Inflammation: Correlates and Prognosis in Framingham
|Study Design:||Observational Model: Defined Population|
|Study Start Date:||July 2000|
|Estimated Study Completion Date:||June 2004|
Recent epidemiologic evidence suggests that inflammation plays a major role in the development of coronary artery disease. High sensitivity C-reactive protein assays have been shown to be independent risk factors for the development of atherosclerosis. Measurements of C-reactive protein also adds to the predictive value of lipid levels in determining the risk of cardiovascular disease. Levels of inflammatory markers may also correlate with response to commonly used lipid lowering agents. The exact role of inflammation in coronary artery disease is not clear; however, it has been suggested that inflammation may be a marker of subclinical cardiovascular disease, or may indicate the presence of vulnerable plaque. In addition to being a possible causative agent in the development of atherogenesis, it has been postulated that inflammatory markers may reflect events that predict the development of myocardial events. The fact that agents such as aspirin and pravastatin, which are known to have anti-inflammatory effects, are effective agents in the prevention of atherosclerosis suggests the possibility that prevention of inflammation may play an important role in reduction of risk for cardiovascular disease.
The study assessed inflammatory markers in 3,765 men and women of the Framingham Study. The markers included inflammatory (C-reactive protein, fibrinogen, soluble intercellular adhesion molecule-1, endothelin-1, monocyte chemotactic protein-1, tumor necrosis factor-alpha) and oxidative stress markers (8-epi-PGF 2alpha, thromboxane B2). The relation between CVD risk factors and systemic markers of vascular inflammation was determined. The relations between inflammatory markers, endothelial dysfunction, and subclinical disease were analyzed. Markers of inflammation were related to prevalent and incident cardiovascular disease events adjusting for standard risk factors. The central hypothesis was that inflammatory markers were independent risk factors for cardiovascular disease events with endothelial dysfunction operating in the causal pathway.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00006403
|Investigator:||Emelia Benjamin||Boston University|