Inflammation: Correlates and Prognosis in Framingham

This study has been completed.
Information provided by:
National Heart, Lung, and Blood Institute (NHLBI) Identifier:
First received: October 12, 2000
Last updated: June 23, 2005
Last verified: March 2005
To determine the relation between cardiovascular disease risk factors and systemic markers of vascular inflammation in the Framingham Study cohort.

Cardiovascular Diseases
Heart Diseases
Coronary Disease

Study Type: Observational
Study Design: Observational Model: Defined Population

Further study details as provided by National Heart, Lung, and Blood Institute (NHLBI):

Study Start Date: July 2000
Estimated Study Completion Date: June 2004
Detailed Description:


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.


Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
No eligibility criteria
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its identifier: NCT00006403

Sponsors and Collaborators
National Heart, Lung, and Blood Institute (NHLBI)
Investigator: Emelia Benjamin Boston University
  More Information

Publications: Identifier: NCT00006403     History of Changes
Other Study ID Numbers: 928
Study First Received: October 12, 2000
Last Updated: June 23, 2005
Health Authority: United States: Federal Government

Additional relevant MeSH terms:
Cardiovascular Diseases
Coronary Artery Disease
Coronary Disease
Arterial Occlusive Diseases
Heart Diseases
Myocardial Ischemia
Pathologic Processes
Vascular Diseases processed this record on November 27, 2015