niels Peter Rønnow Sand7, Lars Melholt Rasmussen8, Michael Hecht Olsen9, Axel Diederichsen10. 1. Department of Cardiology, Rigshospitalet, Copenhagen University Hospital, Blegdamsvej, Copenhagen, Denmark. Electronic address: Soeren.Zoega.Diederichsen@regionh.dk. 2. Department of Cardiology, Odense University Hospital, Odense, Denmark; Centre for Individualized Medicine in Arterial Diseases, Odense University Hospital, Odense, Denmark. 3. Department of Cardiology, Odense University Hospital, Odense, Denmark. 4. Department of Nuclear Medicine, Odense University Hospital, Odense, Denmark; Centre of Health Economics Research, University of Southern Denmark, Odense, Denmark. 5. Department of Cardiology, Sygehus Lillebælt Vejle, Vejle, Denmark. 6. Department of Cardiology, Svendborg Hospital, Svendborg, Denmark. 7. Department of Cardiology, Hospital of South West Denmark, Esbjerg, Denmark; Institute of Regional Health Services Research, University of Southern Denmark, Odense, Denmark. 8. Centre for Individualized Medicine in Arterial Diseases, Odense University Hospital, Odense, Denmark; Department of Clinical Biochemistry and Pharmacology, Odense University Hospital, Odense, Denmark; Cardiovascular Centre of Excellence, University of Southern Denmark, Odense, Denmark. 9. Centre for Individualized Medicine in Arterial Diseases, Odense University Hospital, Odense, Denmark; Cardiovascular Centre of Excellence, University of Southern Denmark, Odense, Denmark; Cardiology Section, Department of Internal Medicine, Holbæk Hospital, Holbæk, Denmark. 10. Department of Cardiology, Odense University Hospital, Odense, Denmark; Centre for Individualized Medicine in Arterial Diseases, Odense University Hospital, Odense, Denmark; Cardiovascular Centre of Excellence, University of Southern Denmark, Odense, Denmark.
Abstract
OBJECTIVES: This study sought to determine the incidence and progression of coronary artery calcification (CAC) in asymptomatic middle-aged subjects and to evaluate the value of a broad panel of biomarkers in the prediction of CAC growth. BACKGROUND: CAC continues to be a major risk factor, but the value of biochemical markers in predicting CAC incidence and progression remains unresolved. METHODS: At baseline, 1,227 men and women underwent traditional risk assessment and a computed tomography (CT) scan to determine the CAC score. Biomarkers of calcium-phosphate metabolism (calcium, phosphate, vitamin D3, parathyroid hormone, osteoprotegerin), lipid metabolism (triglyceride, high- and low-density lipoprotein, total cholesterol), inflammation (C-reactive protein, soluble urokinase-type plasminogen activator receptor), kidney function (creatinine, cystatin C, urate), and myocardial necrosis (cardiac troponin I) were analyzed. A second CT scan was scheduled after 5 years. General linear models were performed to examine the association between biomarkers and ΔCAC score, and additionally, sensitivity analyses were performed in terms of binary and ordinal logistic regressions. RESULTS: A total of 1,006 participants underwent a CT scan after 5 years. Among the 562 participants with a baseline CAC score of 0, 189 (34%) had incident CAC, whereas 214 (48%) of the 444 participants with baseline CAC score >0 had significant progression (>15% annual increase in CAC score). In the multivariate models (n = 1,006), age, sex, hypertension, diabetes, dyslipidemia, and smoking were associated with ΔCAC, whereas the strongest predictor was baseline CAC score. Low-density lipoprotein and total cholesterol levels were independently associated with CAC incidence (n = 562; incidence rate ratio [IRR]: 1.47; 95% confidence interval [CI]: 1.05 to 2.05; and IRR: 1.34; 95% CI: 1.01 to 1.77, respectively), whereas phosphate level was associated with CAC progression (n = 444; IRR: 3.60; 95% CI: 1.42 to 9.11). CONCLUSIONS: In this prospective study, a large part of participants had incident CAC or progression of prevalent CAC at 5 years of follow-up. Low-density lipoprotein and total cholesterol were associated with CAC incidence and phosphate with CAC progression, whereas 12 other biomarkers had little value.
OBJECTIVES: This study sought to determine the incidence and progression of coronary artery calcification (CAC) in asymptomatic middle-aged subjects and to evaluate the value of a broad panel of biomarkers in the prediction of CAC growth. BACKGROUND: CAC continues to be a major risk factor, but the value of biochemical markers in predicting CAC incidence and progression remains unresolved. METHODS: At baseline, 1,227 men and women underwent traditional risk assessment and a computed tomography (CT) scan to determine the CAC score. Biomarkers of calcium-phosphate metabolism (calcium, phosphate, vitamin D3, parathyroid hormone, osteoprotegerin), lipid metabolism (triglyceride, high- and low-density lipoprotein, total cholesterol), inflammation (C-reactive protein, soluble urokinase-type plasminogen activator receptor), kidney function (creatinine, cystatin C, urate), and myocardial necrosis (cardiac troponin I) were analyzed. A second CT scan was scheduled after 5 years. General linear models were performed to examine the association between biomarkers and ΔCAC score, and additionally, sensitivity analyses were performed in terms of binary and ordinal logistic regressions. RESULTS: A total of 1,006 participants underwent a CT scan after 5 years. Among the 562 participants with a baseline CAC score of 0, 189 (34%) had incident CAC, whereas 214 (48%) of the 444 participants with baseline CAC score >0 had significant progression (>15% annual increase in CAC score). In the multivariate models (n = 1,006), age, sex, hypertension, diabetes, dyslipidemia, and smoking were associated with ΔCAC, whereas the strongest predictor was baseline CAC score. Low-density lipoprotein and total cholesterol levels were independently associated with CAC incidence (n = 562; incidence rate ratio [IRR]: 1.47; 95% confidence interval [CI]: 1.05 to 2.05; and IRR: 1.34; 95% CI: 1.01 to 1.77, respectively), whereas phosphate level was associated with CAC progression (n = 444; IRR: 3.60; 95% CI: 1.42 to 9.11). CONCLUSIONS: In this prospective study, a large part of participants had incident CAC or progression of prevalent CAC at 5 years of follow-up. Low-density lipoprotein and total cholesterol were associated with CAC incidence and phosphate with CAC progression, whereas 12 other biomarkers had little value.
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