Rheumatoid arthritis (RA) is characterized by chronic inflammation involving connective tissues throughout the body, particularly diarthrodial joints, eventually leading to joint destruction and physical disability1. In parallel with erosive arthritis, other extraarticular manifestations have been described in the disease, representing systemic activation of the immune system1, which is generally associated with excess mortality2. Atherosclerosis, among others, is considered an extraarticular manifestation of RA3. Well established RA reduces median life expectancy, compared to that of healthy subjects4,5. Overall, about 40% excess mortality has been shown in RA6. In addition to infections and gastrointestinal hemorrhage due to nonsteroidal antiinflammatory drugs (NSAID), cardiovascular (CV) mortality is increased in RA. Besides CV diseases, the leading causes of death in RA are infection and malignancies, which also contribute to increased mortality7,8.
Accelerated atherosclerosis in RA is signified by increased CV morbidity and mortality8–12. Generally, in patients with RA, CV diseases reduce life expectancy by 5 to 10 years on average13–15. In both RA and atherosclerosis, inflammatory immune-mediated processes play central roles, and the 2 diseases share several common pathogenic mechanisms14,16,17. Besides the common inflammatory pathways, RA itself has been considered as an independent risk factor for accelerated CV disease18,19. In a large prospective cohort of women, based on over 100,000 subjects, participants with RA had a significantly increased risk of myocardial infarction compared to those without RA19.
Traditional CV risk …
Address correspondence to Dr. Szodoray; E-mail: szodoray{at}gmail.com