ENDOTHELIAL FUNCTION OF BLOOD VESSELS AND BLOOD RHEOLOGY IN ANCA-ASSOCIATED SYSTEMIC VASCULITIS

Syniachenko O.V.1, Iermolaieva M.V.1, Bevzenko T.B.2, Sedaia L.V.3, Malakhova Z.V.3

Summary. The purpose and objectives: to study the clinical and pathogenetic significance of vascular endothelial function (EFV) and the rheological properties of blood serum (RPB) in microscopic polyangiitis (MPA), Wegener’s granulomatous polyangiitis (GPA) and eosinophilic polyangiitis Churg —Strauss (EPA). Materials and methods. 129 patients with ANCA-SV, among which 59% with MPA, 20% with GPA and 21% with EPA were examined. There were 47% of men and 53% of women among all patients. First degree of disease activity was present in 10% of patients with ANCA-SV, II — in 35%, the III — in 55%. ANCA in serum are found in 74% of patients with MPA, in 79% with GPA, and 44% with EPA. EFV was assessed by levels of endothelin-1, thromboxane-A2, homocysteine (HCys), prostacyclin, nitrites (NO2) and cyclic guanosine monophosphate (cGMP), and the RPB — with the parameters of the volume viscosity (VV), the surface values of viscosity (SV), elasticity (SE), relaxation (SR) and tension (ST) and viscoelasticity modulus. Results. ANCA-SV are accompanied by an imbalance in blood levels of vasoconstrictors and vasodilators, changes in viscous, elastic, viscoelastic, relaxation and interface-active properties of serum, and some nosologies differ with each other by increased (MPA), decreased (GPA) and unchanged (EPA) parametres of cGMP, normal values of ST in GPA, NO2 and SR in EPA, depending on the damage in the heart (in patients with MPA is marked the influence on the content of HCys and VV, in GPA — on SV, SE and SR, in EPA — on HCys, cGMP and ST) and endothelial vascular dysfunction and shifts of physicochemical properties of blood are involved in the development of arrhythmias, myocardial dysfunction, changes in the size of chambers and heart valves. Conclusions: there are marked violations of EFV and RPB in patients with ANCA-SV, which are involved in the pathogenesis of diseases.

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