Beneficial effect of angiotensin-converting enzyme inhibitor on dilated cardiomyopathy induced by autoimmune mechanism against beta 1-adrenoceptor

We have shown that a peptide corresponding to the sequence of the second ex tracellular loop of the human beta1-adrenoceptor (beta1-peptide) was able t o induce an autoimmune cardiomyopathy in rabbits. In this study, we examine d the effect of angiotensin-converting enzyme inhibitor (ACEI) on beta1-pep tide-induced cardiomyopathy. Rabbits were divided into four groups: (1) con trol group (n=6) receiving saline injection; (2) beta1-peptide group (n = 8 ) immunized with beta1-peptide; (3) ACEI group (n = 6), lisinopril (3 mg/da y) given orally and receiving saline injection; and (4) ACEI + beta1-peptid e group (n = 7), lisinopril (3 mg/day) given orally and immunized with beta 1-peptide. Our results showed that, after 1 year, all rabbits in the beta1- peptide group had an increase in heart weight, wall thinning and dilatation s of both ventricles as compared with rabbits in the ACEI + beta1-peptide g roup that had normal heart weight and shape. All rabbits in the pi-peptide group exhibited multifocal degeneration and necrosis of myocardial cells wi th moderate infiltration of inflammatory cells. In the ACEI + beta1-peptide group, three rabbits showed focal degeneration and necrosis of myocardial cells accompanied by mononuclear cells. The lesions in this group were appa rently less marked than those in the beta1-peptide group. In conclusion, AC EI protects the myocardium from injury induced by an autoimmune mechanism a gainst beta1-adrenoceptor.