Plasma catecholamine levels in acute myocardial infarction: Influence of beta-adrenergic blockade and relation to central hemodynamics

Abstract

In a prospective study, 20 patients with acute myocardial infarction were randomly assigned in a double-blind fashion to treatment with intravenous metoprolol followed by oral metoprolol or placebo. All patients underwent hemodynamic monitoring for 24 hours. Plasma adrenaline and noradrenalin levels were estimated at baseline (mean 6.0 ± 0.9 hours from onset of symptoms) and at 1 and 24 hours after the start of therapy. Plasma adrenaline and noradrenalin levels were elevated in all but one patient, with a further increase at 1 hour after administration of metoprolol ( p < 0.05). At baseline pulmonary capillary wedge pressure was directly related to both plasma adrenaline ( r = −0.44; p < 0.05) and noradrenalin levels ( r = −0.44; p < 0.05). There was also an inverse relationship between stroke volume index and the plasma noradrenalin level ( r = −0.44; p < 0.05) but not the plasma adrenaline level. These relationships were lost after the baseline measurements. However, between baseline and 1 hour there was a close relationship between the change in systemic vascular resistance and the changes in both adrenaline ( r = −0.48; p < 0.05) and noradrenalin levels ( r = −0.66; p < 0.01). Thus, in the early stages of myocardial infarction high plasma catecholamine levels are associated with the hemodynamic markers of severe left ventricular damage. Beta-adrenergic blockade with metoprolol produced a further increase in catecholamine levels that was associated with an increase in systemic vascular resistance.