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Atherosclerosis in Rheumatoid Arthritis

This study has been completed.
Sponsor:
Collaborator:
Information provided by (Responsible Party):
C. Michael Stein, Vanderbilt University
ClinicalTrials.gov Identifier:
NCT00037336
First received: May 16, 2002
Last updated: March 14, 2014
Last verified: March 2014
  Purpose

To test the theory that accelerated inflammation-promoted atherosclerosis occurs in patients with rheumatoid arthritis (RA).


Condition
Atherosclerosis
Cardiovascular Diseases
Heart Diseases
Inflammation
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:

BACKGROUND:

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.

DESIGN NARRATIVE:

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.

  Eligibility

Ages Eligible for Study:   18 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Study Population

people with rheumatoid arthritis

Criteria

must meet ACR criteria for RA

  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 ClinicalTrials.gov identifier: NCT00037336

Sponsors and Collaborators
Vanderbilt University
Investigators
Principal Investigator: Charles Stein Vanderbilt University
  More Information

Publications:

Responsible Party: C. Michael Stein, Professor of Medicine, Vanderbilt University
ClinicalTrials.gov Identifier: NCT00037336     History of Changes
Other Study ID Numbers: 1163, R01HL067964
Study First Received: May 16, 2002
Last Updated: March 14, 2014
Health Authority: United States: Federal Government

Additional relevant MeSH terms:
Arteriosclerosis
Arthritis
Arthritis, Rheumatoid
Atherosclerosis
Cardiovascular Diseases
Heart Diseases
Inflammation
Arterial Occlusive Diseases
Autoimmune Diseases
Connective Tissue Diseases
Immune System Diseases
Joint Diseases
Musculoskeletal Diseases
Pathologic Processes
Rheumatic Diseases
Vascular Diseases

ClinicalTrials.gov processed this record on November 24, 2014