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Updated: Jan 10, 2026
Fetal Mouse Cardiovascular Imaging Using a High-frequency Ultrasound 30/45MHZ System
Published on: May 5, 2018
Right Ventricular Myocardial Strain and Proteomic Analysis of Fetuses With Left Ventricular Hypoplasia: A
Jing Ma1,2,3, Sushan Xiao1,2,3, Liu Hong1,2,3
1Department of Ultrasound Union Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan China.
Background And Aims:
Decreased right ventricular (RV) function in fetuses with left ventricular hypoplasia (LVH) increases the risk of adverse outcome. This study aimed to quantitatively evaluate RV myocardial function prenatally in LVH, and explore the relevant mechanism from protein expression.
Methods:
81 singleton fetuses diagnosed with LVH and 81 normal controls were retrospectively included. We used RV global longitudinal strain (RVGLS) derived from two-dimensional speckle tracking imaging to evaluate RV myocardial function and "XGboost" algorithm to select effective factors affecting RV myocardial function in fetuses with LVH. Bioinformatics analysis was performed for differentially expressed proteins between specimens with LVH and normal fetuses.
Results:
In LVH fetuses, RVGLS was significantly lower in fetuses with LVH than in controls (p < 0.001). "XGboost" model showed that RV/LV ratio, LV sphericity index, combined with double outlet right ventricle, and LV end-diastolic dimension z-score had the greatest effect on RVGLS, with SHAP analysis revealing nonlinear relationships between these factors and RVGLS. Proteomics in LVH fetuses demonstrated 144 differentially expressed RV proteins (68 upregulated, 76 downregulated), enriched in extracellular matrix, cytoskeleton, and DNA replication pathways (GO/KEGG). Notably, dysregulated processes included actin depolymerization, cell cycle control, and MCM complex function, suggesting adaptive RV remodeling at molecular levels. Interobserver reproducibility for strain measurements was excellent (ICC > 0.9).
Conclusions:
Impaired RV myocardial function and RV protein spectrum differentiated from normal fetuses have been observed in fetuses with LVH, which shed light on the novel perspective that myogenic developmental abnormalities are not limited to the left heart but also extend to RV cardiomyocytes during the embryonic stage.
