Use of an ultrashort-acting beta-receptor blocker (esmolol) in patients with acute myocardial ischemia and relative contraindications to beta-blockade therapy

↵∗Address for reprints: James M. Kirshenbaum, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis Street, Boston, Massachusetts 02115.

Abstract

The hemodynamic responses io esmolol, an ultrashort-acting (t_1/3= 9 min) beta₁-adrenergic receptor antagonist, were examined in 16 patients with myocardial ischemia and compromised left ventricular function as evidenced by a mean pulmonary capillary wedge pressure of 15 to 25 mm Hg. Esmolol was infused intravenously to a maximal dose of 300 μg/Kg body weight per min for ≤48 h in 16 patients: 9 with acute myocardial infarction, 6 with periinfarction angina and 1 with acute unstable angina. The sinus rate and systolic arterial pressure declined rapidly in all patients from baseline values of 99 ± 12 beats/min and 126 ± 19 mm Hg to 80 ± 14 beats/min (p < 0.05) and 107 ± 20 mm Hg (p ≤0.05) during esmolol treatment. Rate-pressure product decreased by 33% and cardiac index by 14% during esmolol treatment, but pulmonary capillary wedge pressure was not significantly altered by drug infusion (19 ± 3 mm Hg at baseline versus 19 ± 5 during treatment, p = NS). In all patients there was a rapid return toward baseline hemodynamic measurements within 15 min of stopping administration of esmolol, and virtually complete resolution of drug effect was evident within approximately 30 min.

During infusion of esmolol, four of nine patients receiving intravenous nitroglycerin required downward adjustment of nitroglycerin infusion rate to maintain systolic blood pressure >90 mm Hg. Four patients required termination of esmolol infusion because of oliguria or hypotension, but all recovered hemodynamic stability within 30 min of termination of the infusion; one patient required a brief infusion of dopamine.

These results suggest that, even in the presence of moderate left ventricular dysfunction, esmolol safely and effectively lowers both arterial pressure and heart rate in patients with acute ischemia. The titratability and rapid offset of action of esmolol in such patients may broaden the clinical applicability of the adjunctive cardioprotective effect of beta-receptor blockade in the current era of reperfusion therapy for myocardial infarction.

Footnotes

↵∗ Present address: Department of Cardiology, Wayne State University, Detroit, Michigan.
☆ This study was supported in part by Grant 5T32 HL-07049 from the National Heart, Lung, and Blood Institute. Bethesda, Maryland: by a grant from the Dupont Critical Care Corporation. Waukegan, Illinois; and by GCRC Grant MO1 RR00888-10 CLR. Data organization and analysis assisted by the CLINFO data management and analysis system at the Brigham and Women's Hospital, Boston, Massachusetts. This paper was presented in part at the 36th Annual Meeting of the American College of Cardiology, New Orleans, Louisiana, March 1987.