Novel Hemostatic Cardiac Risk Factors in Framingham
|Cardiovascular Diseases Heart Diseases Death, Sudden, Cardiac Myocardial Infarction Thrombosis Atherosclerosis Carotid Artery Diseases|
|Study Start Date:||July 1994|
|Study Completion Date:||May 1998|
Elevation of platelet reactivity plasminogen activator inhibitor, fibrinogen, von Willebrand's factor, and factor VII have been reported to increase myocardial infarction risk. Myocardial infarction and sudden cardiac death are more frequent in the morning when platelet activity is increased and fibrinolysis is decreased. Reduction of recurrent myocardial infarction by aspirin and coumadin suggests causal roles for platelet activity and coagulation. Increases in viscosity and decreases in anti-thrombin III and Protein C have been linked with increased thrombosis. Despite these findings, a coherent picture of these disparate hemostatic indices as cardiac risk factors has yet to emerge.
Platelet reactivty, plasminogen activatator inhibitor, fibrinogen, von Willebrand's factor, factor VII, and other hemostatic risk factors were measured in all 4,000 subjects of the Framingham Offspring Study. The data were combined with the regularly collected Framingham data to: determine the relationships between hemostatic factors and carotid atherosclerosis as assessed by ultrasound; determine the relationship between hemostatic factors and the traditional cardiac risk factors; and determine if hemostatic risk factors independently predict myocardial infarction and cardiac death.
The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00005356
|OverallOfficial:||Geoffrey Tofler||Beth Israel Deaconess Medical Center|