PP.13.17: ARTERIAL STIFFNESS AND SYSTEMIC INFLAMMATION IN PATIENTS WITH RHEMATOID ARTHRITIS AND ANKYLOSING SPONDYLITIS. (June 2015)

• Record Type: Journal Article
• Authors: Dzieza-Grudnik, A.; Sulicka-Grodzicka, J.; Strach, M.; Siga, O.; Klimek, E.; Korkosz, M.; Grodzicki, T.
• Is Part Of: Journal of hypertension. Volume 33(2015)Supplement 1
• Publication Date: 2015-06
• Subjects: Hypertension -- Periodicals; Hypertension -- Periodicals; 616.132005
• DOI: 10.1097/01.hjh.0000468089.25581.2d
• Languages: English
• ISSNs: 1473-5598

Abstract

Abstract : Objective: Patients with inflammatory arthritis have increased cardiovascular risk. The aim of this study was to assess large arterial stiffness and inflammatory markers in patients with short duration rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Figure. No caption available. Design and method: The 77 patients with RA and AS, and 29 healthy subjects were examined. Traditional cardiovascular risk factors, markers of inflammation and endothelial activation (IL-6, IL-18, TNF, hsCRP, fibrinogen, sICAM) as well as carotid-femoral pulse wave velocity (PWV) were measured. The overall measure of inflammation based on the individual values of above-mentioned inflammatory markers were calculated. To compare differences between the groups the Mann-Whitney or Kruskal-Wallis tests were calculated. Results: There were no significant differences in traditional cardiovascular risk factors between examined groups with exception of HDL–cholesterol level (p < 0, 05). The mean duration of disease symptoms was one and six years for RA and AS respectively. The results of inflammatory markers analysis are summarized in Table 1. The positive correlation (r = 0, 23, p < 0, 05) between TNF < alfa> and PWV was observed, but it was no longer significant after adjustment for age. Conclusions: In comparison to healthy subjects, patients with inflammatory arthritis of short duration were not presented increased arterial stiffness despite high grade systemic inflammation. Our findings do not support the hypothesis that systemic inflammation is involved in acceleration of atherosclerosis early in the course of the disease.