EFFECT OF CAPTOPRIL ON MYOCARDIAL BETA-ADRENOCEPTOR DENSITY AND G(I-ALPHA)-PROTEINS IN PATIENTS WITH MILD-TO-MODERATE HEART-FAILURE DUE TO DILATED CARDIOMYOPATHY

In end-stage heart failure due to idiopathic dilated cardiomyopathy be ta(1)-adrenoceptors are downregulated and G(i alpha)-proteins are upre gulated. The aim of the present study was to investigate the influence of the angiotensin-converting enzyme inhibitor captopril on beta-adre noceptor density and G(i alpha)-proteins in sequential endomyocardial biopsies. Nineteen patients with mild to moderate congestive heart fai lure due to idiopathic dilated cardiomyopathy (NYHA Class II-III) were studied before and after 8-11 weeks of therapy. Patients were randomi sed into a captopril and a control group; 9 patients received captopri l 12.5-50 mg per day, (divided in 2-3 doses) p.o. in addition to ''con ventional'' therapy with digoxin and diuretics, and 10 controls receiv ed ''conventional'' therapy only. Echocardiography, spiroergometry, ri ght heart catheterisation and endomyocardial biopsies were performed b efore (baseline) and after treatment. Compared to baseline, captopril increased total beta-adrenoceptor density by selectively increasing be ta(1)-adrenoceptors (31.6 vs 41.2 fmol.mg(-1); p < 0.05) but had no si gnificant effect on G(i alpha)-proteins. The results indicate that tre atment with angiotensin-converting enzyme inhibitors partly restores m yocardial (beta(1)-adrenoceptor density, and this action effect may co ntribute to the clinical improvement of patients with idiopathic dilat ed cardiomyopathy treated in this way.