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Atherosclerosis in Rheumatoid Arthritis

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ClinicalTrials.gov Identifier: NCT00037336
Recruitment Status : Completed
First Posted : May 17, 2002
Last Update Posted : March 17, 2014
National Heart, Lung, and Blood Institute (NHLBI)
Information provided by (Responsible Party):
C. Michael Stein, Vanderbilt University

Tracking Information
First Submitted Date May 16, 2002
First Posted Date May 17, 2002
Last Update Posted Date March 17, 2014
Study Start Date September 2001
Actual Primary Completion Date July 2007   (Final data collection date for primary outcome measure)
Current Primary Outcome Measures Not Provided
Original Primary Outcome Measures Not Provided
Change History
Current Secondary Outcome Measures Not Provided
Original Secondary Outcome Measures Not Provided
Current Other Pre-specified Outcome Measures Not Provided
Original Other Pre-specified Outcome Measures Not Provided
Descriptive Information
Brief Title Atherosclerosis in Rheumatoid Arthritis
Official Title Not Provided
Brief Summary To test the theory that accelerated inflammation-promoted atherosclerosis occurs in patients with rheumatoid arthritis (RA).
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.

Study Type Observational
Study Design Not Provided
Target Follow-Up Duration Not Provided
Biospecimen Not Provided
Sampling Method Not Provided
Study Population people with rheumatoid arthritis
  • Atherosclerosis
  • Cardiovascular Diseases
  • Heart Diseases
  • Inflammation
  • Arthritis, Rheumatoid
Intervention Not Provided
Study Groups/Cohorts Not Provided
Publications *

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
Recruitment Information
Recruitment Status Completed
Enrollment Not Provided
Original Enrollment Not Provided
Actual Study Completion Date July 2007
Actual Primary Completion Date July 2007   (Final data collection date for primary outcome measure)
Eligibility Criteria must meet ACR criteria for RA
Sexes Eligible for Study: All
Ages 18 Years and older   (Adult, Older Adult)
Accepts Healthy Volunteers No
Contacts Contact information is only displayed when the study is recruiting subjects
Listed Location Countries Not Provided
Removed Location Countries  
Administrative Information
NCT Number NCT00037336
Other Study ID Numbers 1163
R01HL067964 ( U.S. NIH Grant/Contract )
Has Data Monitoring Committee Not Provided
U.S. FDA-regulated Product Not Provided
IPD Sharing Statement Not Provided
Current Responsible Party C. Michael Stein, Vanderbilt University
Original Responsible Party Not Provided
Current Study Sponsor Vanderbilt University
Original Study Sponsor National Heart, Lung, and Blood Institute (NHLBI)
Collaborators National Heart, Lung, and Blood Institute (NHLBI)
Principal Investigator: Charles Stein Vanderbilt University
PRS Account Vanderbilt University
Verification Date March 2014