Subclinical left ventricular dysfunction in childhood-onset systemic lupus erythematosus: a two-dimensional speckle-tracking echocardiographic study

Objectives: The main purpose of the study was to investigate left ventricular (LV) subclinical systolic and diastolic dysfunction in childhood-onset systemic lupus erythematosus (c-SLE) patients using two-dimensional speckle-tracking (2DST) echocardiography. We also interrogated possible correlations between impairment of myocardial deformation and the SLE Disease Activity Index 2000 (SLEDAI-2K), as well as the presence of traditional and disease-related cardiovascular risk factors (CRFs).Method: A total of 50 asymptomatic patients and 50 controls (age 14.74 vs. 14.82years, p=0.83) were evaluated by standard and 2DST echocardiography.Results: Despite a normal ejection fraction (EF), there was reduction in all parameters of LV longitudinal and radial deformation in patients compared to controls: peak longitudinal systolic strain (PLSS) [-20.3 (-11 to -26) vs. -22 (-17.8 to -30.4)%, p<0.0001], PLSS rate [-1.190.21 vs. -1.3 +/- 0.25s(-1), p=0.0005], longitudinal strain rate in early diastole [1.7 (0.99-2.95) vs. 2 (1.08-3.00) s(-1), p=0.0034], peak radial systolic strain [33.09 +/- 8.6 vs. 44.36 +/- 8.72%, p<0.0001], peak radial systolic strain rate [1.98 +/- 0.53 vs. 2.49 +/- 0.68s(-1), p<0.0001], and radial strain rate in early diastole [-2.31 +/- 0.88 vs. -2.75 +/- 0.97s(-1), p=0.02]. Peak circumferential systolic strain [-23.67 +/- 3.46 vs. -24.6 +/- 2.86%, p=0.43] and circumferential strain in early diastole [0.37 +/- 0.17 vs. 0.41 +/- 0.15, p=0.27] were similar between patients and controls, although peak circumferential systolic strain rate [-1.5 +/- 0.3 vs. -1.6 +/- 0.3s(-1), p=0.036] was reduced in c-SLE. Further analysis of patients revealed a negative correlation between LV PLSS and SLEDAI-2K (r= -0.52, p<0.0001), and also between LV PLSS and the number of CRFs per patient (r= -0.32, p=0.024).Conclusions: 2DST echocardiography has identified subclinical LV deformation impairment in c-SLE patients. Disease activity and cumulative exposure to CRFs contribute to myocardial compromise.