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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
Layer-Specific Strain Analysis for Detecting Subclinical Cardiac Dysfunction in Systemic Lupus Erythematosus
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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