Nicolas Amabile1, Susan Cheng2, Jean Marie Renard1, Martin G Larson3, Anahita Ghorbani4, Elizabeth McCabe5, Gabriel Griffin6, Coralie Guerin1, Jennifer E Ho7, Stanley Y Shaw8, Kenneth S Cohen9, Ramachandran S Vasan10, Alain Tedgui1, Chantal M Boulanger11, Thomas J Wang12. 1. INSERM, U970, Paris Cardiovascular Research Center - PARCC, 56 Rue Leblanc, 75737 Paris cedex 15, France Université Paris Descartes, Sorbonne Paris Cité, UMR-S970 Paris, France. 2. Framingham Heart Study, Framingham, MA, USA Cardiovascular Division, Brigham and Women's Hospital, Boston, MA, USA. 3. Framingham Heart Study, Framingham, MA, USA Department of Mathematics and Statistics, Boston University, Boston, MA, USA. 4. Cardiology Division, Massachusetts General Hospital, Boston, MA, USA. 5. Department of Mathematics and Statistics, Boston University, Boston, MA, USA Cardiology Division, Massachusetts General Hospital, Boston, MA, USA. 6. Duke University School of Medicine, Durham, NC, USA. 7. Framingham Heart Study, Framingham, MA, USA Cardiology Division, Massachusetts General Hospital, Boston, MA, USA. 8. Cardiology Division, Massachusetts General Hospital, Boston, MA, USA Center for Systems Biology, Massachusetts General Hospital, Boston, MA, USA. 9. Section of Hematology/Oncology, University of Chicago Medical Center, Chicago, IL, USA. 10. Framingham Heart Study, Framingham, MA, USA Sections of Preventive Medicine and Cardiology, Boston University School of Medicine, Boston, MA, USA. 11. INSERM, U970, Paris Cardiovascular Research Center - PARCC, 56 Rue Leblanc, 75737 Paris cedex 15, France Université Paris Descartes, Sorbonne Paris Cité, UMR-S970 Paris, France chantal.boulanger@inserm.fr thomas.j.wang@vanderbilt.edu. 12. Framingham Heart Study, Framingham, MA, USA Cardiology Division, Massachusetts General Hospital, Boston, MA, USA Division of Cardiovascular Medicine, Vanderbilt University Medical Center, 2220 Pierce Avenue, 383 Preston Research Building, Nashville, TN 37232, USA chantal.boulanger@inserm.fr thomas.j.wang@vanderbilt.edu.
Abstract
OBJECTIVE: To examine the relation of endothelial microparticles (EMPs) with cardiometabolic risk in the community. BACKGROUND: Circulating EMPs are small membrane vesicles released after endothelial cell injury. Endothelial microparticles are reportedly increased among individuals with a high burden of cardiovascular risk factors. However, prior investigations have been limited to small, highly selected samples. METHODS: We studied 844 individuals without a history of cardiovascular disease in the Framingham Offspring cohort (mean age 66 ± 9 years, 57% women). We used standardized flow cytometry methods to identify and quantify circulating CD144+ and CD31+/CD41- EMPs. We then used multivariable regression analyses to investigate the relations of EMP phenotypes with cardiovascular and metabolic risk factors. RESULTS: In multivariable analyses, the following cardiovascular risk factors were associated with one or more of the circulating EMP populations: hypertension (P = 0.025 for CD144+,), elevated triglycerides (P = 0.002 for CD144+, P < 0.0001 for CD31+/CD41-), and metabolic syndrome (P < 0.0001 for CD144+,). Overall, each tertile increase in the Framingham risk score corresponded to a 9% increase in log-CD31+/CD41- EMPs (P = 0.022). Furthermore, the presence of hypertriglyceridaemic waist status was associated with 38% higher levels of CD144+ EMPs (P < 0.0001) and 46% higher levels of CD31+/CD41- EMPs (P < 0.0001). CONCLUSION: In a large community-based sample, circulating EMP levels were associated with the presence of cardiometabolic risk factors, particularly dyslipidaemia. These data underscore the potential influence of high-risk metabolic profiles on endothelial integrity. Published on behalf of the European Society of Cardiology. All rights reserved.
OBJECTIVE: To examine the relation of endothelial microparticles (EMPs) with cardiometabolic risk in the community. BACKGROUND: Circulating EMPs are small membrane vesicles released after endothelial cell injury. Endothelial microparticles are reportedly increased among individuals with a high burden of cardiovascular risk factors. However, prior investigations have been limited to small, highly selected samples. METHODS: We studied 844 individuals without a history of cardiovascular disease in the Framingham Offspring cohort (mean age 66 ± 9 years, 57% women). We used standardized flow cytometry methods to identify and quantify circulating CD144+ and CD31+/CD41- EMPs. We then used multivariable regression analyses to investigate the relations of EMP phenotypes with cardiovascular and metabolic risk factors. RESULTS: In multivariable analyses, the following cardiovascular risk factors were associated with one or more of the circulating EMP populations: hypertension (P = 0.025 for CD144+,), elevated triglycerides (P = 0.002 for CD144+, P < 0.0001 for CD31+/CD41-), and metabolic syndrome (P < 0.0001 for CD144+,). Overall, each tertile increase in the Framingham risk score corresponded to a 9% increase in log-CD31+/CD41- EMPs (P = 0.022). Furthermore, the presence of hypertriglyceridaemic waist status was associated with 38% higher levels of CD144+ EMPs (P < 0.0001) and 46% higher levels of CD31+/CD41- EMPs (P < 0.0001). CONCLUSION: In a large community-based sample, circulating EMP levels were associated with the presence of cardiometabolic risk factors, particularly dyslipidaemia. These data underscore the potential influence of high-risk metabolic profiles on endothelial integrity. Published on behalf of the European Society of Cardiology. All rights reserved.
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