Copyright © 1993 by the European Society of Cardiology.
© 1993 The Europen Society of Cardiology
The link between acute haemodynamic adrenergic beta-blockade and long-term effects in patients with heart failure
A study on diastolic function, heart rate and myocardial metabolism following intravenous metoprolol
The Wallenberg Laboratory for Cardiovascular Research, Division of Cardiology, Sahlgrenska Sjukhuset, University of Göteborg Goteborg, Sweden
Received 15 March 1991; revised 1 June 1993; .
Correspondence: Dr Bert Andersson, Kardiologdivisionen, Sahlgrenska Sjukhuset, S-413 45 Goteborg, Sweden.
Abstract
The present study was performed to find possible mechanisms linking the early effects of beta-blockade with the observed long-term effects in patients with heart failure.
In 57 patients with heart failure, 13±3.1 mg of metoprolol was given intravenously. The patients were investigated by invasive haemodynamics (n = 34), including collection of myocardial metabolic data during atrial pacing stress (n = 16), by radionuclide angiography during physiological atrial pacing (n = 13), and by a bedside evaluation (n = 10).
Diastolic function, measured by early peak filling rate, followed changes in heart rate, but was similar when heart rate was held constant by atrial pacing before and after beta-blockade. Following beta-blockade and slower heart rates, diastolic filling volumes were redistributed to late diastole. Metoprolol induced a parallel decrease in coronary sinus flow and myocardial oxygen consumption. Myocardial oxygen consumption following beta-blockade decreased both during spontaneous rhythm (25±15 to 16±8.8 ml. min–1; P = 0.006), and during atrial pacing stress (30±13 to 23±11 ml.min–1; P = 0.004). Cardiac index decreased owing to reduction of heart rate (2.3±1.0 to 1.9±0.64 l.min–1.m2; P = 0.0003), while left ventricular filling pressure was unchanged. Ejection fraction and ventricular volumes were unaltered following atrial pacing or beta-blockade. There was a reflex increase in noradenaline concentration after beta-blockade injection (0.96±0.66 to 1.20±0.91 nmol.l–1; P = 0.002), whereas myocardial noradrenaline overflow was unchanged. There was a trend towards an increase in myocardial lactate consumption after beta-blockade administration during atrial pacing stress.
It is suggested that the surprisingly good tolerability seen after acute administration of beta-blockers to patients with severe heart failure may be explained by prolongation of the diastolic filling phase, which outweighs the negative ino tropic effects. The reduced myocardial metabolic demand may allow the failing myocardium to recover and explain the excellent long-term effect on heart function following beta-blockade treatment.
Key Words: Diastolic function • myocardial metabolism • sympathetic nervous system • noradenalin • lactate
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