류마티스 관절염과 동맥 경화

Abstract

Recently, inflammation has emerged as an important pathogenic mechanism of atherosclerosis. Inflammation has a role in both the initiation and the progression of atherosclerosis and anti-inflammatory agents may have a role in the prevention of cardiovascular disease. C-reactive protein (CRP) is an acute-phase reactant that is a sensitive marker for underlying systemic inflammation. Elevated plasma concentrations of CRP have been reported in patients with acute ischemia or myocardial infarction. Prospective studies indicate that baseline levels of CRP are associated with increased risk of myocardial infarction and stroke among apparently healthy individuals and those with symptomatic angina pectoris or prior myocardial infarction. Furthermore, the value of high-sensitivity testing for CRP appears to be additive to that of total and HDL-cholesterol for cardiovascular risk prediction. The data demonstrating associations between inflammation markers and cardiovascular disease (CVD) have been based on patients without apparent chronic inflammatory conditions. Therefore, it is logical to investigate if the same implications hold among patients with chronic inflammation as an underlying disease. Rheumatoid arthritis is a typical chronic inflammatory disease and CRP well reflects on the disease activity of RA. A number of studies have suggested increased cardiovascular disease and mortality among patients with rheumatoid arthritis. As a potential underlying mechanism for this observation, we have recently shown active untreated RA is associated with an adverse lipid profile that is conventionally accepted as a risk factor for cardiovascular disease. In a subsequent prospective inception cohort study, we have shown the adverse lipid profile can be improved to an extent that is clinically meaningful by effectively treating RA without using a lipid-lowering agent. Our data indicate that better control of rheumatoid arthritis is associated with a better lipid profile that may reduce the risk of cardiovascular disease. We also found morphologic and functional evidence of subclinical accelerated atherosclerosis in patients with RA. We have shown that RA patients had increased intima-media thickness (IMT) of carotid artery and there is decreased vascular endothelial function in patients with RA. The degree of inflammation is well correlated with IMT and endothelial dysfunction in RA patients. In conclusion, RA patients have risk for accelerated atherosclerosis, which may be associated with the inflammation of RA.