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BackgroundSystemic lupus erythematosus is an autoimmune disease associated with reduced number and impaired function of endothelial progenitor cells (EPCs) responsible for vascular regeneration.Aim of the workto assess left ventricular (LV) function of SLE patients using relatively new speckle tracking echocardiography (STE) and examine the relation of any detected abnormalities with peripheral circulating EPC level.Patients and methodsFifty SLE patients and 25 healthy controls were subjected to quantification of peripheral circulating Cluster of differentiation133+/vascular endothelial growth factor receptor2+(CD133+/VEGFR2+) and CD34+/VEGFR2+ EPCs, transthoracic echocardiography (TTE), tissue Doppler imaging (TDI) and STE.ResultsPatients showed a significantly lower CD133+/VEGFR2+ EPCs (p=0.009) and CD34+/VEGFR2+ EPC counts (p=0.0001) compared to controls. TTE/TDI revealed a significantly lower LV ejection fraction (EF) (p=0.007), higher LV end systolic dimensions (p=0.02), myocardial performance index (MPI) (p=0.0001) and mitral flow E/lateral annulus E′ ratio (p=0.002) in patients compared to controls. STE showed a significantly lower global longitudinal strain (GLS) (p<0.001), global circumferential strain (GCS) (p<0.001) and global strain rate during isovolumic relaxation period (GSRivr) (p=0.01) in patients compared to controls. By multiple logistic regression analysis, the independent variables affecting GCS and GSRivr were the prednisolone dose and the LVEF respectively. (95% CI=−0.46 to −0.03; p=0.03 and 95% CI=0.001–0.01; p=0.021; respectively). There was no significant correlation of the GLS, GCS or GSRivr with the EPCs.ConclusionSTE detected subclinical systolic and diastolic abnormalities of LV function in SLE patients. These abnormalities of LV function did not show however any relation with the significantly lower EPC count detected in patients

the egyptian rheumatologist

Assessment of left ventricular function in systemic lupus erythematosus patients by speckle tracking echocardiography: Relation to circulating endothelial progenitor cells