Background: An accumulation of evidence suggests that the local renin-angiotensin system plays a role in the development of cardiac hypertrophy in vivo; however, it remains unknown how the expression of angiotensin II type 1 receptor (AT 1 ), which mediates most of the cardiovascular effects of angiotensin II, is regulated in the left ventricles of human pathologic hearts.Methods and Results: Expression of AT 1 gene in the left ventricle wall of 14 autopsied human hearts was examined by reverse transcription polymerase chain reaction. The levels of AT 1 messenger RNA relative to those of beta-actin messenger RNA in the left ventricle wall were increased 3.8-fold in the hearts with dilated cardiomyopathy (n = 4, P < .05) and 6.2-fold in the noninfarcted areas of hearts with old myocardial infarction (n = 4, P < .05), compared with the control hearts without any cardiac disease (n = 6). The increases in the relative AT 1 messenger RNA level showed a positive correlation with myocyte diameter in the adjacent tissue (r = .927, P < .001 for dilated cardiomyopathy and r = .934, P < .005 for old myocardial infarctions) and with the extent of fibrosis (r = .880, P < .005 for dilated cardiomyopathy and r = .690, P < .05 for old myocardial infarction).Conclusions: Expression of AT 1 in these human pathologic hearts was associated with myocardial cell hypertrophy and extent of fibrosis, a finding that further emphasizes the importance of the local renin-angiotensin system in the remodeling of human hearts with dilated cardiomyopathy and old myocardial infarction.