Effect of prolonged beta-adrenergic blockade induced by atenolol on left ventricular remodeling after acute myocardial infarction in the rat.

Abstract

Beta-adrenergic receptor blockade reduces the mortality rate after acute myocardial infarction (AMI) in humans. However, the effects of beta blockade on left ventricular remodeling remain unknown. Therefore, in the present study we investigated the effect of prolonged beta-adrenergic receptor blockade with atenolol on left ventricular remodeling following AMI in rats. Myocardial infarction (MI) was produced in Wistar-Kyoto rats by ligating the coronary artery. Four groups of rats were studied: sham-operated (n = 10); atenolol (1 g/l in drinking water) treated sham-operated (n = 8); untreated MI (n = 11); atenolol treated MI (n = 10). Hemodynamic measurements were made about 3 weeks after the operation. Infarct size was similar in treated and untreated MI rats (31.2 +/- 2.5% cf. 33.5 +/- 2.0%). MI rats were characterized by increases in left ventricular end-diastolic pressure (LVEDP), right atrial pressure (RAP), right ventricular systolic pressure (RVSP), and left ventricular end-diastolic volume index (LVEDVI), as compared with sham-operated rats. In sham-operated rats, prolonged beta-adrenergic receptor blockade produced only a reduced HR. Atenolol-treated MI rats had a significantly higher LVEDP, RAP and LVEDVI than did rats with untreated MI. Prolonged beta-adrenergic receptor blockade with atenolol appeared to promote left ventricular remodeling after AMI. Thus, the treatment of AMI with beta-adrenergic receptor blockade in the clinical setting should be evaluated with respect to ventricular remodeling during prolonged therapy.