Mahmoud Al Rifai1, Miguel Cainzos-Achirica2, Alka M Kanaya3, Namratha R Kandula4, Zeina Dardardi5, Parag H Joshi6, Jaideep Patel7, Matthew Budoff8, Joseph Yeboah9, Eliseo Guallar10, Roger S Blumenthal5, Michael J Blaha11. 1. Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Department of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Department of Internal Medicine, University of Kansas School of Medicine, Wichita, KS, USA. 2. Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Department of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Bellvitge University Hospital and Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain; RTI Health Solutions, Pharmacoepidemiology and Risk Management, Barcelona, Spain. 3. Department of Medicine, University of California, San Francisco, San Francisco, CA, USA. 4. Feinberg School of Medicine, Division of General Internal Medicine, Northwestern University, Chicago, IL, USA; Feinberg School of Medicine, Department of Preventive Medicine, Northwestern University, Chicago, IL, USA. 5. Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Department of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA. 6. Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Department of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Division of Cardiology, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA. 7. Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Department of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Department of Cardiology, VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, VA, USA. 8. Division of Cardiology, Los Angeles Biomedical Research Institute, Torrance, CA, USA. 9. Department of Cardiology, Wake Forest Baptist Health, Winston-Salem, NC, USA. 10. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA; Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins University, Baltimore, MD, USA. 11. Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Department of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA. Electronic address: mblaha1@jhmi.edu.
Abstract
BACKGROUND AND AIMS: South Asian (SA) individuals are thought to represent a group that is at high-risk for atherosclerotic cardiovascular disease (ASCVD). However, the performance of the Pooled Cohort Equations (PCE) remains uncertain in SAs living in the US. We aimed to study the interplay between predicted 10-year ASCVD risk and coronary artery calcium (CAC) in SAs compared to other racial/ethnic groups. METHODS: We studied 536 SAs from the Mediators of Atherosclerosis in South Asians Living in America (MASALA) study, and 2073 Non-Hispanic Whites (NHWs), 1514 African Americans (AAs), 1254 Hispanics, and 671 Chinese Americans (CAs) from the Multi-Ethnic Study of Atherosclerosis (MESA) who were not currently on statins. We used logistic regression models to assess the association between race/ethnicity and CAC within each ASCVD risk stratum. RESULTS: SAs at low and at intermediate estimated ASCVD risk were more likely to have CAC = 0 compared to NHWs, while SAs at high risk had a similar CAC burden to NHWs. For example, intermediate-risk SAs had a 73% higher odds of CAC = 0 compared to NHWs (95% 1.00-2.99), while high-risk SAs were equally likely to have CAC = 0 (OR 0.95, 95% CI 0.65-1.38) and CAC >100 (OR 0.86, 95% CI 0.61-1.22). CONCLUSIONS: Our results suggest that the extent of ASCVD risk overestimation using the PCEs may be even greater among SAs considered at low and intermediate risk than among NHWs. Studies with incident ASCVD events are required to validate and/or recalibrate current ASCVD risk prediction tools in this group.
BACKGROUND AND AIMS: South Asian (SA) individuals are thought to represent a group that is at high-risk for atherosclerotic cardiovascular disease (ASCVD). However, the performance of the Pooled Cohort Equations (PCE) remains uncertain in SAs living in the US. We aimed to study the interplay between predicted 10-year ASCVD risk and coronary artery calcium (CAC) in SAs compared to other racial/ethnic groups. METHODS: We studied 536 SAs from the Mediators of Atherosclerosis in South Asians Living in America (MASALA) study, and 2073 Non-Hispanic Whites (NHWs), 1514 African Americans (AAs), 1254 Hispanics, and 671 Chinese Americans (CAs) from the Multi-Ethnic Study of Atherosclerosis (MESA) who were not currently on statins. We used logistic regression models to assess the association between race/ethnicity and CAC within each ASCVD risk stratum. RESULTS: SAs at low and at intermediate estimated ASCVD risk were more likely to have CAC = 0 compared to NHWs, while SAs at high risk had a similar CAC burden to NHWs. For example, intermediate-risk SAs had a 73% higher odds of CAC = 0 compared to NHWs (95% 1.00-2.99), while high-risk SAs were equally likely to have CAC = 0 (OR 0.95, 95% CI 0.65-1.38) and CAC >100 (OR 0.86, 95% CI 0.61-1.22). CONCLUSIONS: Our results suggest that the extent of ASCVD risk overestimation using the PCEs may be even greater among SAs considered at low and intermediate risk than among NHWs. Studies with incident ASCVD events are required to validate and/or recalibrate current ASCVD risk prediction tools in this group.
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