Jaideep Patel1, Michael J Blaha2, John W McEvoy2, Sadia Qadir3, Rajesh Tota-Maharaj4, Leslee J Shaw5, John A Rumberger6, Tracy Q Callister7, Daniel S Berman8, James K Min8, Paolo Raggi9, Arthur A Agatston10, Roger S Blumenthal2, Matthew J Budoff11, Khurram Nasir12. 1. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA; Division of Internal Medicine, Virginia Commonwealth University Medical Center-Medical College of Virginia, 1200 E Broad Street, Richmond, VA 23298, USA. Electronic address: jaideepatel@hotmail.com. 2. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA. 3. Division of Cardiology, St. Luke's-Roosevelt Hospital Center, Columbia College of Physicians and Surgeons, New York, NY, USA. 4. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA; Division of Cardiology, Danbury Hospital, Danbury, CT, USA. 5. Division of Cardiology, Emory University, Atlanta, GA, USA. 6. Princeton Longevity Center, Princeton, NJ, USA. 7. Tennessee Heart and Vascular Center, Hendersonville, TN, USA. 8. Cedars-Sinai Medical Center and the Cedars-Sinai Heart Institute, Los Angeles, CA, USA. 9. Division of Cardiology, Mazankowski Alberta Heart Institute, Edmonton, AB, Canada. 10. Center for Prevention and Wellness Research, Baptist Health Medical Group, Miami Beach, FL, USA. 11. Division of Cardiology, Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA. 12. Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA; Center for Prevention and Wellness Research, Baptist Health Medical Group, Miami Beach, FL, USA.
Abstract
BACKGROUND: Risk assessment in the extensive calcified plaque phenotype has been limited by small sample size. OBJECTIVE: We studied all-cause mortality rates among asymptomatic patients with markedly elevated Agatston scores > 1000. METHODS: We studied a clinical cohort of 44,052 asymptomatic patients referred for coronary calcium scans. Mean follow-up was 5.6 years (range, 1-13 years). All-cause mortality rates were calculated after stratifying by Agatston score (0, 1-1000, 1001-1500, 1500-2000, and >2000). A multivariable Cox regression model adjusting for self-reported traditional risk factors was created to assess the relative mortality hazard of Agatston scores 1001 to 1500, 1501 to 2000, and >2000. With the use of post-estimation modeling, we assessed for the presence of an upper threshold of risk with high Agatston scores. RESULTS: A total of 1593 patients (4% of total population) had Agatston score > 1000. There was a continuous graded decrease in estimated 10-year survival across increasing Agatston score, continuing when Agatston score > 1000 (Agatston score 1001-1500, 78%; Agatston score 1501-2000, 74%; Agatston score > 2000, 51%). After multivariable adjustment, Agatston scores 1001 to 1500, 1501 to 2000, and >2000 were associated with an 8.05-, 7.45-, and 13.26-fold greater mortality risk, respectively, than for Agatston score of 0. Compared with Agatston score 1001 to 1500, Agatston score 1501 to 2000 had a similar all-cause mortality risk, whereas Agatston score > 2000 had an increased relative risk (Agatston score 1501-2000: hazard ratio [HR], 1.01 [95% CI, 0.67-1.51]; Agatston score > 2000: HR, 1.79 [95% CI, 1.30-2.46]). Graphical assessment of the predicted survival model suggests no upper threshold for risk associated with calcified plaque in coronary arteries. CONCLUSION: Increasing calcified plaque in coronary arteries continues to predict a graded decrease in survival among patients with extensive Agatston score > 1000 with no apparent upper threshold. Published by Elsevier Inc.
BACKGROUND: Risk assessment in the extensive calcified plaque phenotype has been limited by small sample size. OBJECTIVE: We studied all-cause mortality rates among asymptomatic patients with markedly elevated Agatston scores > 1000. METHODS: We studied a clinical cohort of 44,052 asymptomatic patients referred for coronary calcium scans. Mean follow-up was 5.6 years (range, 1-13 years). All-cause mortality rates were calculated after stratifying by Agatston score (0, 1-1000, 1001-1500, 1500-2000, and >2000). A multivariable Cox regression model adjusting for self-reported traditional risk factors was created to assess the relative mortality hazard of Agatston scores 1001 to 1500, 1501 to 2000, and >2000. With the use of post-estimation modeling, we assessed for the presence of an upper threshold of risk with high Agatston scores. RESULTS: A total of 1593 patients (4% of total population) had Agatston score > 1000. There was a continuous graded decrease in estimated 10-year survival across increasing Agatston score, continuing when Agatston score > 1000 (Agatston score 1001-1500, 78%; Agatston score 1501-2000, 74%; Agatston score > 2000, 51%). After multivariable adjustment, Agatston scores 1001 to 1500, 1501 to 2000, and >2000 were associated with an 8.05-, 7.45-, and 13.26-fold greater mortality risk, respectively, than for Agatston score of 0. Compared with Agatston score 1001 to 1500, Agatston score 1501 to 2000 had a similar all-cause mortality risk, whereas Agatston score > 2000 had an increased relative risk (Agatston score 1501-2000: hazard ratio [HR], 1.01 [95% CI, 0.67-1.51]; Agatston score > 2000: HR, 1.79 [95% CI, 1.30-2.46]). Graphical assessment of the predicted survival model suggests no upper threshold for risk associated with calcified plaque in coronary arteries. CONCLUSION: Increasing calcified plaque in coronary arteries continues to predict a graded decrease in survival among patients with extensive Agatston score > 1000 with no apparent upper threshold. Published by Elsevier Inc.
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