Darae Ko1, Sarah R Preis2, Andrew D Johnson3, Ramachandran S Vasan4, Emelia J Benjamin4, Naomi M Hamburg5, Gary F Mitchell6. 1. Section of Cardiovascular Medicine, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, MA, USA. Electronic address: daraeko@bu.edu. 2. Department of Biostatistics, Boston University School of Public Heath, Boston, MA, USA. 3. Boston University and National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA, USA; National Heart, Lung, and Blood Institute, Division of Intramural Research, Population Sciences Branch, Bethesda, MD, USA. 4. Section of Cardiovascular Medicine, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, MA, USA; Boston University and National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA, USA; Section of Preventive Medicine, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, MA, USA; Department Epidemiology, Boston University School of Public Heath, Boston, MA, USA. 5. Section of Cardiovascular Medicine, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, MA, USA. 6. Cardiovascular Engineering, Inc, Norwood, MA, USA.
Abstract
INTRODUCTION: Association between arterial vascular dysfunction and risk of venous thromboembolism (VTE) is uncertain. We determined the associations between comprehensive measures of arterial vascular function and risk of incident VTE in a community-based cohort study with robust longitudinal follow-up. MATERIALS AND METHODS: In the Framingham Heart Study Original, Offspring, Third Generation, and Omni cohorts, we measured carotid-femoral pulse wave velocity and central pulse pressure (n = 8261, age 51.5 ± 15.5 years, 54% women), flow-mediated dilation and hyperemic velocity (n = 6540, age 47.9 ± 14.1 years, 54% women), and peripheral arterial tonometry ratio (n = 4998, age 54.3 ± 16.0 years, 52% women). Deep venous thrombosis and pulmonary embolism were diagnosed with imaging studies and adjudicated by three Framingham Heart Study physicians. RESULTS AND CONCLUSIONS: The rate of incident VTE was 1.6-2.1 per 1000 person-years during mean follow-up of 8.5-11.2 years. In age- and sex-adjusted Cox proportional hazards regression models, carotid-femoral pulse wave velocity was associated with increased risk of VTE (HR 1.32, 95% CI 1.05-1.66, p = 0.02), however the association was no longer statistically significant after multivariable adjustment (HR 1.24, 95% CI 0.96-1.61, p = 0.10). None of the other vascular variables were associated with the risk of VTE in any of the models. In our comprehensive examination of arterial vascular function and risk of VTE, we did not observe any association between select arterial function measures and risk of VTE after multivariable adjustment.
INTRODUCTION: Association between arterial vascular dysfunction and risk of venous thromboembolism (VTE) is uncertain. We determined the associations between comprehensive measures of arterial vascular function and risk of incident VTE in a community-based cohort study with robust longitudinal follow-up. MATERIALS AND METHODS: In the Framingham Heart Study Original, Offspring, Third Generation, and Omni cohorts, we measured carotid-femoral pulse wave velocity and central pulse pressure (n = 8261, age 51.5 ± 15.5 years, 54% women), flow-mediated dilation and hyperemic velocity (n = 6540, age 47.9 ± 14.1 years, 54% women), and peripheral arterial tonometry ratio (n = 4998, age 54.3 ± 16.0 years, 52% women). Deep venous thrombosis and pulmonary embolism were diagnosed with imaging studies and adjudicated by three Framingham Heart Study physicians. RESULTS AND CONCLUSIONS: The rate of incident VTE was 1.6-2.1 per 1000 person-years during mean follow-up of 8.5-11.2 years. In age- and sex-adjusted Cox proportional hazards regression models, carotid-femoral pulse wave velocity was associated with increased risk of VTE (HR 1.32, 95% CI 1.05-1.66, p = 0.02), however the association was no longer statistically significant after multivariable adjustment (HR 1.24, 95% CI 0.96-1.61, p = 0.10). None of the other vascular variables were associated with the risk of VTE in any of the models. In our comprehensive examination of arterial vascular function and risk of VTE, we did not observe any association between select arterial function measures and risk of VTE after multivariable adjustment.
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