Valentina Valenti1, Bríain Ó Hartaigh1, Iksung Cho1, Joshua Schulman-Marcus1, Heidi Gransar1, Ran Heo1, Quynh A Truong1, Leslee J Shaw1, Joseph Knapper1, Anita A Kelkar1, Sebastiano Sciarretta1, Hyuk-Jae Chang1, Tracy Q Callister1, James K Min2. 1. From the Department of Radiology, Dalio Institute of Cardiovascular Imaging, NewYork-Presbyterian Hospital and the Weill Cornell Medical College, New York, NY (V.V., B.ó.H., I.C., R.H., Q.A.T., J.K.M.); Department of Internal Medicine, Section of Geriatrics, Yale School of Medicine, New Haven, CT (B.ó.H.); Department of Medicine, Division of Cardiology, NewYork Presbyterian Hospital/Weill Cornell Medical College, New York, NY (J.S.-M.); Department of Imaging, and Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA (H.G.); Tennessee Heart and Vascular Institute, Hendersonville (T.Q.C.); Department of Internal Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA (L.J.S., J.K., A.A.K.); IRCCS Neuromed, Pozzilli (IS), Italy (S.S.); Department of Medical-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy (S.S.); and Division of Cardiology, Severance Cardiovascular Hospital and Severance Biomedical Science Institute, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea (H.-J.C.). 2. From the Department of Radiology, Dalio Institute of Cardiovascular Imaging, NewYork-Presbyterian Hospital and the Weill Cornell Medical College, New York, NY (V.V., B.ó.H., I.C., R.H., Q.A.T., J.K.M.); Department of Internal Medicine, Section of Geriatrics, Yale School of Medicine, New Haven, CT (B.ó.H.); Department of Medicine, Division of Cardiology, NewYork Presbyterian Hospital/Weill Cornell Medical College, New York, NY (J.S.-M.); Department of Imaging, and Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA (H.G.); Tennessee Heart and Vascular Institute, Hendersonville (T.Q.C.); Department of Internal Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA (L.J.S., J.K., A.A.K.); IRCCS Neuromed, Pozzilli (IS), Italy (S.S.); Department of Medical-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy (S.S.); and Division of Cardiology, Severance Cardiovascular Hospital and Severance Biomedical Science Institute, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea (H.-J.C.). jkm2001@med.cornell.edu.
Abstract
BACKGROUND: Data regarding coronary artery calcification (CAC) prognosis in diabetic individuals are limited to 5-years follow-up. We investigated the long-term risk stratification of CAC among diabetic compared with nondiabetic individuals. METHODS AND RESULTS: Nine thousand seven hundred and fifteen asymptomatic individuals undergoing CAC scoring were followed for a median (interquartile range) of 14.7 (13.9-15.6) years. The incidence density rate and hazard ratios with 95% confidence intervals were used to calculate all-cause mortality. Incremental prognostic utility of CAC was evaluated using the area under the receiver operator characteristic curve and net reclassification improvement. Diabetics (54.7±10.8 years; 59.4% male) comprised 8.3% of the cohort (n=810), of which 188 (23.2%) died. For CAC=0, the rate of mortality was similar between diabetic and nondiabetic individuals for the first 5 years (P>0.05), with a nonlinear increased risk of mortality for diabetics after 5 years (P<0.05). The adjusted risk of death for those in the highest (CAC>400) versus the lowest (CAC=0) category of CAC increased by a hazards of 4.64 (95% confidence interval =3.74-5.76) and 3.41 (95% confidence interval =2.22-5.22) for nondiabetic and diabetic individuals, respectively. The presence of CAC improved discrimination (area under the receiver operator characteristic curve range: 0.73-0.74; P<0.01) and reclassification (category-free net reclassification improvement range: 0.53-0.50; P<0.001) beyond conventional risk factors in nondiabetic and diabetic individuals, respectively. CONCLUSIONS: CAC=0 is associated with a favorable 5-year prognosis for asymptomatic diabetic and nondiabetic individuals. After 5 years, the risk of mortality increases significantly for diabetic individuals even in the presence of a baseline CAC=0.
BACKGROUND: Data regarding coronary artery calcification (CAC) prognosis in diabetic individuals are limited to 5-years follow-up. We investigated the long-term risk stratification of CAC among diabetic compared with nondiabetic individuals. METHODS AND RESULTS: Nine thousand seven hundred and fifteen asymptomatic individuals undergoing CAC scoring were followed for a median (interquartile range) of 14.7 (13.9-15.6) years. The incidence density rate and hazard ratios with 95% confidence intervals were used to calculate all-cause mortality. Incremental prognostic utility of CAC was evaluated using the area under the receiver operator characteristic curve and net reclassification improvement. Diabetics (54.7±10.8 years; 59.4% male) comprised 8.3% of the cohort (n=810), of which 188 (23.2%) died. For CAC=0, the rate of mortality was similar between diabetic and nondiabetic individuals for the first 5 years (P>0.05), with a nonlinear increased risk of mortality for diabetics after 5 years (P<0.05). The adjusted risk of death for those in the highest (CAC>400) versus the lowest (CAC=0) category of CAC increased by a hazards of 4.64 (95% confidence interval =3.74-5.76) and 3.41 (95% confidence interval =2.22-5.22) for nondiabetic and diabetic individuals, respectively. The presence of CAC improved discrimination (area under the receiver operator characteristic curve range: 0.73-0.74; P<0.01) and reclassification (category-free net reclassification improvement range: 0.53-0.50; P<0.001) beyond conventional risk factors in nondiabetic and diabetic individuals, respectively. CONCLUSIONS: CAC=0 is associated with a favorable 5-year prognosis for asymptomatic diabetic and nondiabetic individuals. After 5 years, the risk of mortality increases significantly for diabetic individuals even in the presence of a baseline CAC=0.
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