Beta-adrenergic blockade in acute myocardial infarction: a haemodynamic and radionuclide study

While long term beta-adrenergic blockade, introduced in theconvalescent stage of myocardial infarction, may reduce subsequentmortality, the value of early beta-blockade in the acute phaseis less certain. Therefore, the influence of beta-blockade onleft ventricular performance and eventual infarct size was assessedin 61 consecutive patients with acute myocardial infarction.Metoprolol (15 mg i. v. followed by 200 mg day^-1 orally) orplacebo was administered in a double-blind, randomised fashionwith a median delay of 5.9 hours from onset of symptoms. After15 days of double blind therapy all patients were started onopen treatment with metoprolol. All patients underwent haemodynamicmonitoring for 24 hours and serial radionuclide ventriculographyand thallium 201 scintigraphy.In the first hour metoprolol produceda decrease in cardiac output (1.3 l min^-1; P<0.001) due toa reduction in heart rate (15 min^-1; P<0-001) and a decreasein left ventricular stroke work index (10.7 g m m²; P<0.001)due to a reduction in mean arterial pressure (10 mmHg; P<0.001).There was then a gradual attenuation in these changes. Whilemetoprolol produced an increase in pulmonary capillary wedgepressure and in both end-diastolic and end-systolic volumes(P<0.05), these changes were confined to patients with abaseline pulmonary capillary wedge pressure below the medianof 13 mm Hg mercury. There was no significant change in strokevolume or in ejection fraction in response to metoprolol. Therewas no significant difference between the groups in left ventricularperformance, as assessed by radionuclide ventriculography, orin scintigraphic infarct size, either at the end of the 15 daysdouble-blind treatment or after 3 months open treatment withmetoprolol.Thus, early intervention with metoprolol in acutemyocardial infarction appeared to reduce myocardial oxygen consumptionwith no adverse haemodynamic effect. However, metoprolol failedto preserve left ventricular function, or to reduce apparentinfarct size. These data suggest that the modest reduction inmortality reported in the acute phase studies of beta-blockadein myocardial infarction, is unlikely to be due to infarct reduction.It is more likely to be due to a secondary prevention or toan antiarrhythmic effect.