Key points are not available for this paper at this time.
Design
Review
RA may model inflammation's effects on arterial stiffness for future trials; leaves open whether targeted therapies alter CV outcomes.
Inflammation is a key element in atheroma formation, playing a pivotal role in the initiation, progression and propagation of the disease. Circulating levels of several cytokines including IL-6 and TNF-a are elevated in subjects with atherosclerosis, and correlate with disease burden. Levels of the acute phase reactant C-reactive protein (CRP) also predict the risk of future cardiovascular events both in subjects with known cardiovascular disease (CVD), and in apparently healthy individuals. Moreover, the incidence of CVD is increased in patients with chronic systemic inflammatory diseases such as rheumatoid arthritis (RA), and the inflammatory process of RA resembles the one seen in atherosclerosis. Both diseases involve activation of macrophages, T-cells, especially CD4þCD28and B-cells as well as increased expression of adhesion molecules and increased circulating levels of TNF-a and CRP. These facts make RA a useful “model” to investigate the relationship between systemic inflammation and CVD. The mechanism
No takes yet. Share an insight, caveat, or question.
Mäki-Petäjä et al. (2010) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: