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Atherosclerosis in Rheumatoid Arthritis

This study has been completed.
National Heart, Lung, and Blood Institute (NHLBI)
Information provided by (Responsible Party):
C. Michael Stein, Vanderbilt University Identifier:
First received: May 16, 2002
Last updated: March 14, 2014
Last verified: March 2014
To test the theory that accelerated inflammation-promoted atherosclerosis occurs in patients with rheumatoid arthritis (RA).

Cardiovascular Diseases
Heart Diseases
Arthritis, Rheumatoid

Study Type: Observational

Resource links provided by NLM:

Further study details as provided by Vanderbilt University:

Study Start Date: September 2001
Study Completion Date: July 2007
Primary Completion Date: July 2007 (Final data collection date for primary outcome measure)
Detailed Description:


Premature cardiovascular disease is a major cause of mortality in rheumatoid arthritis (RA). The mechanisms underlying accelerated atherosclerosis and its relationship to inflammation in RA are poorly understood. Recent studies indicate that inflammation through the effects of inflammatory cytokines, and oxidative stress, through lipid peroxidation, are important in the pathogenesis of atherosclerosis. The study's hypothesis is that accelerated, inflammation-promoted atherosclerosis occurs in RA.


The study tests the hypotheses: 1) that structural and functional vascular damage is more frequent and more severe in patients with established RA than matched controls and is related to cumulative disease severity; 2) that this impairment of vascular integrity is associated with clinical and laboratory markers of inflammation, plasma homocysteine concentrations, and oxidative stress. To address these two hypotheses the relationship between longstanding inflammation and vascular integrity will be determined in a cross-sectional study of 75 patients with established RA in whom prospectively obtained clinical data are available for 15 years, and 75 matched non-RA controls. Endothelium-dependent, flow-mediated dilation of the brachial artery measured by ultrasound, and coronary calcium volume measured by electron beam computed tomography (EBCT) will provide functional and structural measures of vascular integrity, respectively. F2-isoprostane excretion, a reliable index of lipid peroxidation in vivo, homocysteine and lipid concentrations will be measured. Vascular integrity, oxidative stress, lipids and homocysteine will be compared in controls and RA patients. In the RA patients the relationship between RA activity and damage indices obtained over 15 years and vascular function and damage measures will be determined. Using the same techniques we will address hypothesis 3) that the rate of progression of vascular disease in patients with early RA can be altered by control of inflammation. In a prospective cohort of 100 patients with early RA receiving usual clinical care and 100 matched non-RA controls followed over 24 months the relationship between clinical and biochemical measures of inflammation and vascular integrity will be determined by comparing "responders" and "non-responders". These studies will provide a basic understanding of the interrelationship between inflammation, lipids, oxidative stress and vascular damage, and will suggest strategies for reversing or preventing such damage in RA and, potentially, other diseases.


Ages Eligible for Study:   18 Years and older   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Study Population
people with rheumatoid arthritis
must meet ACR criteria for RA
  Contacts and Locations
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Please refer to this study by its identifier: NCT00037336

Sponsors and Collaborators
Vanderbilt University
National Heart, Lung, and Blood Institute (NHLBI)
Principal Investigator: Charles Stein Vanderbilt University
  More Information


Responsible Party: C. Michael Stein, Professor of Medicine, Vanderbilt University Identifier: NCT00037336     History of Changes
Other Study ID Numbers: 1163
R01HL067964 ( US NIH Grant/Contract Award Number )
Study First Received: May 16, 2002
Last Updated: March 14, 2014

Additional relevant MeSH terms:
Cardiovascular Diseases
Heart Diseases
Arthritis, Rheumatoid
Joint Diseases
Musculoskeletal Diseases
Pathologic Processes
Arterial Occlusive Diseases
Vascular Diseases
Rheumatic Diseases
Connective Tissue Diseases
Autoimmune Diseases
Immune System Diseases processed this record on March 24, 2017