Contribution of ventricular remodeling to pathogenesis of heart failure inrats

We previously reported an approximately 50% incidence of rats with symptoms of congestive heart failure (CHF) at 8 wk postinfrarenal aorto-caval fistu la. However, it was not clear whether compensatory ventricular remodeling c ould continue beyond 8 wk or whether the remaining animals would have devel oped CHF or died. Therefore, the intent of this study was to complete the c haracterization of this model of sustained volume overload by determining t he morbidity and mortality and the temporal response of left ventricular (L V) remodeling and function beyond 8 wk. The findings demonstrate an upper l imit to LV hypertrophy and substantial increases in LV volume and complianc e, matrix metalloproteinase activity, and collagen volume fraction associat ed with the development of CHF. There was an 80% incidence of morbidity and mortality following 21 wk of chronic volume overload. These findings indic ate that the development of CHF is triggered by marked ventricular dilatati on and increased compliance occurring once the myocardial hypertrophic resp onse is exhausted.