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Microvascular function is impaired in ankylosing spondylitis and improves after TNFα blockade
  1. I.C. van Eijk (i.v.eijk{at}janvanbreemen.nl)
  1. Jan van Breemen Institute, Netherlands
    1. M.J.L. Peters (mjl.peters{at}vumc.nl)
    1. VU University Medical Center, Netherlands
      1. E.H. Serne (e.serne{at}vumc.nl)
      1. VU University Medical Center, Netherlands
        1. I.E. van der Horst-Bruinsma (ie.vanderhorst{at}vumc.nl)
        1. VU University Medical Center, Netherlands
          1. B.A.C. Dijkmans (bac.dijkmans{at}vumc.nl)
          1. VU University Medical Center, Netherlands
            1. Y.M. Smulders (y.smulders{at}vumc.nl)
            1. VU University Medical Center, Netherlands
              1. M.T. Nurmohamed (m.nurmohamed{at}janvanbreemen.nl)
              1. VU University Medical Center, Netherlands

                Abstract

                Objectives: Ankylosing spondylitis (AS) is associated with increased cardiovascular morbidity and mortality. Microvascular function has been linked to several risk factors for cardiovascular disease. Inflammation in AS may cause microvascular dysfunction. To test this, we assessed microvascular function in 1] AS patients compared to healthy controls and 2] AS patients before and after one month of anti-TNFα treatment with etanercept.

                Methods: Fifteen consecutive AS patients, who were scheduled for etanercept treatment according to the ASAS guidelines, and 12 healthy controls matched for age and sex, were recruited. Endothelium-dependent and -Vindependent vasodilatation in skin were evaluated with laser Doppler fluxmetry after iontophoresis of acetylcholine and sodium nitroprusside, respectively. Videomicroscopy was used to measure recruitment of skin capillaries after arterial occlusion.

                Results: Compared to healthy controls, AS patients had impaired endothelium-dependent vasodilatation and capillary recruitment. Following anti-TNFα treatment, microvascular function improved significantly for both endothelium-dependent vasodilatation (P=0.03) and capillary recruitment (P=0.006). A significant correlation was observed between changes in endothelium-dependent vasodilatation and changes in ESR (r=-0.56; P=0.03).

                Conclusion: Microvascular dysfunction is present in AS patients, with active disease, but improves as inflammation regresses after TNFα blockade.

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