The Canadian journal of cardiology · 2024
Adaptation of Left Ventricular Function and Myocardial Microstructure in Fetuses With Right Ventricular Hypoplasia.
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Ma Jing, Li Yuman, Cao Haiyan, Yuan Yaping, Chen Shizhen, Hong Liu, Zhang Li, Zhou Xin, Xie Mingxing
Аннотация
BACKGROUND: In this study we evaluated changes in left ventricular (LV) function and myocardial microstructure in fetuses with right ventricular hypoplasia (RVH) using 2-dimensional speckle tracking echocardiography, diffusion tensor cardiovascular magnetic resonance imaging, and proteomics analysis.
METHODS: Fifty-one singleton fetuses diagnosed with RVH and 51 normal fetuses were retrospectively included. LV global longitudinal strain and global circumferential strain were acquired using 2-dimensional speckle tracking echocardiography. Fraction anisotropy, mean diffusivity, and helix angle were measured using diffusion tensor cardiovascular magnetic resonance imaging in 4 fetal specimens with RVH and 3 normal fetal specimens. Bioinformatics analysis was performed for differentially expressed proteins between RVH and normal specimens.
RESULTS: In RVH fetuses, LV global longitudinal strain and regional longitudinal strain were significantly lower than in controls (P < 0.001), whereas LV sphericity index and LV global circumferential strain were increased. In RVH fetuses, fraction anisotropy was higher in middle and apical segments than in normal fetuses (P < 0.001). LV mean diffusivity was reduced in all of the segments (P < 0.001). Circumferentially oriented myocytes and left-handed oriented myocytes were increased, but right-handed oriented myocytes were decreased (P < 0.001). Using proteomics, 95 myocardial proteins differed with upregulation of 66 and downregulation in RVH hearts including myocardial contractile fibrillar proteins and cell membrane protein complexes.
CONCLUSIONS: In fetal RVH, the left ventricle demonstrates altered function with reduced longitudinal but augmented circumferential strain, which might support its need to augment its preload and consequent cardiac output. Decreased right-handed and increased circumferentially oriented myocytes might contribute to this adaptation. The left ventricle in fetal RVH also demonstrates a differential expression of various myocardial proteins.
METHODS: Fifty-one singleton fetuses diagnosed with RVH and 51 normal fetuses were retrospectively included. LV global longitudinal strain and global circumferential strain were acquired using 2-dimensional speckle tracking echocardiography. Fraction anisotropy, mean diffusivity, and helix angle were measured using diffusion tensor cardiovascular magnetic resonance imaging in 4 fetal specimens with RVH and 3 normal fetal specimens. Bioinformatics analysis was performed for differentially expressed proteins between RVH and normal specimens.
RESULTS: In RVH fetuses, LV global longitudinal strain and regional longitudinal strain were significantly lower than in controls (P < 0.001), whereas LV sphericity index and LV global circumferential strain were increased. In RVH fetuses, fraction anisotropy was higher in middle and apical segments than in normal fetuses (P < 0.001). LV mean diffusivity was reduced in all of the segments (P < 0.001). Circumferentially oriented myocytes and left-handed oriented myocytes were increased, but right-handed oriented myocytes were decreased (P < 0.001). Using proteomics, 95 myocardial proteins differed with upregulation of 66 and downregulation in RVH hearts including myocardial contractile fibrillar proteins and cell membrane protein complexes.
CONCLUSIONS: In fetal RVH, the left ventricle demonstrates altered function with reduced longitudinal but augmented circumferential strain, which might support its need to augment its preload and consequent cardiac output. Decreased right-handed and increased circumferentially oriented myocytes might contribute to this adaptation. The left ventricle in fetal RVH also demonstrates a differential expression of various myocardial proteins.