This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. OBJECTIVE: This study will examine to what extent atherosclerosis and cardiovascular morbidity are explained by systemic inflammation in rheumatoid arthritis (RA), accounting for the competing influence of established cardiovascular risk factors.
The aims are: (1) To determine the extent of atherosclerosis that is explained by cumulative systemic inflammation in RA; (2) To determine the role of inflammation in the progression of atherosclerosis in patients with RA; and (3) To determine the role of ongoing inflammatory disease activity as a risk factor for cardiac and cerebrovascular atherothrombotic events in RA. RESEARCH PLAN AND METHODS: 680 members of an established cohort of RA patients will undergo two non-invasive procedures to measure atherosclerosis: high resolution B-mode ultrasound of the carotid intima-medial thickness (IMT) and ankle-arm systolic blood pressure index. These measures will be compared to the severity of joint damage, which reflects cumulative inflammation in RA. The influence of inflammation on the progression of carotid IMT will be examined, and the influence of ongoing inflammatory disease activity on the incidence of cardiac and cerebrovascular events in the RA cohort will be assessed. Data analysis will focus on correlations between the measures of inflammation and atherosclerosis and the predictive power of inflammatory changes and cardiac/cerebrovascular endpoints. CLINICAL
Persons with rheumatoid arthritis (RA) experience an increased risk of cardiovascular disease compared to the general population. This protocol is designed to determine the role of long-term systemic inflammation in the development of atherosclerosis in persons with RA and to compare the measures of inflammation to cardiovascular risk factors as predictors of cardiac and cerebrovascular morbidity, and it will point the way for future research into the mechanisms of atherogenesis. In addition, it will have implications for the management of patients with RA and other inflammatory diseases, by extending the current indications for anti-inflammatory therapy to the prevention of atherosclerosis. This would ultimately lengthen the life expectancy and improve the quality of life of people with inflammatory diseases.
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