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Left ventricular (LV) hypertrophy and dilatation are important compensatory responses to chronic volume overload. Although LV function is initially preserved by these responses, the continued structural remodeling of the myocardium ultimately becomes maladaptive, leading to the development of heart failure. We have shown previously that increased myocardial matrix metalloproteinase (MMP) activity precedes LV dilatation induced by a chronic volume overload. Accordingly, this study focused on the effects of MMP inhibition therapy (PD 166793, 1 mg x kg(-1) x d(-1)) on LV size and function in a rat model of volume overload-induced heart failure.

Effects of Matrix Metalloproteinase Inhibition on Ventricular Remodeling Due to Volume Overload