title: Different type of carotid arterial wall remodeling in rheumatoid arthritis compared with healthy subjects: a case-control study.
abstract: OBJECTIVE
  Rheumatoid arthritis (RA) is associated with an increased cardiovascular (CV) risk, but mechanisms behind this increased risk have not been fully elucidated. Carotid arterial remodeling is the change of structural properties in response to hemodynamic or metabolic factors aimed at keeping wall stress within certain limits. This process might become maladaptive when stress on the arterial wall increases beyond these limits. We investigated whether maladaptive carotid arterial remodeling is present in RA compared with control subjects.
  
  
  METHODS
  The 2 cohorts were 96 patients with RA and 274 healthy subjects, who were investigated cross-sectionally. Carotid intima-media thickness (cIMT) and interadventitial diameter (IAD) were assessed by B-mode carotid ultrasonography. Lumen diameter (LD), circumferential wall stress (CWS), and circumferential wall tension (CWT) were calculated. Linear regression analyses were used to investigate the association between presence of RA and carotid arterial remodeling.
  
  
  RESULTS
  Compared with healthy subjects, RA was associated with a 0.40 mm (9.3%) greater LD, 0.41 mm (7.8%) greater IAD, 10% higher CWS, and 8% higher CWT. The groups had comparable cIMT. Associations remained similar after exclusion of patients with prior CV disease and after adjustment for demographic factors and CV risk factors.
  
  
  CONCLUSIONS
  RA is associated with maladaptive outward carotid arterial remodeling. These results are relevant because maladaptive outward remodeling is associated with plaque instability and rupture. These results indicate an alternative pathway, beyond the traditional CV risk factors, in RA that amplifies the CV risk.
authors.affiliation: Department of Rheumatology, Jan van Breemen Research Institute - Reade, The Netherlands. Alper.vanSijl@vumc.nl
authors.forename: Alper M
authors.initials: AM
authors.lastname: Van Sijl
authors.forename: Katja
authors.initials: K
authors.lastname: Van Den Hurk
authors.forename: Mike J L
authors.initials: MJ
authors.lastname: Peters
authors.forename: Vokko P
authors.initials: VP
authors.lastname: Van Halm
authors.forename: Giel
authors.initials: G
authors.lastname: Nijpels
authors.forename: Coen D A
authors.initials: CD
authors.lastname: Stehouwer
authors.forename: Y V O M
authors.initials: YV
authors.lastname: Smulders
authors.forename: Alexandre E
authors.initials: AE
authors.lastname: Voskuyl
authors.forename: Jacqueline M
authors.initials: JM
authors.lastname: Dekker
authors.forename: Michael T
authors.initials: MT
authors.lastname: Nurmohamed
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D050197:Atherosclerosis / Q000150:complications; D001783:Blood Flow Velocity; D002318:Cardiovascular Diseases / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D059168:Carotid Intima-Media Thickness; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011673:Pulsatile Flow; D017539:Tunica Intima / Q000473:pathology* / Q000503:physiopathology; D017540:Tunica Media / Q000473:pathology* / Q000503:physiopathology; D059289:Vascular Stiffness / Q000502:physiology