Dynamic coronary obstruction as a cause of angina pectoris: Implications regarding therapy

The strong link demonstrated at autopsy between coronary atherosclerosis and angina pectoris led to the important concept that a fixed obstruction of 1 or more coronary arteries was the pathophysiologic cause of angina: myocardial ischemia and angina occurred when myocardial oxygen demand out-stripped the capacity of the diseased coronary artery to deliver oxygen. Therapeutic strategies were based on attempts to lower myocardial oxygen needs induced by physical and emotional stress. However, the finding that dynamic increases in coronary vascular resistance can also either precipitate ischemia or reduce the threshold of myocardial oxygen consumption (MVO₂) at which it occurs has profoundly altered our understanding of the pathophysiologic features of angina and, therefore, its treatment. Dynamic coronary obstruction can occur at the large-vessel level, causing Prinzmetal's or variant angina. It is also possible that in some patients a continuum of large-vessel coronary vasoconstrictor tone exists, causing the common clinical situation manifested by angina with variable thresholds of onset. Recent studies have demonstrated that increases in the resistance offered to flow by small coronary arteries too small to be imaged by angiography can also decrease anginal threshold. The fact that ischemia can be precipitated by dynamic increases in large- or small-vessel coronary resistance has important implications for the therapy of angina pectoris. In those persons who mostly have a dynamic component contributing to their coronary obstruction, primary intervention with vasodilator therapy, including nitrates and calcium-channel blocking agents, are probably most effective therapeutically. In those persons with fixed obstruction and little evidence of a dynamic component, the traditional therapeutic approach designed to reduce myocardial oxygen consumption would be most efficacious. This would include the use of nitrates and β blockers. On the other hand, those persons who have a combination of fixed and dynamic obstruction might benefit either from interventions designed either to lower MVO₂ or to relieve obstruction; some patients might require both approaches for optimal symptomatic control. The recognition that dynamic influences can profoundly exacerbate the degree of coronary obstruction at either the large- or small-vessel level should influence medical approaches to the alleviation of ischemic pain and result in more effective treatment of anginal syndromes.