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European Heart Journal 1984 5(5):366-373;
Copyright © 1984 by the European Society of Cardiology.
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© 1984 The European Society of Cardiology

Enhanced haemodynamic effects of propranolol in acute myocardial infarction

B. SILKE, G.I.C. NELSON, S.P. VERMA, M. HUSSAIN, R.C. AHUJA, C. WALKER and S.H. TAYLOR1

University Department of Cardiovascular Studies and Department of Medical Cardiology, The General Infirmary Leeds, U.K.

Received 15 August 1983; revised 23 November 1983; .

1Correspondence to: Dr. S.H. Taulor, Department of Cardiology, The General Infirmary, Great George Street, Leeds LS1 3EX, U.K.

Abstract

To evaluate the possible influence of sympathetic activation on the haemodynamic response to intravenous beta-blockade, the dose-response characteristics of three boluses of propranolol were evaluated in 8 patients with uncomplicated infarction and compared in a similar number of patients with stable angina. Following a control period, when haemodynamic stability was confirmed, propranolol 2, 2 and 4 mg (cumulative dosage 2, 4 and 8 mg) was injected into the central circulation at 15 min intervals. Despite close matching in baseline control haemodynamic variables between the groups, in stable angina, pro pranolol resulted in dose-related depression of cardiac output without change in systemic blood pressure, whereas following myocardial infarction the drug induced significantly greater falls in cardiac output (P>0-05) and a dose-related decrease in systemic blood pressure. Despite the greater effects of propranolol on cardiac output following myocardial infarction, the left ventricular filling pressure was increased to a lesser extent compared with stable angina. The explanation for this observation may reside in a greater susceptibility of the left ventricular wall to increase its compliance, under conditions of high sympathetic stimulation, following beta-blockade. These data support experimental and biochemical evidence of sym pathetic activation in myocardial infarction; the hyperadrenergic state conditions an augmented haemody namic response to competitive antagonism of sympathetic stimulation at cardiac beta-adrenocep tors.

Key Words: Beta-blockade • haemodynamics • myocardial infarction • propranolol • sympathetic activation


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