Gradual pressure overload via aortic banding in young guinea pigs led to left ventricular hypertrophy, with approximately 50% developing myocardial decompensation and dyspnea.
Gradual aortic banding in young guinea pigs provides a valuable preclinical model for studying the transition from compensatory left ventricular hypertrophy to heart failure.
Left ventricular hypertrophy has been produced in the guinea pig by a procedure that gradually increases left ventricular afterload. A mildly constricting band was placed around the ascending aortas of very young guinea pigs (225-275 g). With growth to 500-1,000 g, left ventricular systolic pressure increased and left ventricular hypertrophy developed. In approximately 50% of these animals, the hypertrophy was associated with normal left ventricular function and with no unusual symptoms or evidence of heart failure. The other animals developed dyspnea, which appeared an average of 41 days after banding. Dyspneic animals had normal body weight, markedly increased right ventricular and lung weights, decreased left ventricular norepinephrine content, diminished maximum left ventricular pressure generating capacity, and a significantly higher incidence of left ventricular interstitial and perivascular fibrosis. These findings demonstrate that even when left ventricular overload is imposed gradually by banding the aortas of young animals, myocardial decompensation ultimately ensues in a significant proportion of such animals. The slow imposition of loading, the slow rate of decompensation, and the ability to identify animals in heart failure by clinical dyspnea make this model uniquely valuable for studies on the mechanisms of heart failure.
Siri et al. (1989) studied Left ventricular hypertrophy and heart failure. Aortic banding (mildly constricting band around the ascending aorta) was evaluated on Development of dyspnea and myocardial decompensation. Gradual pressure overload via aortic banding in young guinea pigs led to left ventricular hypertrophy, with approximately 50% developing myocardial decompensation and dyspnea.