Leslee J Shaw1, James K Min2, Khurram Nasir3, Joe X Xie1, Daniel S Berman4, Michael D Miedema5, Seamus P Whelton6, Zeina A Dardari6, Alan Rozanski7, John Rumberger8, C Noel Bairey Merz4, Mouaz H Al-Mallah9, Matthew J Budoff10, Michael J Blaha6. 1. Emory University School of Medicine, 1462 Clifton Rd NE, Room 529, Atlanta, GA, USA. 2. Department of Radiology and Medicine, Weill Cornell Medical College, 413 E. 69th St, Suite 108, New York, NY, USA. 3. Cardiology & Center for Outcomes Research and Evaluation, Yale New Haven Hospital, Yale University, 1 Church Street, Suite 200, New Haven, CT, USA. 4. Departments of Imaging and Medicine and the Smidt Heart Institute, Cedars-Sinai, 8700 Beverly Blvd, Los Angeles, CA, USA. 5. Cardiovascular Prevention, Minneapolis Heart Institute Foundation, Minneapolis Heart Institute, 920 East 28th Street, Suite 600, Minneapolis, MN, USA. 6. Johns Hopkins Ciccarone Center for Prevention of Heart Disease, Blalock 524D1, 600 N Wolfe St. Baltimore, MD, USA. 7. Department of Medicine, St. Luke's Roosevelt Hospital Center, 1111 Amsterdam Ave, New York, NY, USA. 8. Princeton Longevity Center, Princeton Forrestal Village, 136 Main Street, Princeton, NJ, USA. 9. Cardiac Sciences Department, King Abdul-Aziz Cardiac Center, Mail Code: 1413, Riyadh, Saudia Arabia. 10. Cardiology, Los Angeles Biomedical Research Center, 1124 W. Carson St., RB-2 Torrance, CA, USA.
Abstract
Aims: Pathologic evidence supports unique sex-specific mechanisms as precursors for acute cardiovascular (CV) events. Current evidence on long-term CV risk among women when compared with men based on measures of coronary artery calcium (CAC) remains incomplete. Methods and results: A total of 63 215 asymptomatic women and men were enrolled in the multicentre, CAC Consortium with median follow-up of 12.6 years. Pooled cohort equation (PCE) risk scores and risk factor data were collected with the Agatston score and other CAC measures (number of lesions and vessels, lesion size, volume, and plaque density). Cox proportional hazard models were employed to estimate CV mortality (n = 919). Sex interactions were calculated. Women and men had average PCE risk scores of 5.8% and 9.1% (P < 0.001). Within CAC subgroups, women had fewer calcified lesions (P < 0.0001) and vessels (P = 0.017), greater lesion size (P < 0.0001), and higher plaque density (P = 0.013) when compared with men. For women and men without CAC, long-term CV mortality was similar (P = 0.67), whereas detectable CAC was associated with 1.3-higher hazard for CV death among women when compared with men (P < 0001). Cardiovascular mortality was higher among women with more extensive, numerous, or larger CAC lesions. The relative hazard for cardiovascular disease (CVD) mortality for women and men was 8.2 vs. 5.1 for multivessel CAC, 8.6 vs. 5.9 for ≥5 CAC lesions, and 8.5 vs. 4.4 for a lesion size ≥15 mm3, respectively. Additional explorations revealed that women with larger sized and more numerous CAC lesions had 2.2-fold higher CVD mortality (P < 0.0001) as compared to men. Moreover, CAC density was not predictive of CV mortality in women (P = 0.51) but was for men (P < 0.001), when controlling for CAC volume and cardiac risk factors. Conclusion: Our overall findings support that measures beyond the Agatston score provide important clues to sex differences in atherosclerotic plaque and may further refine risk detection and focus preventive strategies of care.
Aims: Pathologic evidence supports unique sex-specific mechanisms as precursors for acute cardiovascular (CV) events. Current evidence on long-term CV risk among women when compared with men based on measures of coronary artery calcium (CAC) remains incomplete. Methods and results: A total of 63 215 asymptomatic women and men were enrolled in the multicentre, CAC Consortium with median follow-up of 12.6 years. Pooled cohort equation (PCE) risk scores and risk factor data were collected with the Agatston score and other CAC measures (number of lesions and vessels, lesion size, volume, and plaque density). Cox proportional hazard models were employed to estimate CV mortality (n = 919). Sex interactions were calculated. Women and men had average PCE risk scores of 5.8% and 9.1% (P < 0.001). Within CAC subgroups, women had fewer calcified lesions (P < 0.0001) and vessels (P = 0.017), greater lesion size (P < 0.0001), and higher plaque density (P = 0.013) when compared with men. For women and men without CAC, long-term CV mortality was similar (P = 0.67), whereas detectable CAC was associated with 1.3-higher hazard for CV death among women when compared with men (P < 0001). Cardiovascular mortality was higher among women with more extensive, numerous, or larger CAC lesions. The relative hazard for cardiovascular disease (CVD) mortality for women and men was 8.2 vs. 5.1 for multivessel CAC, 8.6 vs. 5.9 for ≥5 CAC lesions, and 8.5 vs. 4.4 for a lesion size ≥15 mm3, respectively. Additional explorations revealed that women with larger sized and more numerous CAC lesions had 2.2-fold higher CVD mortality (P < 0.0001) as compared to men. Moreover, CAC density was not predictive of CV mortality in women (P = 0.51) but was for men (P < 0.001), when controlling for CAC volume and cardiac risk factors. Conclusion: Our overall findings support that measures beyond the Agatston score provide important clues to sex differences in atherosclerotic plaque and may further refine risk detection and focus preventive strategies of care.
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