title: Non-invasive assessment of arterial stiffness indices by applanation tonometry and pulse wave analysis in patients with rheumatoid arthritis treated with TNF-alpha blocker remicade (infliximab).
abstract: Rheumatoid arthritis (RA) is accompanied by long lasting inflammation, which may lead to arterial dysfunction and premature aging of the arteries. The purpose of this clinical work was to determine the modification of carotid-radial pulse wave velocity (PWV) and aortic augmentation index (AIx) in young-aged RA patients and the influence of treatment with anti-TNF-alpha (infliximab) on these measures. We examined 68 RA patients (mean age 40.68 yrs) with moderate or high disease activity (DAS28 5.37 +/- 0.94) and 87 controls (mean age 38.10 yrs). PWV and AIx were assessed non-invasively by applanation tonometry. A blood test included serum lipid profile, and high-sensitivity CRP measurements. We found that in RA patients, AIx (p < 0.001) was significantly higher while PWV (p = 0.315) did not differ as compared to control. Multiple regression analysis revealed the presence of RA is an independent predictor for AIx (R2 = 0.718, adjusted R2 = 0.707; p < 0.001). Analysis (Mann-Whitney test) in 15 RA patients revealed lowering of PWV (p = 0.004) under infliximab therapy with no change in AIx (p = 0.573), suggesting the improvement of arterial wall function by anti-TNF-alpha therapy. We conclude that increased AIx is more prominent in RA patients as compared to the controls. PWV appears to be a less sensitive marker for the detection of enhanced development of arterial stiffness in relatively young-aged RA patients. However, PWV may serve as a good marker to discern effects of infliximab on artery elasticity.
authors.affiliation: Institute of Experimental and Clinical Medicine at Vilnius University, Lithuania. alma.cypiene@santa.lt
authors.forename: Alma
authors.initials: A
authors.lastname: Cypiene
authors.forename: Aleksandras
authors.initials: A
authors.lastname: Laucevicius
authors.forename: Algirdas
authors.initials: A
authors.lastname: Venalis
authors.forename: Ligita
authors.initials: L
authors.lastname: Ryliskyte
authors.forename: Jolanta
authors.initials: J
authors.lastname: Dadoniene
authors.forename: Zaneta
authors.initials: Z
authors.lastname: Petrulioniene
authors.forename: Milda
authors.initials: M
authors.lastname: Kovaite
authors.forename: Violetta
authors.initials: V
authors.lastname: Laskova
authors.forename: Jonas
authors.initials: J
authors.lastname: Gintautas
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001158:Arteries / Q000187:drug effects / Q000502:physiology*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000473:pathology*; D015992:Body Mass Index; D002339:Carotid Arteries / Q000473:pathology; D004548:Elasticity; D005260:Female; D006801:Humans; D000069285:Infliximab; D008297:Male; D008365:Manometry; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab