SUMMARYThe objective of the present study was to determine if carvedilol protects against myocardial degeneration and fibrotic change, and reduces mortality in TO2 hamsters.Carvedilol was administered intraperitoneally to 8 week-old TO2 hamsters for 21 weeks at a dose of 11 mg/kg/day. There were 15 TO2 hamsters in the carvedilol group (group C) and 10 in the untreated group (group N). The control group consisted of 11 Fb hamsters (group F). The mortality rate was determined from the number of surviving hamsters after 29 weeks. Myocardial fibrosis was evaluated by MRI and histopathological examination. EF and LVDd were determined by echocardiography at 8 and 29 weeks, while the MRI score was calculated at 29 weeks.Mortality, histopathological fibrosis, and MRI score were all lower in group C than in group N. Carvedilol had a protective effect against myocardial fibrosis and decreased the mortality rate in TO2 hamsters. ( 2-4) Following this, β-blocker therapy became used for the treatment of chronic heart failure.We previously performed MRI studies in a hamster model of cardiomyopathy (Bio 14.6 hamster) and found abnormal sites of enhancement as well as delayed enhancement. We proposed that the enhanced areas were regions of myocardial degeneration and fibrosis. 5) Carvedilol is a β-blocker that also has α-blocking and antioxidant effects, which have been shown to reduce the mortality rate of patients with moderate to severe chronic cardiac failure by 35% to 65%, in addition to also lowering the rehospitalization rate. 3,4) In the present study, we assessed the effects of carvedilol [6][7][8] in another hamster model of dilated cardiomyopathy, the BioFrom the