Human chymase activates not only angiotensin II but also transforming growth factor-S , a major stimulator of myocardial fibrosis, while rat chymase activates transforming growth factor-S , but not angiotensin II. To clarify the role of chymase-dependent transforming growth factor-S activation, we evaluated whether chymase inhibition prevents cardiac fibrosis and cardiac dysfunction after myocardial infarction in rats. Myo-

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Background-Left ventricular aneurysm repair (LVR) reduces LV wall stress and improves LV function. However, as we reported previously, the initial improvement of LVR was short-term because of LV remodeling but could be maintained longer with postoperative use of an angiotensin-converting enzyme (ACE) inhibitor. Atrial natriuretic peptide (ANP) has been used to treat patients with heart failure by natriuretic and vasodilatory actions. Recent reports have suggested that ANP inhibits the rennin-angiotensin system. In this study, the effects of ANP after LVR were evaluated. Methods and Results-Rats that had an LV aneurysm 4 weeks after left anterior descending artery ligation underwent LVR by plicating the LV aneurysm and were randomized into 2 groups: LVRϩA group was intravenously administrated with 10 g/h of carperitide, recombinant ␣-hANP, by osmotic-pump for 4 weeks, and the LVR group was given normal saline.

The operative results improved with the selection of the procedures, with elective operation, and mitral plasty for less cardiac dilatation. The mid-term results of clinical status and LV function showed the effectiveness of the operation.

Chronic chymase inhibition prevented myocardial fibrosis and preserved cardiac function after LVR. A chymase inhibition could be an important strategy for management after LV repair surgery.