Patients with antiphospholipid syndrome display endothelial perturbation

Background : there is strong evidence that antiphospholipid antibodies (aPL) perturb endothelium both in vitro and in experimental animal models. by inducing a vasculopathy and an endothelial pro-inflammatory/coagulant phenotype. However, few contrasting studies raised the issue about the possibility to detect a comparable endothelial perturbation in antiphospholipid syndrome (APS) patients. The aim of this observational case-control study was to evaluate several parameters of endothelial perturbation in patients with APS and without any other atherosclerosis risk factor.
Patients and Methods : we investigated plasma levels of soluble adhesion molecules (s-ICAM-1, s-VCAM-1, s-E-selectin), soluble thrombomodulin (sTM), von Willebrand factor (vWF) and tissue plasminogen activator (t-PA) by solid-phase assays in 40 selected APS patients and 40 age- and sex-matched healthy
subjects. In addition, we evaluated circulating endothelial cells by flow cytometry and brachial artery
flow-mediated vasodilation. Patients and controls were free of conditions known to affect both the biological and the functional endothelial parameters.
Results : plasma levels of sTM, s-E-selectin and s-VCAM-1 did not differ from controls, while a significant increase in s-ICAM-1 (P ¼ 0.029), t-PA (P ¼ 0.003) and vWF titres (P ¼ 0.002) was found. Circulating mature endothelial cells were also significantly higher in patients than in controls (P ¼ 0.05) and decreased during both vitamin K antagonists (P ¼ 0.001) and antiplatelet (P ¼ 0.032) treatments. Mean brachial artery flow-mediated vasodilation responses were significantly impaired compared to healthy
subjects (P ¼ 0.0001).
Conclusions : as a whole these findings indicate that APS patients display an endothelial perturbation in the absence of other detectable traditional risk factors for atherosclerosis.