Arterial stiffness, antiphospholipid antibodies, and pulmonary arterial hypertension in systemic lupus erythematosus

BackgroundThe aim of this study is to evaluate the role of arterial stiffness in pulmonary arterial hypertension (PAH) in systemic lupus erythematosus (SLE) patients and its relationship with antiphospholipid antibody (aPL).MethodsMeasurement of brachial ankle pulse wave velocity (baPWV), carotid arterial stiffness, and pulmonary vascular resistance (PVR) was performed in 51 patients with SLE. PAH was diagnosed if the pulmonary artery systolic pressure was >40 mmHg. Information concerning SLE duration, medication, and serum autoantibodies was recorded. SLE activity was assessed by the SLE disease activity index (SLEDAI).ResultsaPL was present in 10 patients (20%), and PAH was detected in 6 patients (12%). The prevalence of Raynaud's phenomenon, baPWV, positive aPL, and titers of IgG anticardiolipin antibody (aCL) were increased in SLE with PAH; however, no difference was found in inflammatory markers, disease duration, and SLEDAI compared to SLE without PAH. Carotid artery deformation and right ventricular function were reduced in patients with PAH (all p < 0.05). Carotid artery circumferential strain (r = 0.34, p = 0.021), radial strain (r = −0.30, p = 0.045), and baPWV (r = 0.46, p = 0.001) showed significant correlation between IgG aCL. Univariate and multiple regression analysis revealed that the only significant independent predictors of the presence of PAH were baPWV, carotid artery stiffness, and IgG aCL.ConclusionArterial stiffness might contribute to the pathogenesis of PAH related to SLE as well as aPLs. Furthermore, the significant association of aPL with arterial stiffness suggests its important role in PAH with SLE.