Multimodal ultrasound imaging of a rat model with ischemic heart failure and its relationship to histopathology.

OBJECTIVE

To investigate the value of multimodal ultrasound imaging in assessing ischemic heart failure, and to analyze the relationship between ultrasound parameters and histopathology.

METHODS

Thirty male healthy SD rats were randomly divided into a control (n = 10) and a model group (n = 20). The rat model of ischemic heart failure (IHF) was established by the ligation of left anterior descending artery for 4 weeks. Left ventricular ejection fraction (LVEF) and left ventricular cardiac output (LVCO) were determined with routine echocardiography. Global longitudinal strain (GLS) and global circumferential strain (GCS) were determined with Speckle Tracking. Myocardial oxygen saturation (sO) was measured with photoacoustic (PA) imaging. Hematoxylin and eosin (H&E) staining, transmission electron microscopy, and Masson staining were performed to determine mitochondrial damage and myocardial fibrosis. Enzyme-linked immunosorbent assay (ELISA) was performed to detect the serum levels of cardiac troponin I (cTNT) and N-terminal B-type natriuretic peptide (NT-pro BNP). Pearson correlation analysis was employed to analyze the correlation among LVEF, LVCO, GLS, GCS, sO, mitochondrial impairment, fibrosis, cTNT and NT-pro BNP.

RESULTS

Echocardiography revealed significant systolic function changes in the model group as compared to the control group, characterized by decreased LVEF and CO. The serum levels of cTn-T and NT-proBNP were increased, suggesting myocardial injury and functional impairment. GLS and GCS in the model group was reduced as compared to the control group. Concurrently, a marked reduction in sO was observed in the anterior wall of the model rats, whereas that in the posterior wall showed no significant change. Histopathologic examinations unveiled pronounced cellular and subcellular damage, such as disorganization of myocardial fibers and mitochondrial impairment, with the model group presenting a higher Flameng score. Masson's trichrome staining revealed increased myocardial fibrosis. Correlation analyses pinpointed significant associations between echocardiographic parameters, degree of mitochondrial damage, fibrosis, and the levels of cTn-T and NT-proBNP in the model group. This indicated the interrelated nature of structural changes and functional impairment in IHF. Notably, GLS showed the strongest correlations with indicators of myocardial injury. However, anterior wall sO did not demonstrate a significant correlation with either histopathologic damage or serum biomarker levels.

CONCLUSIONS

Myocardial GLS is a sensitive indicator of pathological myocardial remodeling in heart failure. The multimodal ultrasound can be applied to assess pathologic remodeling in IHF rats.