Endothelial Vasomotor Function in the Framingham Study
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|ClinicalTrials.gov Identifier: NCT00005751|
Recruitment Status : Completed
First Posted : May 26, 2000
Last Update Posted : May 13, 2016
|Condition or disease|
|Cardiovascular Diseases Heart Diseases|
Current research suggests that loss of the vasodilator, anti-thrombotic, and anti-inflammatory properties of the vascular endothelium plays a dynamic role in the pathogenesis of cardiovascular disease. Impaired endothelial function, including impaired nitric oxide-dependent vasodilation is associated with cardiovascular disease risk factors. Further, there is growing evidence that endothelial function can be improved by risk modification. However, the available studies have not definitively resolved the issue of the cross-sectional correlates of endothelial dysfunction because they have been limited to small samples of highly selected patients. For example, it remains unclear whether hypercholesterolemia, hypertension, or elevated glucose levels are independent determinants of endothelial dysfunction. Most importantly, no study has shown a relation between endothelial dysfunction and increased cardiovascular risk. Such a demonstration would increase our understanding of the pathogenesis of cardiovascular disease and aid clinicians in identifying high risk individuals who would benefit most from intervention.
Using non-invasive brachial artery ultrasound, endothelial function was examined in about 3,800 men and women of the Framingham Heart Study. The cross-sectional correlates of endothelial function with known coronary risk factors were examined and cross-sectional analyses were performed on the relation of endothelial function to prevalent cardiovascular disease. Observations were made of the adjusted relation of endothelial function to incident and recurrent cardiovascular events. The central hypothesis was that the presence of endothelial dysfunction was an independent risk factor for cardiovascular disease events.
The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.
|Study Type :||Observational|
|Study Start Date :||December 1998|
|Actual Study Completion Date :||November 2003|
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00005751
|OverallOfficial:||Emilia Benjamin||Boston University|