title: Effect of 1-year anti-TNF-α therapy on aortic stiffness, carotid atherosclerosis, and calprotectin in inflammatory arthropathies: a controlled study.
abstract: BACKGROUND
  Premature arterial stiffening and atherosclerosis are increased in patients with inflammatory arthropathies such as rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA). The proinflammatory protein calprotectin is associated with inflammatory arthropathies, vascular pathology, and acute coronary events. We examined the long-term effects of treatment with tumor necrosis factor (TNF)-α antagonists on aortic stiffness and carotid intima media thickness (CIMT) in patients with inflammatory arthropathies, and the relationships to the levels of calprotectin.
  
  
  METHODS
  Fifty-five patients with RA, AS, or PsA and a clinical indication for anti-TNF-α therapy were included and followed with regular examinations for 1 year. Thirty-six patients starting with anti-TNF-α therapy were compared with a nontreatment group of 19 patients. Examinations included assessments of aortic stiffness (aortic pulse wave velocity, aPWV), CIMT, and plasma calprotectin.
  
  
  RESULTS
  After 1 year, aPWV (mean (s.d.)) was improved in the treatment group, but not in the control group (-0.54 [0.79] m/s vs. 0.06 [0.61] m/s, respectively; P = 0.004), and CIMT progression (median (quartile cut-points, 25th and 75th percentiles)) was reduced in the treatment group compared to the control group (-0.002 [-0.038, 0.030] mm vs. 0.030 [0.011, 0.043] mm, respectively; P = 0.01). In multivariable analyses, anti-TNF-α therapy over time was associated with improved aPWV (P = 0.02) and reduced CIMT progression (P = 0.04), and calprotectin was longitudinally associated with aPWV (P = 0.02).
  
  
  CONCLUSIONS
  Long-term anti-TNF-α therapy improved aortic stiffness and CIMT progression in patients with inflammatory arthropathies. Calprotectin may be a soluble biomarker reflecting aortic stiffening in these patients.
authors.affiliation: Department of Cardiology B, Oslo University Hospital Ullevaal, Oslo, Norway. kristin.angel@medisin.uio.no
authors.forename: Kristin
authors.initials: K
authors.lastname: Angel
authors.forename: Sella A
authors.initials: SA
authors.lastname: Provan
authors.forename: Magne K
authors.initials: MK
authors.lastname: Fagerhol
authors.forename: Petter
authors.initials: P
authors.lastname: Mowinckel
authors.forename: Tore K
authors.initials: TK
authors.lastname: Kvien
authors.forename: Dan
authors.initials: D
authors.lastname: Atar
mesh_terms: D000328:Adult; D000368:Aged; D018501:Antirheumatic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D015535:Arthritis, Psoriatic / Q000188:drug therapy* / Q000503:physiopathology; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002340:Carotid Artery Diseases / Q000188:drug therapy* / Q000503:physiopathology; D059168:Carotid Intima-Media Thickness; D018450:Disease Progression; D005260:Female; D006801:Humans; D039841:Leukocyte L1 Antigen Complex / Q000097:blood / Q000187:drug effects / Q000502:physiology*; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013167:Spondylitis, Ankylosing / Q000188:drug therapy* / Q000503:physiopathology; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D059289:Vascular Stiffness / Q000187:drug effects / Q000502:physiology*
chemical_list: D018501:Antirheumatic Agents; D039841:Leukocyte L1 Antigen Complex; D014409:Tumor Necrosis Factor-alpha