| Abstract: | Traditionally when considering the pharmacologic basis of therapy in angina pectoris, attention is focussed on alterations of coronary blood flow. Yet the diseased coronary arteries in these patients often do not appear to be capable of responding to vasodilatory drugs. Since the pain of myocardial ischemia is relieved by a number of interventions without an increase in coronary blood flow, the concept herein considered is that angina pector is best viewed as an unfavorable relation between myocardial oxygen requirements and availability. Thus, the clinical value of the major antianginal agents is thought to be based importantly upon their actions to reduce myocardial oxygen consumption rather than to increase coronary blood flow.Sublingual nitroglycerin possesses a powerful dilator effect on veins which reduces venous return and thereby the size of the heart and intra-myocardial tension; thus myocardial oxygen requirements are diminished.The beta-adrenergic receptor blocking drug, propranolol (Inderal®), inhibits sympathetic stimulation of the heart at rest and during exercise. Thus, myocardial oxygen requirements are diminished by the reduction in heart rate and diminished contractility. As a result of this latter action, cardiac output is reduced and thereby arterial pressure and intramyocardial tension is lowered. In patients with advanced heart disease and borderline cardiac compensation, propranolol is hazardous because it removes the availability of one of the important reserve mechanisms for maintaining cardiac compensation—the sympathetic support of the failing heart.The introduction of electrical stimulation of the carotid sinus nerves as a means of therapy in patients with angina pectoris has provided a powerful tool for the treatment of patients with refractory ischemic pain. |
