title: Endothelium-dependent and independent dilation capability of peripheral arteries in patients with systemic lupus erythematosus and antiphospholipid syndrome.
abstract: OBJECTIVE
  The study evaluated the systemic inflammatory response and endothelium-dependent and independent function of the brachial artery (BA) in systemic lupus erythematosus (SLE) patients with and without antiphospholipid syndrome (APS).
  
  
  METHODS
  The study group consisted of 42 women with SLE (21 without APS; mean age 36.1 ± 9.1, and 21 with APS; mean age 43.9 ± 13.1) and 22 healthy controls (mean age 43.5 ± 10.3). Endothelium-dependent functional response was evacuate using the flow-mediated vasodilatation (FMD) of brachial artery and endothelium-independent vasodilatation by application of glyceryl trinitrate (GTN). Using biochemical methods, circulating inflammatory markers were determined.
  
  
  RESULTS
  In comparison to controls, in both groups of patients endothelium-dependent dilation of BA was significantly reduced, and there were no differences in FMD between patients with or without APS: SLE - 7.7% (11.9-12.1), SLE+APS 7.8% (2.4-12.8), controls - 14.6% (11.2-21.1), p<0.001. However, endothelium-independent dilation of the brachial artery was significantly lower in SLE-APS patients than in controls and also lower than in the SLE group: SLE - 24.3% (15.0-28.6), SLE+APS-17.4% (13.1-22.6), controls - 23.0% (17.8-30.1), p=0.015 vs. p=0.027. Patients with SLE had significantly higher values of VCAM-1, hs-CRP, and fibrinogen than controls. In patients with SLE+APS, an additional significant increase of inflammatory markers was registered.
  
  
  CONCLUSIONS
  The results of our study indicate that patients with SLE have deteriorated endothelium-dependent and those with APS also independent vascular function which could be, together with increased inflammatory response, involved in vascular complications in these patients. The presence of APS aggravates systemic inflammatory response.
authors.affiliation: Department of Vascular Diseases, University Medical Centre Ljubljana, Slovenia.
authors.forename: M
authors.initials: M
authors.lastname: Stalc
authors.forename: M
authors.initials: M
authors.lastname: Tomsic
authors.forename: M K
authors.initials: MK
authors.lastname: Jezovnik
authors.forename: P
authors.initials: P
authors.lastname: Poredos
mesh_terms: D000328:Adult; D016736:Antiphospholipid Syndrome / Q000000981:diagnostic imaging / Q000276:immunology / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000276:immunology / Q000503:physiopathology*; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000276:immunology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D007249:Inflammation / Q000000981:diagnostic imaging / Q000276:immunology / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000000981:diagnostic imaging / Q000276:immunology / Q000503:physiopathology*; D008875:Middle Aged; D005996:Nitroglycerin; D017524:Slovenia; D018608:Ultrasonography, Doppler; D014664:Vasodilation; D014665:Vasodilator Agents
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D014665:Vasodilator Agents; D005996:Nitroglycerin