Mariana J Kaplan1. 1. Division of Rheumatology, University of Michigan Medical School, Ann Arbor, Michigan 48109-0680, USA. makaplan@med.umich.edu
Abstract
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-alpha 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.
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-tumornecrosis factor-alpha 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.
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