title: Tumor necrosis factor-alpha antagonists improve aortic stiffness in patients with inflammatory arthropathies: a controlled study.
abstract: The chronic inflammatory state of rheumatoid arthritis and other inflammatory arthropathies, such as ankylosing spondylitis and psoriatic arthritis, contributes to the accelerated atherosclerosis associated with these conditions. This study evaluates the effect of treatment with tumor necrosis factor (TNF)-alpha antagonists on arterial stiffness in patients with inflammatory arthropathies. A total of 60 patients with rheumatoid arthritis, ankylosing spondylitis, or psoriatic arthritis and clinical indication for anti-TNF-alpha therapy were included. Thirty-five patients started with anti-TNF-alpha therapy and were compared with a nontreatment group of 25 patients. Aortic stiffness (aortic pulse wave velocity), augmentation index, and disease activity were assessed at baseline and after 3 months. Aortic pulse wave velocity (mean+/-SD) was reduced in the treatment group but not in the control group (-0.50+/-0.78 m/s versus 0.05+/-0.54 m/s, respectively; P=0.002). Concomitantly, C-reactive protein and the disease activity score were reduced in the treatment group (-9.3+/-20.2 mg/L [P<0.001] and -0.74+/-0.91 [P=0.004]). Augmentation index remained unchanged in both groups (0.1+/-7.1% versus -1.0+/-5.8%, respectively; P=0.53). In a multivariate linear regression model, only treatment with TNF-alpha antagonist and change in mean arterial pressure predicted alterations in aortic pulse wave velocity. In summary, anti-TNF-alpha therapy improved aortic stiffness in patients with inflammatory arthropathies. These findings support the idea that anti-inflammatory treatment has a favorable effect on cardiovascular risk in patients with inflammatory arthropathies.
authors.affiliation: Department of Cardiology, Oslo University Hospital Aker, 0514 Oslo, Norway. kristin.angel@medisin.uio.no
authors.forename: Kristin
authors.initials: K
authors.lastname: Angel
authors.forename: Sella Aarrestad
authors.initials: SA
authors.lastname: Provan
authors.forename: Hanne Løvdahl
authors.initials: HL
authors.lastname: Gulseth
authors.forename: Petter
authors.initials: P
authors.lastname: Mowinckel
authors.forename: Tore Kristian
authors.initials: TK
authors.lastname: Kvien
authors.forename: Dan
authors.initials: D
authors.lastname: Atar
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D015535:Arthritis, Psoriatic / Q000175:diagnosis / Q000188:drug therapy; D001172:Arthritis, Rheumatoid / Q000175:diagnosis / Q000188:drug therapy*; D050197:Atherosclerosis / Q000175:diagnosis* / Q000453:epidemiology; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000187:drug effects; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011336:Probability; D012016:Reference Values; D018570:Risk Assessment; D012720:Severity of Illness Index; D013167:Spondylitis, Ankylosing / Q000175:diagnosis / Q000188:drug therapy; D018709:Statistics, Nonparametric; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000627:therapeutic use; D014655:Vascular Resistance / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D014409:Tumor Necrosis Factor-alpha