Gowtham R Grandhi1, Mohammadhassan Mirbolouk2, Zeina A Dardari2, Mouaz H Al-Mallah3, John A Rumberger4, Leslee J Shaw5, Ron Blankstein6, Michael D Miedema7, Daniel S Berman8, Matthew J Budoff9, Harlan M Krumholz10, Michael J Blaha2, Khurram Nasir11. 1. Center for Outcomes Research and Evaluation, Yale New Haven Hospital, New Haven, Connecticut. 2. The Johns Hopkins Ciccarone Center for Prevention of Cardiovascular Disease, Baltimore, Maryland. 3. Houston Methodist DeBakey Heart and Vascular Center, Houston Methodist Hospital, Houston, Texas. 4. Princeton Longevity Center, Princeton, New Jersey. 5. Weill Cornell Medical College, New York, New York. 6. Cardiovascular Division and Department of Radiology, Brigham and Women's Hospital, Boston, Massachusetts. 7. Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota. 8. Department of Imaging, Cedars-Sinai Medical Center, Los Angeles, California. 9. Department of Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, California. 10. Center for Outcomes Research and Evaluation, Yale New Haven Hospital, New Haven, Connecticut; Section of Cardiovascular Medicine, Department of Medicine, Yale School of Medicine, New Haven, Connecticut; Department of Health Policy and Management, Yale School of Public Health, New Haven, Connecticut. 11. Division of Cardiovascular Prevention and Wellness, Houston Methodist DeBakey Heart & Vascular Center, and Center for Outcomes Research (COR) Houston Methodist, Houston, Texas. Electronic address: knasir@houstonmethodist.org.
Abstract
OBJECTIVES: This study sought to evaluate the association and burden of coronary artery calcium (CAC) with long-term, cause-specific mortality across the spectrum of baseline risk. BACKGROUND: Although CAC is a known predictor of short-term, all-cause mortality, data on long-term and cause-specific mortality are inadequate. METHODS: The CAC Consortium cohort is a multicenter cohort of 66,636 participants without coronary heart disease (CHD) who underwent CAC testing. The following risk factors (RFs) were considered: 1) current cigarette smoking; 2) dyslipidemia; 3) diabetes mellitus; 4) hypertension; and 5) family history of CHD. RESULTS: During the 12.5-years median follow-up, 3,158 (4.7%) deaths occurred; 32% were cardiovascular disease (CVD) deaths. Participants with CAC scores ≥400 had a significantly increased risk for CHD and CVD mortality (hazard ratio [HR]: 5.44; 95% confidence interval [CI]: 3.88 to 7.62; and HR: 4.15; 95% CI: 3.29 to 5.22, respectively) compared with CAC of 0. Participants with ≥3 RFs had a smaller increased risk for CHD and CVD mortality (HR: 2.09; 95% CI: 1.52 to 2.85; and HR: 1.84; 95% CI: 1.46 to 2.31, respectively) compared with those without RFs. Across RF strata, CAC added prognostic information. For example, participants without RFs but with CAC ≥400 had significantly higher all-cause, non-CVD, CVD, and CHD mortality rates compared with participants with ≥3 RFs and CAC of 0. CONCLUSIONS: Across the spectrum of RF burden, a higher CAC score was strongly associated with long-term, all-cause mortality and a greater proportion of deaths due to CVD and CHD. Absence of CAC identified people with a low risk over 12 years of follow-up, with most deaths being non-CVD in nature, regardless of RF burden.
OBJECTIVES: This study sought to evaluate the association and burden of coronary artery calcium (CAC) with long-term, cause-specific mortality across the spectrum of baseline risk. BACKGROUND: Although CAC is a known predictor of short-term, all-cause mortality, data on long-term and cause-specific mortality are inadequate. METHODS: The CAC Consortium cohort is a multicenter cohort of 66,636 participants without coronary heart disease (CHD) who underwent CAC testing. The following risk factors (RFs) were considered: 1) current cigarette smoking; 2) dyslipidemia; 3) diabetes mellitus; 4) hypertension; and 5) family history of CHD. RESULTS: During the 12.5-years median follow-up, 3,158 (4.7%) deaths occurred; 32% were cardiovascular disease (CVD) deaths. Participants with CAC scores ≥400 had a significantly increased risk for CHD and CVD mortality (hazard ratio [HR]: 5.44; 95% confidence interval [CI]: 3.88 to 7.62; and HR: 4.15; 95% CI: 3.29 to 5.22, respectively) compared with CAC of 0. Participants with ≥3 RFs had a smaller increased risk for CHD and CVD mortality (HR: 2.09; 95% CI: 1.52 to 2.85; and HR: 1.84; 95% CI: 1.46 to 2.31, respectively) compared with those without RFs. Across RF strata, CAC added prognostic information. For example, participants without RFs but with CAC ≥400 had significantly higher all-cause, non-CVD, CVD, and CHD mortality rates compared with participants with ≥3 RFs and CAC of 0. CONCLUSIONS: Across the spectrum of RF burden, a higher CAC score was strongly associated with long-term, all-cause mortality and a greater proportion of deaths due to CVD and CHD. Absence of CAC identified people with a low risk over 12 years of follow-up, with most deaths being non-CVD in nature, regardless of RF burden.
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