Different Type of Carotid Arterial Wall Remodeling in Rheumatoid Arthritis Compared with Healthy Subjects: A Case-Control Study

Alper M. van Sijl*, Katja van den Hurk, Mike J. L. Peters, Vokko P. Van Halm, Giel Nijpels, Coen D. A. Stehouwer, Yvo M. Smulders, Alexandre E. Voskuyl, Jacqueline M. Dekker, Michael T. Nurmohamed

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

15 Citations (Web of Science)

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. Conclusion. 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. (First Release Oct 1 2012; J Rheumatol 2012;39:2261-6; doi:10.3899/jrheum.120617)
Original languageEnglish
Pages (from-to)2261-2266
JournalJournal of Rheumatology
Volume39
Issue number12
DOIs
Publication statusPublished - Dec 2012

Keywords

  • RHEUMATOID ARTHRITIS
  • CAROTID ARTERIAL WALL REMODELING
  • CARDIOVASCULAR DISEASE

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