Transition from Hypertrophy to Heart Failure in Rats with Pressure-Overload

Objective To investigate whether chronic pressure-overload induced by suprarenal abdominal aortic banding may progress into left ventricular failure in animal model.Methods Eight-week old male Wistar rats were enrolled and suprarenal abdominal aorta was ligated by 7-0 nylon suture against a 23-gauge needle.Rats with LV hypertrophy(LVH,n = 10),age-matched sham-operated rats(Sham,n = 10)and normal control rats(Con,n = 10)were assessed at 20 and 38 weeks after aortic banding.The ratio of heart weight to body weight was calculated and cardiac hemodynamic parameters were obtained by multi-functional physiology recorder and echocardiography.H.E.and picrosirius red staining methods were used to display collagen content in the rat hearts.Results Twelve weeks after banding,LVH rats showed LV wall hypertrophy with normal cavity dimensions and decreased diastolic function(E/A ratio:LVH:1.0±0.25,Con:1.6±0.12).After 38 weeks of pressure overload,LV wall thickness was decreased and cavity dilated with a fall in left ventricular ejection fraction,and further deterioration of systolic and diastolic function was evident(EF:LVH:44.8±8.42,Con:70.9±5.19;Max dP/dt:LVH:4916±1267.3,Con:14225±932.1;Min dP/dt:LVH:-3246±1217.3,Con:-12138±725.2).In contrast to LVH rats,the sham-operated rats showed no change in LV diastolic cavity dimension,and systolic and diastolic functions did not deteriorate or improved.H.E.and picrosirius red staining showed severe fibrosis in heart tissue of LVH animals.Conclusions This model of pressure overload is characterized initially by concentric LV hypertrophy with compensated LV chamber performance;however,markedly abnormal diastolic filling is present.The transition from compensated hypertrophy to heart failure is gradually emerged with LV dilation and impairment of systolic function.