Comprehensive drug management of angina pectoris.
Our current understanding of the pathophysiology of angina and myocardial ischemia includes both anatomic and dynamic mechanisms. The relative contribution made by hemodynamically important atherosclerotic obstruction and dynamic coronary artery obstruction, either by arterial spasm or arteriolar constriction, to the pathophysiology of ischemia in any given patient should be delineated. This information appears to be useful in identifying patients likely to achieve major benefit from vasodilators on the one hand or beta-adrenergic blocking agents on the other. A number of agents are now available within these two pharmacologic classes. There are some differences in action of these various agents that require thorough familiarity of effects of these drugs so that their action can be optimized. Practically speaking, the large majority of patients with an angina syndrome will respond to nitrates. Nitrates are extremely safe and cheap; thus, their use for relief or prevention of the acute ischemic episode remains the initial treatment of choice. When symptoms are more than mild to moderate in severity, or unacceptably controlled in frequency using nitrates alone, other pharmacologic measures are needed (Fig. 2). In patients with a predominant symptom of effort angina, suggesting that a hemodynamically important atherosclerotic-type obstruction is responsible for the syndrome, beta-adrenergic blocking drugs can be very helpful. If effort angina remains unacceptably controlled or adverse effects occur, a calcium-channel antagonist may be added or substituted. These latter agents do not exacerbate bronchospasm or peripheral vascular disease, and they offer a distinct advantage over beta-adrenergic blocking agents in patients with angina who have such disorders. Where the predominant symptom is rest angina, or the patient has other evidence suggesting coronary spasm or arteriolar vasoconstriction, a calcium-channel antagonist may result in a very favorable response. This therapy should be extended not only to patients in whom coronary spasm occurs spontaneously but to those in whom it can be provoked by stimuli such as effort or cold. When spasm is superimposed upon hemodynamically important atherosclerotic obstruction, the favorable response does not seem to be as great as that seen when spasm exists alone. In these cases, coronary bypass surgery, plexectomy , and other nonpharmacologic approaches may have to be added to the pharmacologic regimen.(ABSTRACT TRUNCATED AT 400 WORDS)
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000787:Angina Pectoris / Q000188:drug therapy*; D000788:Angina Pectoris, Variant / Q000188:drug therapy; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D003326:Coronary Circulation / Q000187:drug effects; D003329:Coronary Vasospasm / Q000188:drug therapy; D004359:Drug Therapy, Combination; D006801:Humans; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D014665:Vasodilator Agents / Q000627:therapeutic use
D000319:Adrenergic beta-Antagonists; D002121:Calcium Channel Blockers; D014665:Vasodilator Agents