Cardiovascular Disease in Rheumatoid Arthritis
Cardiovascular Disease in Rheumatoid Arthritis
Purpose of Review: Individuals with rheumatoid arthritis are at increased risk for morbidity and mortality from cardiovascular disease (CVD). The purpose of this review is to discuss recent advances in our understanding of the pathogenesis, prevalence, treatment, and prevention of accelerated atherosclerotic disease in rheumatoid arthritis.
Recent Findings: Recent reports have highlighted the increased risk for silent myocardial infarction and sudden death in rheumatoid arthritis, and the potential roles of traditional and nontraditional risk factors for CVD, including abnormal revascularization of damaged peripheral blood vessels and genetic polymorphisms. Several studies have also added important information on the possible role of anti-tumor necrosis factor-a therapy, other disease modifying antirheumatic drugs, and nonsteroidal anti-inflammatory drugs in decreasing CVD risk.
Summary: 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. Good control of the inflammation, immunologic disturbances, and metabolic changes seen in rheumatoid arthritis are crucial in the prevention of this potentially lethal complication. There is a need for heightened awareness of the increased risk for silent ischemia, early myocardial infarction, and sudden death. Further exploration of the mechanisms of vascular repair and their potential role in premature atherosclerosis is needed.
Rheumatoid arthritis, a chronic inflammatory disease that affects 1% of the general population, is associated with increased mortality, which is predominantly due to accelerated coronary artery and cerebrovascular atherosclerosis. Indeed, women with rheumatoid arthritis are twice as likely to suffer a myocardial infarction compared with women without rheumatoid arthritis, and this increased risk is also seen in men. Largely because of this heightened risk for atherosclerotic disease, overall life expectancy in rheumatoid arthritis is significantly reduced, with standardized mortality rates ranging from 1.28 to 3.0. This phenomenon is not restricted to individuals with established rheumatoid arthritis, because increased mortality in patients who are positive for rheumatoid factor and have early inflammatory polyarthritis has also been reported.
Importantly, cardiovascular events occur approximately a decade earlier in the rheumatoid arthritis cohort, suggesting that - like in diabetes mellitus - rheumatoid arthritis is a significant independent risk factor for premature ischemic heart disease. Furthermore, previous studies have suggested that traditional cardiovascular risk factors do not fully account for the increased propensity for vascular complications in rheumatoid arthritis. Moreover, immune dysregulation, inflammation, and metabolic disturbances characteristic of rheumatoid arthritis may play an important role in the development of early atherosclerosis and premature mortality.
It appears that variables that increase cardiovascular mortality in rheumatoid arthritis are present very early during the natural history of the disease, because patients with new onset, rheumatoid factor positive rheumatoid arthritis exhibit evidence of abnormal endothelial function, which is a good predictor of future development of atherosclerosis. Rheumatoid arthritis extra-articular manifestations, usually related to uncontrolled inflammation, are associated with increased cardiovascular mortality, further suggesting that processes intrinsic to the pathogenesis of rheumatoid arthritis play important roles in cardiovascular damage and its clinical consequences. However, despite the increased risk for vascular events, strategies to prevent cardiovascular disease (CVD) are similar among women with and those without rheumatoid arthritis. This review highlights recent investigations focusing on the impact of CVD in rheumatoid arthritis, explores novel potential mechanisms implicated in the increased propensity to atherosclerotic disease, and discusses the potential role of disease-modifying antirheumatic drugs (DMARDs) and other novel therapies in promoting and/or preventing premature CVD in rheumatoid arthritis.
Purpose of Review: Individuals with rheumatoid arthritis are at increased risk for morbidity and mortality from cardiovascular disease (CVD). The purpose of this review is to discuss recent advances in our understanding of the pathogenesis, prevalence, treatment, and prevention of accelerated atherosclerotic disease in rheumatoid arthritis.
Recent Findings: Recent reports have highlighted the increased risk for silent myocardial infarction and sudden death in rheumatoid arthritis, and the potential roles of traditional and nontraditional risk factors for CVD, including abnormal revascularization of damaged peripheral blood vessels and genetic polymorphisms. Several studies have also added important information on the possible role of anti-tumor necrosis factor-a therapy, other disease modifying antirheumatic drugs, and nonsteroidal anti-inflammatory drugs in decreasing CVD risk.
Summary: 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. Good control of the inflammation, immunologic disturbances, and metabolic changes seen in rheumatoid arthritis are crucial in the prevention of this potentially lethal complication. There is a need for heightened awareness of the increased risk for silent ischemia, early myocardial infarction, and sudden death. Further exploration of the mechanisms of vascular repair and their potential role in premature atherosclerosis is needed.
Rheumatoid arthritis, a chronic inflammatory disease that affects 1% of the general population, is associated with increased mortality, which is predominantly due to accelerated coronary artery and cerebrovascular atherosclerosis. Indeed, women with rheumatoid arthritis are twice as likely to suffer a myocardial infarction compared with women without rheumatoid arthritis, and this increased risk is also seen in men. Largely because of this heightened risk for atherosclerotic disease, overall life expectancy in rheumatoid arthritis is significantly reduced, with standardized mortality rates ranging from 1.28 to 3.0. This phenomenon is not restricted to individuals with established rheumatoid arthritis, because increased mortality in patients who are positive for rheumatoid factor and have early inflammatory polyarthritis has also been reported.
Importantly, cardiovascular events occur approximately a decade earlier in the rheumatoid arthritis cohort, suggesting that - like in diabetes mellitus - rheumatoid arthritis is a significant independent risk factor for premature ischemic heart disease. Furthermore, previous studies have suggested that traditional cardiovascular risk factors do not fully account for the increased propensity for vascular complications in rheumatoid arthritis. Moreover, immune dysregulation, inflammation, and metabolic disturbances characteristic of rheumatoid arthritis may play an important role in the development of early atherosclerosis and premature mortality.
It appears that variables that increase cardiovascular mortality in rheumatoid arthritis are present very early during the natural history of the disease, because patients with new onset, rheumatoid factor positive rheumatoid arthritis exhibit evidence of abnormal endothelial function, which is a good predictor of future development of atherosclerosis. Rheumatoid arthritis extra-articular manifestations, usually related to uncontrolled inflammation, are associated with increased cardiovascular mortality, further suggesting that processes intrinsic to the pathogenesis of rheumatoid arthritis play important roles in cardiovascular damage and its clinical consequences. However, despite the increased risk for vascular events, strategies to prevent cardiovascular disease (CVD) are similar among women with and those without rheumatoid arthritis. This review highlights recent investigations focusing on the impact of CVD in rheumatoid arthritis, explores novel potential mechanisms implicated in the increased propensity to atherosclerotic disease, and discusses the potential role of disease-modifying antirheumatic drugs (DMARDs) and other novel therapies in promoting and/or preventing premature CVD in rheumatoid arthritis.
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