Joonseok Kim1, Matthew J Budoff2, Khurram Nasir3, Nathan D Wong4, Joseph Yeboah5, Mouaz H Al-Mallah6, Steve Shea7, Zeina A Dardari8, Roger S Blumenthal8, Michael J Blaha9, Miguel Cainzos-Achirica10. 1. Division of Cardiovascular Health and Disease, Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45257, USA; Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Department of Cardiology, The Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA. 2. Division of Cardiology, Los Angeles Biomedical Research Center at Harbor-UCLA, Division of Cardiology, Torrance, CA 90502, USA. 3. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Department of Cardiology, The Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA; Center for Prevention and Wellness Research, Baptist Health South Florida, Miami, FL 33139, USA. 4. Division of Cardiology, University of California, Irvine, CA 92697, USA. 5. Division of Cardiology, Department of Medicine, Wake Forest University, Winston-Salem, NC 27157, USA. 6. Division of Cardiology, Henry Ford Hospital, Detroit, MI 48202, USA; King Saud bin Abdulaziz University for Health Sciences, King Abdullah International Medical Research Center, King Abdulaziz Cardiac Center, Ministry of National Guard, Health Affairs, Saudi Arabia. 7. Departments of Medicine and Epidemiology, Columbia University, New York, NY 10032, USA. 8. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Department of Cardiology, The Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA. 9. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Department of Cardiology, The Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA; Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins University, Baltimore, MD 21205, USA. Electronic address: mblaha1@jhmi.edu. 10. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Department of Cardiology, The Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA; Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins University, Baltimore, MD 21205, USA.
Abstract
BACKGROUND AND AIMS: TAC is associated with incident CVD and all-cause mortality. Nevertheless, the independent 10-year prognostic value of TAC in individuals with CAC = 0 beyond traditional risk factors is not well established. METHODS: 3415 MESA participants with baseline CAC = 0 were followed for CHD, CVD events and all-cause mortality. TAC was measured in the ascending and descending aorta in all participants and quantified using Agatston's score. Multivariable Cox proportional hazards regression models were used to study the associations between TAC and incident CHD, CVD events and all-cause mortality. Likelihood ratio tests were used to compare prediction models including traditional risk factors plus TAC versus risk factors alone. RESULTS: 406 participants (11.9%) had TAC>0 at baseline. Over a median follow-up of 11.3 years, unadjusted event rates per 1000 person-years were higher in TAC>0 than in TAC = 0 participants: CHD 2.18 vs. 2.03; CVD 6.85 vs. 3.42; all-cause mortality 12.84 vs. 4.96. However, in multivariable Cox regression analyses adjusting for CVD risk factors, neither TAC>0, TAC>100 nor log(TAC+1) were independently associated with any of the study outcomes, nor improved their prediction compared to traditional risk factors alone (p value of likelihood ratio tests >0.05). CONCLUSIONS: In a multi-ethnic, modern US population of asymptomatic individuals with CAC = 0 at baseline, the prevalence of TAC>0 was low, and TAC did not improve 10-year estimation of prognosis beyond traditional risk factors. In the presence of CAC = 0, measurement of TAC is unlikely to provide sufficient additional prognostic information to further improve risk assessment.
BACKGROUND AND AIMS: TAC is associated with incident CVD and all-cause mortality. Nevertheless, the independent 10-year prognostic value of TAC in individuals with CAC = 0 beyond traditional risk factors is not well established. METHODS: 3415 MESAparticipants with baseline CAC = 0 were followed for CHD, CVD events and all-cause mortality. TAC was measured in the ascending and descending aorta in all participants and quantified using Agatston's score. Multivariable Cox proportional hazards regression models were used to study the associations between TAC and incident CHD, CVD events and all-cause mortality. Likelihood ratio tests were used to compare prediction models including traditional risk factors plus TAC versus risk factors alone. RESULTS: 406 participants (11.9%) had TAC>0 at baseline. Over a median follow-up of 11.3 years, unadjusted event rates per 1000 person-years were higher in TAC>0 than in TAC = 0 participants: CHD 2.18 vs. 2.03; CVD 6.85 vs. 3.42; all-cause mortality 12.84 vs. 4.96. However, in multivariable Cox regression analyses adjusting for CVD risk factors, neither TAC>0, TAC>100 nor log(TAC+1) were independently associated with any of the study outcomes, nor improved their prediction compared to traditional risk factors alone (p value of likelihood ratio tests >0.05). CONCLUSIONS: In a multi-ethnic, modern US population of asymptomatic individuals with CAC = 0 at baseline, the prevalence of TAC>0 was low, and TAC did not improve 10-year estimation of prognosis beyond traditional risk factors. In the presence of CAC = 0, measurement of TAC is unlikely to provide sufficient additional prognostic information to further improve risk assessment.
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