FOR THE DEGREE OF
DOCTOR OF MEDICINE
Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder of unknown etiology marked by a symmetric, peripheral polyarthritis and various systemic manifestations. The process involves an inflammatory response of the synovium secondary to hyperplasia of synovial cells, excess synovial fluid, and the development of fibrous tissue(pannus) in the synovium. The pathology of the disease process often leads to the destruction of articular cartilage and ankylosis of the joints.
The most common cause of death in RA is cardiovascular disease, accounting for more than 50% of the mortality (2). The most likely explanation is that the inflammation associated with RA has an impact on the vasculature. The pathogenic mechanisms involved in accelerated cardiovascular complications in rheumatoid arthritis appear to be complex and multifactorial. Both traditional and nontraditional risk factors potentially contribute to the increased cardiovascular risk. There is a need for heightened awareness of the increased risk for silent ischemia, early myocardial infarction, and sudden death (4). The underlying cause of ischaemic heart disease (IHD), appears to be accelerated in patients with RA. The reason for this may be related to clustering of classical cardiac risk factors such as dyslipidaemia, a prothrombotic state and other processes.
However, classical risk factors, though important, do not appear to be sufficient to explain the accelerated atherosclerosis associated with RA (5) . This is possibly due to the systemic inflammation associated with RA, which may make RA itself (like diabetes) an independent risk factor for the development of IHD (6). Accumulating evidence suggests that systemic inflammation indeed has an important role in the development of atherosclerosis (7), and markers of inflammatory activity such as C reactive protein (CRP) are predictive of cardiovascular risk in the general population (8). A higher risk of sudden cardiac death is associated with particular HLA–DRB1 genotypes that are more frequent in patients with RA. and this can explain in part the higher risk of sudden death in these patients (9).
There is evidence that the presentation of coronary heart disease is different in RA patients compared with individuals without RA. Ischemic heart disease may be clinically silent in many RA patients, and there appears to be a higher risk of unrecognized myocardial infarction and sudden cardiac death. RA patients also have a lower likelihood of demonstrating angina symptoms (10). Enhanced inflammatory process may promote the development of heart dysfunction in inflammatory arthritis.
In seropositive RA, the extent of inflammation has been shown to predict CV disease and overall mortality (9), so aggressive coronary heart disease prevention strategies should be tested for persons with rheumatoid arthritis to decrease mortality (12).
AIMS AND OBJECTIVES
1. To determine the prevalence of silent IHD in rheumatoid arthritis patients.
2. To identify the predictors of silent IHD in patients with rheumatoid arthritis.
3. To study the correlation between silent IHD and RA disease activity.
MATERIALS AND METHODS
The present study will be carried out in department of General Medicine, N.S.C.B. Medical College & Hospital,...