Objective: To observe the pathological changes of heart failure induced by aortic arch stenosis in rats.
Methods: Twenty four chronic heart failure models were established by cutting the second left rib along the sternum to open the chest, and transcatheter aortical constriction (TAC) was performed between the brachiocephalic trunk and the left common carotid artery, and another eight rats were taken for sham operation. Echocardiography, hemodynamics and N-terminal pro-brain natriuretic peptide (NT proBNP) were measured at 12 weeks after TAC in the sham operation group and 4 weeks, 8 weeks and 12 weeks after TAC in the model group respectively, and myocardial histopathology was observed.
Results: In the model group, NT proBNP increased significantly at 4 weeks, peaked at 8 weeks (P<0.05), and declined at 12 weeks after TAC; The results of echocardiography showed that in the model group, ejection fraction (EF), fraction shortening (FS), left ventricular end systolic volume (LVESV), left ventricular end diastolic volume (LVESV), left ventricular end diastolic volume (LVEDV) and left ventricular end diastolic volume (LVESV) were significantly increased at 4 weeks, 8 weeks and 12 weeks after TAC (P<0.05), respectively; Hemodynamic examination showed that the left ventricular pressure maximum rate of rise (dp/dtmax) decreased and the left ventricular pressure maximum rate of fall (- dp/dtmax) increased in the model group after TAC (P<0.05); Pathological observation showed that in the model group, myocardial cells were hypertrophy and disordered at 4 weeks after TAC, connective tissue hyperplasia and inflammatory cell infiltration at 8 weeks, and myocardial cells were apoptosis and collagen fiber deposition at 12 weeks.
Conclusion: In the rat heart failure model induced by aortic arch stenosis, the myocardium appears compensatory hypertrophy 4 weeks after TAC, the initial reaction of myocardial decompensation 8 weeks after TAC, and myocardial fibrosis 12 weeks after TAC, forming irreversible heart failure.