Sina Kianoush1, Mahmoud Al Rifai1, Miguel Cainzos-Achirica2, Mouaz H Al-Mallah3, Geoffrey H Tison4, Joseph Yeboah5, Michael D Miedema6, Matthew A Allison7, Nathan D Wong8, Andrew P DeFilippis9, William Longstreth10, Khurram Nasir11, Matthew J Budoff8, Kunihiro Matsushita12, Michael J Blaha13. 1. Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins Medical Institutions, Baltimore, MD, USA. 2. Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins Medical Institutions, Baltimore, MD, USA; RTI Health Solutions, Barcelona, Spain. 3. Division of Cardiovascular Medicine, Henry Ford Hospital, Detroit, MI, USA; King Saud bin Abdulaziz University for Health Sciences, King Abdullah International Medical Research, Saudi Arabia. 4. Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Division of Cardiology, University of California, San Francisco, CA, USA. 5. Department of Heart and Vascular Center of Excellence, Wake Forest Baptist Health, Winston-Salem, North Carolina, USA. 6. Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA. 7. Department of Family Medicine and Public Health, University of California - San Diego, San Diego, CA, USA. 8. Los Angeles Biomedical Research Institute, Torrance, CA, USA; University of Washington, Seattle, WA, USA. 9. Division of Cardiovascular Medicine, University of Louisville, Jewish Hospital/Kentucky One Health, Louisville, KY, USA. 10. Department of Neurology, University of Washington, Seattle, WA, USA. 11. Center for Prevention and Wellness Research, Baptist Health Medical Group, Miami Beach, FL, USA. 12. Departments of Epidemiology and Biostatistics, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA. 13. Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins Medical Institutions, Baltimore, MD, USA. Electronic address: mblaha1@jhmi.edu.
Abstract
BACKGROUND AND AIMS: Atherosclerosis is a systemic disease. We examined whether the cumulative burden of thoracic extra-coronary calcification (ECC) improves prediction of stroke, transient ischemic attack (TIA), and stroke mortality beyond traditional risk factors and coronary artery calcium (CAC). METHODS: We followed a total of 6805 participants (mean age 62.1 ± 10.2 years, 47.2% male) from the Multi-Ethnic Study of Atherosclerosis (MESA) over a median of 12.1 years. The presence or absence of calcification at 4 thoracic ECC sites (mitral valve annulus, aortic valve, aortic root, and thoracic aorta) was determined from baseline cardiac-gated non-contrast CT scans. A multisite thoracic ECC score, ranging 0-4, was calculated by summing the 4 individual sites, which were treated as binary variables. Multivariable Cox proportional hazards regression models, controlled for traditional risk factors and CAC, were used to estimate hazard ratios for ischemic (primary endpoint) and hemorrhagic stroke, total stroke, TIA, and stroke mortality with increasing thoracic ECC. RESULTS: With an increasing number of thoracic ECC sites, there was a significant (p < 0.05) multivariable adjusted step-wise increase in the risk for ischemic stroke (n = 184), total stroke (n = 235), and TIA (n = 85), but not hemorrhagic stroke (n = 32) and stroke mortality (n = 42). Thoracic ECC increased the c-statistic and net reclassification index beyond traditional risk factors and CAC, but the results were not significant (p > 0.10). CONCLUSIONS: Although multisite thoracic ECC is independently associated with ischemic stroke, total stroke, and TIA, the incremental predictive value of thoracic ECC beyond traditional risk factors and CAC appears to be minimal.
BACKGROUND AND AIMS: Atherosclerosis is a systemic disease. We examined whether the cumulative burden of thoracic extra-coronary calcification (ECC) improves prediction of stroke, transient ischemic attack (TIA), and stroke mortality beyond traditional risk factors and coronary artery calcium (CAC). METHODS: We followed a total of 6805 participants (mean age 62.1 ± 10.2 years, 47.2% male) from the Multi-Ethnic Study of Atherosclerosis (MESA) over a median of 12.1 years. The presence or absence of calcification at 4 thoracic ECC sites (mitral valve annulus, aortic valve, aortic root, and thoracic aorta) was determined from baseline cardiac-gated non-contrast CT scans. A multisite thoracic ECC score, ranging 0-4, was calculated by summing the 4 individual sites, which were treated as binary variables. Multivariable Cox proportional hazards regression models, controlled for traditional risk factors and CAC, were used to estimate hazard ratios for ischemic (primary endpoint) and hemorrhagic stroke, total stroke, TIA, and stroke mortality with increasing thoracic ECC. RESULTS: With an increasing number of thoracic ECC sites, there was a significant (p < 0.05) multivariable adjusted step-wise increase in the risk for ischemic stroke (n = 184), total stroke (n = 235), and TIA (n = 85), but not hemorrhagic stroke (n = 32) and stroke mortality (n = 42). Thoracic ECC increased the c-statistic and net reclassification index beyond traditional risk factors and CAC, but the results were not significant (p > 0.10). CONCLUSIONS: Although multisite thoracic ECC is independently associated with ischemic stroke, total stroke, and TIA, the incremental predictive value of thoracic ECC beyond traditional risk factors and CAC appears to be minimal.
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