Subclinical atherosclerosis in young patients with rheumatoid arthritis and low disease activity

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E. Bartoloni Bocci *
S. Marchesi
F. Delle Monache
G. Vaudo
A. Giordano
F. Ragni Alunni
C. Angrisani
E. Mannarino
Y. Shoenfeld
R. Gerli
(*) Corresponding Author:
E. Bartoloni Bocci | office@pagepress.org

Abstract

Background: There is an increasing body of evidence suggesting that subjects with rheumatoid arthritis (RA) are characterized by acceleration of atherosclerotic process of arterial wall. However, all investigations performed so far to evaluate subclinical atherosclerosis in RA included subjects without selection for age and degree of disease activity that may represent confounding factors in such an evaluation. Objectives: To verify signs of accelerated subclinical atherosclerosis in young subject suffering from RA but with low disease activity. Methods: Thirty-two patients with RA and 28 age- and sex-matched control subjects with non-inflammatory rheumatic diseases were enrolled. Inclusion criteria were age less than 60 and low disease activity with score £3.2 according to DAS28, while subjects with traditional risk factors for and/or overt cardiovascular disease were ruled out from the study. Both patients and controls underwent evaluation of carotid and femoral artery intima-media thickness by ultrasounds. Results: Patients had higher intima-media thickness than controls of all the sites evaluated at carodit artery level, whereas there were no differences at the comparison of the superficial and common femoral artery wall. At the univariate analysis, a positive correlation between LDL cholesterol levels and intima-media thickness at the carotid bifurcation was found. Conclusions: Young patients with RA and low disease activity have acceleration of atherosclerosis development as shown by increased intima-media thickness of carotid artery with respect to subjects without inflammatory rheumatic disease. It is conceivable that the organic damage of arterial wall could be the result of persistent endothelial dysfunction induced by chronic inflammation and immune dysregulation which characterize RA.

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