Key result
SLE is linked to ~2-point worse GLS and increased epicardial adipose tissue vs controls.
Why the study?
Systemic lupus erythematosus can cause myocardial damage and left ventricular dysfunction, and the role of epicardial adipose tissue thickness in this process is unclear.
Case-Control (n=98)
No
Absolute Event Rate: -18.2% vs -20%
p-value: p=<0.001
Increased epicardial adipose tissue thickness correlates with early subclinical left ventricular systolic dysfunction in systemic lupus erythematosus patients, detectable by 2D speckle-tracking echocardiography.
EAT thickness may flag subclinical LV dysfunction in SLE; this Level 5 finding leaves open causal links and therapeutic implications.
Background Systemic lupus erythematosus (SLE) can cause myocardial damage and left ventricular dysfunction in patients. Abnormal deposition of epicardial adipose tissue (EAT) can promote the occurrence and development of cardiovascular diseases. The aim of this study was to investigate changes in EAT thickness in patients with SLE and apply two-dimensional speckle tracking echocardiography (2D-STE) to study the correlation between EAT and left ventricular systolic function. Patients and methods This case–control study recruited a total of 67 SLE patients as the case group and 31 healthy individuals as the control group. Left ventricular systolic function parameters were measured using 2D-STE. Changes and correlations in laboratory indicators, EAT, and left ventricular systolic function parameters were compared between groups. Results Compared with the control group, the case group showed significantly increased EAT and diastolic left ventricular posterior wall thickness (LVPWD) ( P <0.05). High-density lipoprotein cholesterol (HDL-C), apical two-chamber longitudinal strain (AP2C LS), apical three-chamber longitudinal strain (AP3C LS), apical four-chamber longitudinal strain (AP4C LS), and global longitudinal strain (GLS) were significantly reduced ( P < 0.05). The 18-segment left ventricular longitudinal strain was further grouped according to coronary artery supply; the LAD, RCA, and LCX groups in the patient cohort all showed reductions compared with the healthy control group ( P < 0.05). Spearman correlation analysis revealed that EAT was negatively correlated with GLS ( r = −0.39, P < 0.05), LAD group ( r = −0.26, P < 0.05), RCA group ( r = −0.47, P < 0.05), and LCX group ( r = −0.29, P < 0.05), and positively correlated with duration of illness (DT) ( r = 0.41, P < 0.05) and age ( r = 0.45, P < 0.05). Multiple linear regression analysis confirmed that EAT is an important influencing factor of left ventricular longitudinal strain function ( P < 0.05). Conclusion Increased epicardial adipose tissue thickness is negatively correlated with left ventricular systolic function. EAT can effectively reflect changes in left ventricular systolic function in SLE patients, providing a basis for clinical management and early intervention.
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Lin et al. (2026) conducted a case-control in Systemic lupus erythematosus (n=98). Systemic lupus erythematosus vs. Healthy individuals was evaluated on Global longitudinal strain (GLS) (p=<0.001). Patients with systemic lupus erythematosus exhibited significantly increased epicardial adipose tissue thickness and reduced global longitudinal strain (-18.2% vs -20.0%) compared to healthy controls, with epicardial fat independently predicting systolic dysfunction.
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