Improvement of myocardial metabolism in coronary arterial disease by beta-blockade.

Abstract

Twenty patients with angina pectoris associated with obstructive coronary arterial disease were investigated by stressing the heart by atrial pacing. Arterial and coronary sinus blood was sampled and the time taken to provoke angina (pacing time) measured. Nine of the patients acted as a control group and did not receive beta-blocking drugs. In this group both pacing time and myocardial lactate extraction were reproducible provided that 45 minutes rest was allowed between pacing tests: we have called this period the myocardial recovery time. The 11 remaining patients were paced before and after beta-blockade, the rate being kept constant for each patient. In contrast to the control group, beta-blockade improved myocardial metabolism as shown by increased myocardial lactate extraction (P<002) and decreased glucose extraction (P<O0O1). The pacing time to angina was increased (P<001) and the degree of ST segment depression was decreased (P<0 05). There was no significant effect on systolic or diastolic bloodpressure, myocardial oxygen extraction, or extraction offree fatty acids and potassium.Failure to allow adequate time for full myocardial recovery after pacing will invalidate assessment of antianginal drugs. When this precaution is taken beta-blocking drugs are seen to improve nyocardialmetabolism independently of their effects on heart rate and blood pressure.Adrenergic beta-receptor antagonists are well established in the treatment of angina pectoris (Jackson et al., 1975). Their beneficial effects are related to the reduction of left ventricular work by a reduction in heart rate, arterial pressure, and velocity of myocardial contraction (Robinson, 1971). By eliminating the effect of heart rate by means of atrial pacing, Balcon (1971) concluded that the main beneficial effect of propranolol and practolol was the reduction of heart rate.The interpretation of an atrial pacing stress test relies to a large extent on the subjective sensation of chest pain. The addition of arterial and coronary sinus sampling, and particularly estimation of lactate, provides a more objective measurement of the response of the left ventricle to stress. This study demonstrates the reproducibility of the change in lactate extraction when the atrial pacing rate is constant and the time interval between successive pacing tests is also adequate. The beneficial effects of adrenergic beta-receptor antagonists in patients with obstructive coronary arterial disease is also confirmed.

Beta adrenergic receptor blockade of feline myocardium. Cardiac mechanics, energetics, and beta adrenoceptor regulation.

“…In contrast, no primary effect of propranolol on the oxygen consumption of normal isolated myocardium is apparent in these data. Thus, although it has been postulated that fl-adrenoceptor blockade has an effect on myocardial metabolism that is independent of its effect on either cardiac autonomic nervous control (53) or hemodynamic variables (67,68), no support for these concepts is found either in these data or in other recent data (69) derived in a somewhat less direct manner.…”

Angina with normal coronary arteriograms. Value of coronary sinus lactate estimation in diagnosis and treatment.

“…We have recently shown that beta-blockers have a similar beneficial effect (Jackson et al, 1977). Of 19 patients with abnormal lactate metabolism, 15 responded to glyceryl trinitrate and 16 to propranolol.…”

Preoperative β-blocker use: is titration to a heart rate of 60 beats per minute a consistently attainable goal?

“…This finding may have a significant impact in light of evidence that intravenous therapy alone may be difficult to titrate; 35% of patients treated with intravenous atenolol, in the study by Mangano et al [1], had intraoperative tachycardia. In addition, the beneficial effects of b-blockade are multifactorial; even if they are administered in submaximal doses, b-blockade may cause reductions of myocardial metabolism, oxygen demand, shear stress, inflammatory responses, platelet aggregability, and plaque disruption [17,23,37,38]. Additional data are needed to determine which degree of blockade is required to achieve these beneficial effects.…”