Medical Thesis
PREVALENCE OF SILENT ISCHEMIC HEART DISEASE IN PATIENTS OF
RHEUMATOID ARTHRITIS
THESIS FOR THE DEGREE OF DOCTOR OF MEDICINE (GENERAL MEDICINE)
INTRODUCTION
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
RHEUMATOID ARTHRITIS
THESIS FOR THE DEGREE OF DOCTOR OF MEDICINE (GENERAL MEDICINE)
INTRODUCTION
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