Alexander C Razavi1, S M Iftekhar Uddin2, Zeina A Dardari2, Daniel S Berman3, Matthew J Budoff4, Michael D Miedema5, Albert D Osei2, Olufunmilayo H Obisesan2, Khurram Nasir6, Alan Rozanski7, John A Rumberger8, Leslee J Shaw9, Laurence S Sperling10, Seamus P Whelton2, Martin Bødtker Mortensen11, Michael J Blaha2, Omar Dzaye12. 1. Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Emory Center for Heart Disease Prevention, Emory University School of Medicine, Atlanta, Georgia, USA. 2. Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. 3. Department of Imaging, Cedars-Sinai Medical Center, Los Angeles, California, USA. 4. Lundquist Institute, Harbor-UCLA Medical Center, Torrance, California, USA. 5. Minneapolis Heart Institute and Foundation, Minneapolis, Minnesota, USA. 6. Division of Cardiovascular Prevention and Wellness, Houston Methodist DeBakey Heart and Vascular Center, Houston, Texas, USA. 7. Division of Cardiology, Mount Sinai, St Luke's Hospital, New York, New York, USA. 8. Department of Cardiac Imaging, Princeton Longevity Center, Princeton, New Jersey, USA. 9. Department of Radiology, Weill Cornell Medicine, New York, New York, USA. 10. Emory Center for Heart Disease Prevention, Emory University School of Medicine, Atlanta, Georgia, USA. 11. Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark. 12. Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Electronic address: odzaye@jhmi.edu.
Abstract
BACKGROUND: Coronary artery calcium (CAC) is a marker of plaque burden. Whether CAC improves risk stratification for incident sudden cardiac death (SCD) beyond atherosclerotic cardiovascular disease (ASCVD) risk factors is unknown. OBJECTIVES: SCD is a common initial manifestation of coronary heart disease (CHD); however, SCD risk prediction remains elusive. METHODS: The authors studied 66,636 primary prevention patients from the CAC Consortium. Multivariable competing risks regression and C-statistics were used to assess the association between CAC and SCD, adjusting for demographics and traditional risk factors. RESULTS: The mean age was 54.4 years, 33% were women, 11% were of non-White ethnicity, and 55% had CAC >0. A total of 211 SCD events (0.3%) were observed during a median follow-up of 10.6 years, 91% occurring among those with baseline CAC >0. Compared with CAC = 0, there was a stepwise higher risk (P trend < 0.001) in SCD for CAC 100 to 399 (subdistribution hazard ratio [SHR]: 2.8; 95% CI: 1.6-5.0), CAC 400 to 999 (SHR: 4.0; 95% CI: 2.2-7.3), and CAC >1,000 (SHR: 4.9; 95% CI: 2.6-9.9). CAC provided incremental improvements in the C-statistic for the prediction of SCD among individuals with a 10-year risk <7.5% (ΔC-statistic = +0.046; P = 0.02) and 7.5% to 20% (ΔC-statistic = +0.069; P = 0.003), which were larger when compared with persons with a 10-year risk >20% (ΔC-statistic = +0.01; P = 0.54). CONCLUSIONS: Higher CAC burden strongly associates with incident SCD beyond traditional risk factors, particularly among primary prevention patients with low-intermediate risk. SCD risk stratification can be useful in the early stages of CHD through the measurement of CAC, identifying patients most likely to benefit from further downstream testing.
BACKGROUND: Coronary artery calcium (CAC) is a marker of plaque burden. Whether CAC improves risk stratification for incident sudden cardiac death (SCD) beyond atherosclerotic cardiovascular disease (ASCVD) risk factors is unknown. OBJECTIVES: SCD is a common initial manifestation of coronary heart disease (CHD); however, SCD risk prediction remains elusive. METHODS: The authors studied 66,636 primary prevention patients from the CAC Consortium. Multivariable competing risks regression and C-statistics were used to assess the association between CAC and SCD, adjusting for demographics and traditional risk factors. RESULTS: The mean age was 54.4 years, 33% were women, 11% were of non-White ethnicity, and 55% had CAC >0. A total of 211 SCD events (0.3%) were observed during a median follow-up of 10.6 years, 91% occurring among those with baseline CAC >0. Compared with CAC = 0, there was a stepwise higher risk (P trend < 0.001) in SCD for CAC 100 to 399 (subdistribution hazard ratio [SHR]: 2.8; 95% CI: 1.6-5.0), CAC 400 to 999 (SHR: 4.0; 95% CI: 2.2-7.3), and CAC >1,000 (SHR: 4.9; 95% CI: 2.6-9.9). CAC provided incremental improvements in the C-statistic for the prediction of SCD among individuals with a 10-year risk <7.5% (ΔC-statistic = +0.046; P = 0.02) and 7.5% to 20% (ΔC-statistic = +0.069; P = 0.003), which were larger when compared with persons with a 10-year risk >20% (ΔC-statistic = +0.01; P = 0.54). CONCLUSIONS: Higher CAC burden strongly associates with incident SCD beyond traditional risk factors, particularly among primary prevention patients with low-intermediate risk. SCD risk stratification can be useful in the early stages of CHD through the measurement of CAC, identifying patients most likely to benefit from further downstream testing.
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