BackgroundMyocardial fibrosis can result in right ventricular (RV) dysfunction, a critical factor in poor clinical outcomes and high mortality rates among patients with pulmonary hypertension (PH). Decreased RV myocardial strain rates have been reported in PH patients. The expression of FOXO3A may play a crucial role in myocardial fibrosis; however, the relationship between myocardial fibrosis, speckle‐tracking echocardiography (STE), and the transcription factor FOXO3A remains unclear. This study aimed to explore the relationship between the molecular mechanisms of myocardial fibrosis and noninvasive ultrasound evaluation indices to provide a reliable molecular foundation for the early diagnosis of right heart dysfunction in clinical settings.MethodsA progressive right heart failure (RHF) rat model was established through subcutaneous injections of monocrotaline. Rats were divided into baseline, 2‐week, 4‐week, and 6‐week groups based on the disease course. RV structure, function, and myocardial strain were assessed via echocardiography. Myocardial fibrosis severity was determined using PSR staining. The correlation between myocardial strain and RV myocardial fibrosis was analyzed. FOXO3A, collagen I, collagen III, and BNP expressions were tested using western blotting.ResultsAs the disease progressed, the right ventricle significantly expanded, and the RV fractional area change (FAC), tricuspid annular plane systolic excursion (TAPSE), RV global longitudinal strain (RVLS global), and RV free wall longitudinal strain (RVLS FW) gradually declined. However, the reductions in RVLS global and RVLS FW occurred earlier than that of RVFAC, TAPSE. Significant correlations were observed between RVLS global, RVLS FW, and collagen deposition. FOXO3A expression gradually decreased with disease progression, while BNP, collagen I, and collagen III expressions gradually increased.ConclusionsDecreases in RVLS global and RVLS FW in RHF rats occurred earlier than RVFAC and were associated with RV myocardial fibrosis. Furthermore, FOXO3A may have a protective role in the process of RV myocardial fibrosis.

Background Myocardial fibrosis may lead to right ventricular (RV) dysfunction, which is a key determinant to poor clinical prognosis and high mortality in patients with pulmonary hypertension (PH). Reduced right ventricular myocardial strain rate was reported in PH patients. The expression of FOXO3A may have an essential role in myocardial fibrosis. However, the relationship between myocardial fibrosis and speckle-tracking echocardiography (STE) or transcription factor FOXO3A is unclear. Therefore, we aimed to exploring the relationship between the molecular mechanism of myocardial fibrosis and the noninvasive ultrasound evaluation index in order to provide a reliable molecular basis for the early diagnosis of right heart dysfunction in clinic. Methods Progressive right heart failure (RHF) rat model was established by subcutaneous injection of monocrotaline. Rats divided into baseline, 2-week, 4-week and 6-week according to the course of disease. Right ventricular structure, function and myocardial strain were determined via echocardiography. The degree of myocardial fibrosis was determined by PSR staining. The correlation of myocardial strain to RV myocardial fibrosis was analyzed. The expression of FOXO3A, collagen I, collagen III and BNP were test via western blotting. Results As the disease progresses, the right ventricle significantly expands, RV fractional area change (FAC), RV global longitudinal strain (RVLS global) and RV free wall longitudinal strain (RVLS FW) gradually decreases. While the reduction of RVLS global, RVLS FW appeared earlier than that of RVFAC. Significant correlations were observed between RVLS global, RVLS FW and collagen deposition. FOXO3A expression gradually decreased with the disease progression, while the expression of BNP, collagen I, collagen III gradually increased. Conclusions Decreased of RVLS global, RVLS FW in RHF rats are happened earlier than RVFAC, and have associated with RV myocardial fibrosis. While, FOXO3A may plays a protective role in the process of RV myocardial fibrosis.