Suzette J Bielinski1, Cecilia Berardi2, Paul A Decker3, Phillip S Kirsch4, Nicholas B Larson5, James S Pankow6, Michele Sale7, Mariza de Andrade8, Hugues Sicotte9, Weihong Tang10, Naomi Q Hanson11, Christina L Wassel12, Joseph F Polak13, Michael Y Tsai14. 1. Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. Electronic address: bielinski.suzette@mayo.edu. 2. Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA; Montefiore Medical Center, Bronx, NY, USA. Electronic address: ceci.berardi@gmail.com. 3. Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. Electronic address: Decker.Paul@mayo.edu. 4. Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. Electronic address: Phillip_kirsch@uhc.com. 5. Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. Electronic address: Larson.Nicholas@mayo.edu. 6. Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN, USA. Electronic address: pankow@umn.edu. 7. Center for Public Health Genomics, University of Virginia, VA, USA. Electronic address: msale@virginia.edu. 8. Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. Electronic address: mandrade@mayo.edu. 9. Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. Electronic address: Sicotte.Hugues@mayo.edu. 10. Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN, USA. Electronic address: tang0097@umn.edu. 11. Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA. Electronic address: hanso047@umn.edu. 12. Department of Epidemiology, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: cwassel@pitt.edu. 13. Department of Radiology, Tufts Medical Center, Tufts University School of Medicine, Boston, MA, USA. Electronic address: jpolak@tufts-nemc.org. 14. Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA. Electronic address: tsaix001@umn.edu.
Abstract
OBJECTIVE: P-selectin is a cellular adhesion molecule that has been shown to be crucial in development of coronary heart disease (CHD). We sought to determine the role of P-selectin on the risk of atherosclerosis in a large multi-ethnic population. METHODS: Data from the Multi-Ethnic Study of Atherosclerosis (MESA), including 1628 African, 702 Chinese, 2393 non-Hispanic white, and 1302 Hispanic Americans, were used to investigate the association of plasma P-selectin with CHD risk factors, coronary artery calcium (CAC), intima-media thickness, and CHD. Regression models were used to investigate the association between P-selectin and risk factors, Tobit model for CAC, and Cox regression for CHD events. RESULTS: Mean levels of P-selectin differed by ethnicity and were higher in men (P<0.001). For all ethnic groups, P-selectin was positively associated with measures of adiposity, blood pressure, current smoking, LDL, and triglycerides and inversely with HDL. A significant ethnic interaction was observed for the association of P-selectin and prevalent diabetes; however, P-selectin was positively associated with HbA1c in all groups. Higher P-selectin levels were associated with greater prevalence of CAC. Over 10.1 years of follow-up, there were 335 incident CHD events. There was a positive linear association between P-selectin levels and rate of incident CHD after adjustment for traditional risk factors. However, association was only significant in non-Hispanic white Americans (HR: 1.81, 95% CI 1.07 to 3.07, P=0.027). CONCLUSION: We observed ethnic heterogeneity in the association of P-selectin and risk of CHD.
OBJECTIVE:P-selectin is a cellular adhesion molecule that has been shown to be crucial in development of coronary heart disease (CHD). We sought to determine the role of P-selectin on the risk of atherosclerosis in a large multi-ethnic population. METHODS: Data from the Multi-Ethnic Study of Atherosclerosis (MESA), including 1628 African, 702 Chinese, 2393 non-Hispanic white, and 1302 Hispanic Americans, were used to investigate the association of plasma P-selectin with CHD risk factors, coronary artery calcium (CAC), intima-media thickness, and CHD. Regression models were used to investigate the association between P-selectin and risk factors, Tobit model for CAC, and Cox regression for CHD events. RESULTS: Mean levels of P-selectin differed by ethnicity and were higher in men (P<0.001). For all ethnic groups, P-selectin was positively associated with measures of adiposity, blood pressure, current smoking, LDL, and triglycerides and inversely with HDL. A significant ethnic interaction was observed for the association of P-selectin and prevalent diabetes; however, P-selectin was positively associated with HbA1c in all groups. Higher P-selectin levels were associated with greater prevalence of CAC. Over 10.1 years of follow-up, there were 335 incident CHD events. There was a positive linear association between P-selectin levels and rate of incident CHD after adjustment for traditional risk factors. However, association was only significant in non-Hispanic white Americans (HR: 1.81, 95% CI 1.07 to 3.07, P=0.027). CONCLUSION: We observed ethnic heterogeneity in the association of P-selectin and risk of CHD.
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