Key result
Fetal left ventricular hypoplasia linked to impaired RV myocardial function and 144 altered proteins.
Why the study?
Decreased right ventricular function in fetuses with left ventricular hypoplasia increases adverse outcome risks, but quantitative prenatal evaluation and underlying protein expression mechanisms needed exploration.
Cross-Sectional (n=162)
Fetuses with left ventricular hypoplasia show impaired right ventricular myocardial function and altered protein expression, indicating that developmental abnormalities extend to the right ventricle.
Answers are grounded in this paper and cite their sources.
Suggests fetal right ventricular strain may help risk-stratify left ventricular hypoplas.
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: < 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.
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Ma et al. (2025) conducted a cross-sectional in Left ventricular hypoplasia (n=162). Left ventricular hypoplasia vs. Normal controls was evaluated on Right ventricular global longitudinal strain (RVGLS) and differentially expressed RV proteins (p=< 0.001). Fetuses with left ventricular hypoplasia demonstrated impaired right ventricular myocardial function and 144 differentially expressed RV proteins compared to normal controls (P<0.001).
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