Spasm is only one type of dynamic stenosis typically responsible for variant angina; spasm with or without transient intraluminal plugging, superimposed on a wide range of old or fresh, fixed stenoses, is largely responsible for unstable angina; physiological changes of tone around pliable coronary stenoses probably account for the variable exercise tolerance and for spontaneous attacks in patients with stable angina. Sustained spasms, not responsive to nitrates and thrombosis, are likely to be involved at different times or simultaneously in acute coronary occlusion causing myocardial infarction. Acute or worsening phases of coronary diseases are largely caused by dynamic stenoses, whereas stable, fixed-threshold, predictable angina may be the only feature of quiescent phases of coronary disease.