Ventricular Remodeling in the Dog

Background Progressive ventricular remodeling after myocardial damage is associated with a poor prognosis. Optimal prevention of the histopathological processes involved in remodeling requires a more complete understanding of the mechanisms involved in initiating and maintaining these structural changes. Since the sympathetic nervous system and the renin-angiotensin system may be involved in the remodeling process, the structural effects of pharmacological inhibitors have been evaluated in a canine model of localized myocardial injury resulting from transmyocardial DC shock. Methods and Results The study is comprised of two protocols run in series. In protocol 1, zofenopril (Z), a converting enzyme inhibitor (CEI), prevented the increase in left ventricular mass (LVM) and end-diastolic volume (LVV) observed in the control group (C) at 16 weeks (Z: LVM, 69.8+3.4 to 65.4+2.6 g, P=NS; LVV, 45.4±2.7 to 51.6±2.7 mL, P=NS; C: LVM, 68.4±3.2 to 91.4+2.9 g, P=.0001; LVV, 56.6±3.0 to 71.9±2.4 mL, P=.0003). Terazosin, an a,-adrenoceptor antagonist, failed to prevent remodeling at 16 weeks despite con-