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Haemodynamic and metabolic effects of atenolol in patients with angina pectoris
Insights
Atenolol improved myocardial metabolism and relieved angina in patients with heart disease by enhancing lactate extraction, potentially by reducing free fatty acid utilization. However, it did not fully prevent pacing-induced pressure increases.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Pharmacology
Background:
- Angina pectoris is often linked to impaired myocardial metabolism.
- Understanding how beta-blockers affect cardiac function and substrate utilization is crucial for managing ischemic heart disease.
Purpose of the Study:
- To investigate the effects of atenolol on myocardial substrate metabolism and cardiac function in patients with angina pectoris.
- To assess the relationship between metabolic changes, angina relief, and hemodynamic parameters.
Main Methods:
- Measurements included myocardial substrate extraction, coronary sinus flow, left ventricular pressure, and cardiac output in 11 angina patients.
- Hemodynamic and metabolic parameters were assessed at three pacing rates before and after atenolol administration (0.2 mg/kg).
Main Results:
- Atenolol reduced maximal dP/dt and KV max, and cardiac output at the lowest pacing rate, but did not alter left ventricular pressures or myocardial oxygen uptake.
- Angina was abolished in most patients after atenolol, accompanied by increased myocardial lactate and pyruvate extraction, and decreased arterial free fatty acids.
- The improvement in lactate extraction correlated with angina relief but did not prevent pacing-induced increases in end-diastolic pressure.
Conclusions:
- Atenolol improves myocardial metabolic efficiency in angina patients, evidenced by enhanced lactate extraction, possibly due to reduced free fatty acid utilization.
- The metabolic improvements are associated with angina relief, though not all hemodynamic changes induced by pacing are prevented.
Abstract:
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 of hydroxybutyrate and acetoacetate fell after atenolol, 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 relief of angina, but did not abolish the rise in end-diastolic pressure induced by pacing.