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Connective tissue diseases and noninvasive evaluation of atherosclerosis

Authors Ardita G, Failla G, Finocchiaro PM, Mugno F, Attanasio L, Timineri S, Di Salvo MM

Received 17 November 2013

Accepted for publication 30 March 2014

Published 18 June 2014 Volume 2014:2 Pages 53—57

DOI https://doi.org/10.2147/JVD.S57728

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 5


Giorgio Ardita, Giacomo Failla, Paolo Maria Finocchiaro, Francesco Mugno, Luigi Attanasio, Salvatore Timineri, Michelangelo Maria Di Salvo

Cardiovascular Department, Angiology Unit, Ferrarotto Hospital, Catania, Italy

Abstract: Connective tissue diseases (CTDs) are associated with increased risk of cardiovascular disease due to accelerated atherosclerosis. In patients with autoimmune disorders, in addition to traditional risk factors, an immune-mediated inflammatory process of the vasculature seems to contribute to atherogenesis. Several pathogenetic mechanisms have been proposed, including chronic inflammation and immunologic abnormalities, both able to produce vascular damage. Macrovascular atherosclerosis can be noninvasively evaluated by ultrasound measurement of carotid or femoral plaque. Subclinical atherosclerosis can be evaluated by well-established noninvasive techniques which rely on ultrasound detection of carotid intima-media thickness. Flow-mediated vasodilatation and arterial stiffness are considered markers of endothelial dysfunction and subclinical atherosclerosis, respectively, and have been recently found to be impaired early in a wide spectrum of autoimmune diseases. Carotid intima-media thickness turns out to be a leading marker of subclinical atherosclerosis, and many studies recognize its role as a predictor of future vascular events, both in non-CTD individuals and in CTD patients. In rheumatic diseases, flow-mediated dilatation and arterial stiffness prove to be strongly correlated with inflammation, disease damage index, and with subclinical atherosclerosis, although their prognostic role has not yet been conclusively shown. Systemic lupus erythematosus, rheumatoid arthritis, and likely antiphospholipid syndrome are better associated with premature and accelerated atherosclerosis. Inconclusive results were reported in systemic sclerosis.

Keywords:
rheumatic disease, subclinical atherosclerosis, arterial stiffness, accelerated atherosclerosis

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