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Updated: Feb 26, 2026

Transthoracic Speckle Tracking Echocardiography for the Quantitative Assessment of Left Ventricular Myocardial Deformation
Published on: October 20, 2016
Análisis de Deformación Específico por Capa para Detectar Disfunción Cardíaca Subclínica en el Lupus Eritematoso
Mert Gürsoy1, Murat Kazım Ersanlı1, Hasan Ali Barman1
1Cerrahpasa Institute of Cardiology, Department of Cardiology, Istanbul University-Cerrahpasa, Istanbul, Turkey.
Background:
Cardiac involvement in systemic lupus erythematosus (SLE) is often subclinical and underdiagnosed. Although impaired global longitudinal strain (GLS) is well documented in SLE, data on layer-specific myocardial deformation are scarce. This study aimed to assess left and right ventricular function in SLE patients using speckle tracking echocardiography (STE), focusing on layer-specific LV strain and its association with disease activity.
Methods:
We included 43 SLE patients and 40 age- and sex-matched healthy controls in a cross-sectional design. All subjects underwent conventional transthoracic echocardiography and STE. Global longitudinal strain (GLS) of the left ventricle (LV) was measured separately for endocardial, mid-myocardial, and epicardial layers. Right ventricular (RV) free wall strain was also assessed. Correlation between strain parameters and SLEDAI-2K score was analyzed.
Results:
While conventional echocardiographic parameters, including LV ejection fraction, were similar between groups, STE revealed significant myocardial impairment in SLE patients. LV endocardial and mid-myocardial GLS were significantly reduced in SLE patients compared to controls (-15.7% vs. -20.3% and -18.1% vs. -20.1%, respectively; p < 0.001). Epicardial strain showed a nonsignificant reduction (p = 0.081). RV free wall strain was also lower in SLE patients (-26.1% vs. -29.8%, p = 0.001). LV endocardial strain strongly correlated with SLEDAI-2K (ρ = 0.716, p < 0.001), while RV strain did not.
Conclusion:
STE detects early biventricular myocardial involvement in SLE, with evidence of systolic dysfunction predominantly at the LV endocardial level.
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