Fredrik Olson1, Jonathan Engborg2, Mette H Grønhøj2, Niels P Sand3, Jess Lambrechtsen4, Flemming H Steffensen5, Mads Nybo6, Oke Gerke7, Hans Mickley2, Axel C P Diederichsen8. 1. Department of Cardiology, Odense University Hospital, Sdr. Boulevard 29, Dk-5000, Odense C, Denmark. Electronic address: fredrik.anders.olsson@rsyd.dk. 2. Department of Cardiology, Odense University Hospital, Sdr. Boulevard 29, Dk-5000, Odense C, Denmark. 3. Department of Cardiology, Sydvestjyst Hospital, Finsensgade 35, DK-6700, Esbjerg, Denmark. 4. Department of Cardiology, Svendborg Hospital, Valdemarsgade 53, DK-5700, Svendborg, Denmark. 5. Department of Cardiology, Vejle Hospital, Kabbeltoft 25, DK-7100, Vejle, Denmark. 6. Department of Clinical Biochemistry, Odense University Hospital, Sdr. Boulevard 29, DK-5000, Odense C, Denmark. 7. Department of Nuclear Medicine, Odense University Hospital, Sdr. Boulevard 29, DK-5000, Odense C, Denmark. 8. Department of Cardiology, Odense University Hospital, Sdr. Boulevard 29, Dk-5000, Odense C, Denmark. Electronic address: Axel.Diederichsen@rsyd.dk.
Abstract
BACKGROUND:High-sensitive troponin I (hs-TnI) is an individual predictor of future cardiovascular disease (CVD). However, the relationship between hs-TnI and coronary artery calcification (CAC) as determined by computed tomography (CT) has not previously been investigated in a general population. METHODS: 1173 randomized, middle-aged subjects without known CVD underwent a non-contrast cardiac-CT scan for CAC determination. Hs-TnI was detected using ARCHITECT STAT High Sensitive Troponin-I immunoassay. Total 10-year cardiovascular mortality risk was estimated using HeartScore. The relationship between hs-TnI and CAC was assessed using logistic regression analyses and receiver operating characteristic curves (ROC). RESULTS:Concentrations of hs-TnI above the limit of detection were measured in 89.3% of all subjects. Presence of CAC (Agatston score >0) was detected in 29% in the lowest hs-TnI quartile compared with 55% in the highest, with a stepwise increase over the quartiles. In fully adjusted regression models with dichotomous CAC outcomes, hs-TnI was able to predict presence of CAC (OR: 1.25, 95% CI: 1.03-1.51, p = 0.025) and an Agatston score >100 (OR: 1.36, 95% CI: 1.08-1.71, p = 0.009). Subjects in the fourth hs-TnI quartile had an increased risk for presence of CAC (OR: 1.56, 95% CI: 1.06-2.26, p = 0.024) and for an Agatston score >100 (OR: 1.82, 95% CI: 1.04-3.18, p = 0.035), when compared with the first quartile. Addition of hs-TnI to HeartScore improved the ROCAUC from 0.671 to 0.695 (p < 0.0001). CONCLUSION: Hs-TnI was associated with CAC in a Danish middle-aged population without previously known CVD. This is a step towards understanding hs-TnI as a risk marker for CVD.
RCT Entities:
BACKGROUND: High-sensitive troponin I (hs-TnI) is an individual predictor of future cardiovascular disease (CVD). However, the relationship between hs-TnI and coronary artery calcification (CAC) as determined by computed tomography (CT) has not previously been investigated in a general population. METHODS: 1173 randomized, middle-aged subjects without known CVD underwent a non-contrast cardiac-CT scan for CAC determination. Hs-TnI was detected using ARCHITECT STAT High Sensitive Troponin-I immunoassay. Total 10-year cardiovascular mortality risk was estimated using HeartScore. The relationship between hs-TnI and CAC was assessed using logistic regression analyses and receiver operating characteristic curves (ROC). RESULTS: Concentrations of hs-TnI above the limit of detection were measured in 89.3% of all subjects. Presence of CAC (Agatston score >0) was detected in 29% in the lowest hs-TnI quartile compared with 55% in the highest, with a stepwise increase over the quartiles. In fully adjusted regression models with dichotomous CAC outcomes, hs-TnI was able to predict presence of CAC (OR: 1.25, 95% CI: 1.03-1.51, p = 0.025) and an Agatston score >100 (OR: 1.36, 95% CI: 1.08-1.71, p = 0.009). Subjects in the fourth hs-TnI quartile had an increased risk for presence of CAC (OR: 1.56, 95% CI: 1.06-2.26, p = 0.024) and for an Agatston score >100 (OR: 1.82, 95% CI: 1.04-3.18, p = 0.035), when compared with the first quartile. Addition of hs-TnI to HeartScore improved the ROCAUC from 0.671 to 0.695 (p < 0.0001). CONCLUSION: Hs-TnI was associated with CAC in a Danish middle-aged population without previously known CVD. This is a step towards understanding hs-TnI as a risk marker for CVD.
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