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Am J Cardiol. 1981 Oct;48(4):797-803.

Dynamic coronary tone in precipitation, exacerbation and relief of angina pectoris.


Until recently, understanding of the pathogenesis of angina pectoris was based primarily on the concept of a fixed stenosis of one or more coronary arteries: Myocardial ischemia and angina occurred when myocardial oxygen consumption (MVO2) outstripped the capacity of the diseased coronary artery to delivery oxygen. Therapeutic strategies focused on interventions designed to reduce MVO2. The concept of dynamic obstruction, first applied to coronary spasm induced at rest and more recently to spasm induced by exercise, adds an additional important pathophysiologic mechanism responsible for causing angina pectoris. This study deals with the possibility that the concept of "spasm," as commonly understood, is too narrowly defined. It develops the hypothesis that subcritical increases in large vessel coronary tone occur, either in a "normal" coronary artery or in one with an existing lesion, that augment the degree of large vessel coronary resistance but not enough to exceed the vasodilator reserve of the coronary arterioles. Hence, although total coronary resistance, and thereby coronary flow, is unaltered at rest, the impingement on arteriolar vasodilator reserve would diminish the capacity to augment flow in response to increases in MVO2. Such coronary constriction would not precipitate angina at rest but would increase anginal threshold. Conversely, dilatation of a stenotic coronary artery could decrease the degree of obstruction and increase anginal threshold. This concept of dynamic coronary obstruction in the presence of "normal" or diseased coronary arteries implies a direct role for coronary vasodilators in some patients with angina pectoris, even when frank coronary spasm is absent. Also implicit in this hypothesis is the concept that dynamic and fixed components to obstruction may contribute variably to the degree of obstruction in different patients. Some patients with largely fixed obstruction would benefit mainly from attempts to lower MVO2 with nitrates and beta blocking agents. Dynamic coronary obstruction may constitute the major mechanism responsible for angina in other patients. In these persons nitrates or calcium channel blocking agents might provide the most efficacious form of therapy. Both fixed and dynamic obstruction may play an important role in symptom production in yet other patients. In such persons attempts to decrease MVO2 and the magnitude of coronary obstruction might provide the most successful form of therapy.

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