Haemodynamic and metabolic effects of atenolol in patients with angina pectoris.

Abstract

SUMMARY Myocardial substrate extraction, coronary sinus flow, left ventricular pressure, and cardiac output were measured in 11 patients with angina pectoris at three pacing rates before and after atenolol (0.2 mg/kg). Left ventricular pressures, and the product of systolic pressure time index and heart rate did not change, but max dP/dt and KV max fell after atenolol. Only at the lowest pacing rate did the drug reduce cardiac output. Coronary sinus blood flow and myocardial oxygen uptake did not change after atenolol. At the highest pacing rate before atenolol four patients developed angina, accompanied by a rise in end-diastolic pressure. After atenolol angina was abolished in three, but the end-diastolic pressure still rose at the highest pacing rate. Myocardial lactate extraction ratio fell as heart rate increased, and was lower in the patients who developed angina. After atenolol, lactate extraction ratio increased significantly at the highest and lowest pacing rates. Myocardial pyruvate extraction rose after the drug. Arterial concentrations ofhydroxybutyrate and acetoacetate fell after atenoldl, but the decrease in their extraction was not significant. Myocardial extraction of free fatty acids was related to arterial concentration, which fell after atenolol. The changes in lactate and pyruvate extraction after atenolol were related inversely to changes in arterial free fatty acid concentration suggesting that the improvement in myocardial metabolism could have been secondary to reduced peripheral lipolysis. The increase in lactate extraction was associated with reliefofangina, but did not abolish the rise in end-diastolic pressure induced by pacing.The beneficial effect of beta-adrenergic blocking drugs in angina has been attributed to a reduction in myocardial oxygen demand secondary to their haemodynamic actions.1-3 When heart rate is controlled by atrial pacing, beta blockade has little effect upon myocardial oxygen consumption.45 Studies in which patients with angina have been paced before and after beta-blocking drugs have yielded conflicting results; some have shown no beneficial effect,3 6 while others have shown an improvement in anginal threshold or lactate extraction,4 suggesting that beta blockade may modify myocardial metabolism independently of its haemodynamic actions. The possible direct effects of beta-blocking drugs upon the human myocardium are poorly understood, and though their actions upon peripheral metabolism are well documented8 the relevance of these to the heart has not been established.Atenolol is a cardioselective beta-adrenergic antagonist without intrinsic sympathomimetic acReceived for publication 12 November 1979 tivity,9 and is effective in the treatment of angina.'0 When heart rate is controlled, atenolol does not change myocardial oxygen consumption or coronary blood flow.5 This study describes the effects of atenolol upon myocardial substrate extraction, coronary sinus blood flow, and systemic haemodynamics during pacing in 11 patients with angina, and attempts to id...

Atenolol Depresses Post-Ischaemic Recovery in the Isolated Rat Heart

“…The employed atenolol concentration allowed us to compare our results to those of previous studies w x 8,11,16,19,20 . The selected ischaemia condition induces reproducible myocardial dysfunction in control hearts without leading to arrest.…”

Improved myocardial lactate extraction after propranolol in coronary artery disease: effected by peripheral glutamate and free fatty acid metabolism.

“…The propranolol induced decrease in contractility and oxygen uptake was probably counterbalanced by left ventricular dilatation with a subsequent increase in wall tension.2 4 Coronary sinus blood flow and systemic haemodynamics were not influenced by propranolol. Beta adrenergic blockers may cause regional redistribution of myocardial blood flow in favour of ischaemic areas.19 This effect has been reported to be eliminated during pacing.20 Thus, the changes in substrate exchange across the heart found in the present study cannot be attributed to the haemodynamic effects of propranolol.…”

Haemodynamic effects of intravenous amrinone in patients with impaired left ventricular function.

“…We feel that the time of heparinisation may be in part responsible for the reduction in arterial free fatty acid at 20 minutes. 12 We find it interesttng that in this paper8 10 ml contrast injected into the venous system should alter myocardial metabolism as much as a similar intracoronary bolus or larger left ventricular injection. This suggests that multiple doses of contrast may not have an additive effect upon myocardial metabolism, as suggested by Timmis et al It is obvious that all invasive procedures affect variables measured, but we hope, like others, to design our experiments to keep this to a minimum.…”