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LV scar was minimized and LV wall stress decreased by the reduced LV size.6 However, at late phase, LV redilation developed and LV systolic function deteriorated. Ratcliffe et al12 performed LVR as we did in a sheep MI model. They also showed that the initial improvement of LV function, followed by LV remodeling 6 weeks after LVR. The remodeling caused LV size and LV function to return to preoperative values. These negative results after LVR prompted us to consider adjuvant therapies to improve operative outcomes. After MI, the heart develops remodeling as follows: during the early phase in the first few days ; , there is expansion of the infracted tissue leading to early LV chamber dilation and increased mechanical stress on the remaining viable myocardium. In the late phase, there is ongoing progressive remodeling of the remote areas of the LV, characterized by further chamber dilation, myocardial hypertrophy, and progressive deterioration in systolic pump function.13 The tissue reninangiotensin system RAS ; is activated after MI, and plays an important role not only in early but also in late remodeling.14 ACE-I is well known to prevent remodeling after MI, both clinically and experimentally.7, 8 Mulder et al have shown that ACE-I exerted markedly beneficial effects even when treatment was started late into the evolution of heart failure after MI.15 The LV aneurysm model in our study should be one in the late remodeling course after MI. Once the LVR reduces LV volume, mechanical stress on the remote myocardium is decreased. However, activated-tissue RAS might work for progressive remodeling and deteriorate the LV function late after LVR. We propose a hypothesis in which the progressive remodeling after LVR and the subsequent functional deterioration of the LV is associated with activated-tissue RAS. We designed this prospective study in accord with this hypothesis to investigate the effect of LVR with ACE-I administration. In this study, LV systolic function was restored in the early phase after LVR. Without medication, however, LV redilation developed and LV systolic function deteriorated in the late phase, as in our previous study.6 In this study ACE-I per se had only a little effect on LV systolic function eg, a small increase of FAC in ACE-I group ; . However, when ACE-I.

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