Comparisons of the Framingham and Pooled Cohort Equation Risk Scores for Detecting Subclinical Vascular Disease in Blacks Versus Whites

• Authors: Matthew L Topel, Emory University; Jia Shen, Emory University; Alanna A. Morris, Emory University; Ibhar Al Mheid, Emory University; Salman Sher, Emory University; Sandra B Dunbar, Emory University; Viola Vaccarino, Emory University; Laurence S Sperling, Emory University; Gary H. Gibbons, National Institutes of Health; Greg Martin, Emory University; Arshed Ali Quyyumi, Emory University
• Journal Title: American Journal of Cardiology
• Volume: Volume 121, Number 5
• Publisher: Elsevier: 12 months | 2018-03-01, Pages 564-569
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1016/j.amjcard.2017.11.031
• Subjects: Health Sciences, Epidemiology; Health Sciences, General
• Keywords: Science & Technology; Life Sciences & Biomedicine; Cardiac & Cardiovascular Systems; Cardiovascular System & Cardiology; INTIMA-MEDIA THICKNESS; CARDIOVASCULAR EVENTS; ARTERIAL STIFFNESS; HEART-DISEASE; AUGMENTATION INDEX; AFRICAN-AMERICANS; PREDICTION; VALIDATION; ADULTS; METAANALYSIS

Abstract

The pooled cohort Atherosclerotic Cardiovascular Disease (ASCVD) risk calculator is designed to improve cardiovascular risk estimation compared with the Framingham Risk Score, particularly in blacks. Although the ASCVD risk score better predicts mortality and incident cardiovascular disease in blacks, less is known about its performance for subclinical vascular disease measures, including arterial stiffness and carotid intima-media thickness. We sought to determine if the ASCVD risk score better identifies subclinical vascular disease in blacks compared with the Framingham risk score. We calculated both the Framingham and ASCVD cohort risk scores in 1,231 subjects (mean age 53 years, 59% female, 37% black) without known cardiovascular disease and measured the extent of arterial stiffness, as determined by pulse wave velocity (PWV), central pulse pressure (CPP), and central augmentation index (CAIx), and subclinical atherosclerosis, as determined by carotid-IMT (C-IMT). Compared with whites, blacks had higher CAIx (23.9 ± 10.2 vs 22.1 ± 9.6%, p = 0.004), CPP (36.4 ± 10.5 vs 34.9 ± 9.8 mmHg, p = 0.014), PWV (7.6 ± 1.5 vs 7.3 ± 1.3 m/s, p = 0.004), and C-IMT (0.67 ± 0.10 vs 0.65 ± 0.10 mm, p = 0.005). In a multivariable analysis including race and Framingham risk score, race remained an independent predictor of all measures of subclinical vascular disease; however, models with race and the ASCVD risk score showed that race was not an independent predictor of subclinical vascular disease. In conclusion, greater subclinical vascular disease in blacks was not estimated by the Framingham risk score. The new ASCVD risk score provided a better estimate of racial differences in vascular function and structure.