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Noninvasive indices based on speckle tracking echocardiography (STE) are increasingly used in right ventricular (RV) function measurement, however, their correlations with the pathologic mechanisms of dysfunction in pulmonary hypertension has not been established. The aim of our study was to assess the characterization of RV myocardial mechanics using three-dimensional (3D) STE and its association with molecular and cellular mechanisms in a RV pressure overload model.
Pulmonary artery banding (PAB) was used to induce RV pressure overload in beagles. 3D-STE was performed before and after 3 months in PAB and sham-operated beagles. Subsequently, the hearts were investigated by histology and analyzed for gene and protein expression.
3D-STE measurements revealed a significant decrease in longitudinal strain and increase in radial and circumferential strain. PAB-induced pressure overload resulted in RV hypertrophy, increased interstitial fibrosis and reduced capillary density. The protein expression of p53 and caspase-3 were elevated, whereas hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor (VEGF), connexin 43 (Cx43) and Bcl-2 were decreased in PAB group. Messenger ribonucleic acid expression of HIF-1α, Cx43, VEGF and Bcl-2 were reduced, whereas caspase-3 was increased in PAB group. RV longitudinal, radial and circumferential strain significantly correlated with interstitial fibrosis, and expression of p53, VEGF, Cx43 and Bcl-2.
PAB causes pressure overload–induced RV hypertrophy and remodeling that occur at the structural, histological, and molecular levels in beagles. The significant correlations of RV 3D-STE indices with hemodynamic, molecular and cellular parameters indicate that 3D-STE may be a valuable tool for assessment of ventricular function in RV pressure overload.