Transient regional myocardial ischemia appears to underlie symptoms such as angina pectoris and represents a key pathophysiologic step, since it is an objective marker of disease activity and is capable of causing disabling symptoms and damage to left ventricular myocardium. A study of the characteristics of transient ischemia in and out of the hospital has shown that symptoms are an inconsistent underestimation of these events. Ischemia is generally prolonged, mostly asymptomatic, and usually accompanied by a regional decrease in myocardial perfusion. Studies out of the hospital have also shown that these episodes are frequently triggered by a wide range of ordinary everyday activities. These new features of transient ischemia are worth noting when searching for relevant causes that are present during everyday life and when trying to choose more rational therapy. More detailed studies of patient activity have shown that different levels of mental arousal are the most common triggering mechanism causing ischemia out of the hospital. In addition, the occurrence of transient ischemia during everyday life displays a circadian rhythm, with an increase and peak occurrence between 6:00 A.M. and 12 noon each day. The day-to-day variability of ischemia is marked, indicating functional disturbances of coronary stenoses against a background of a severe reduction in cross-sectional area. The examination of proximal stenoses has shown that the reduction in cross-sectional area is usually underestimated by conventional angiography; pressure gradients across coronary stenoses are common and, with reduced poststenotic blood pressure, can jeopardize perfusion; disturbances of vessel caliber and antegrade flow can accompany many of the ordinary everyday activities known to trigger ischemia detected in Holter tapes studied out of the hospital; and there is clear-cut evidence of endothelial dysfunction in these patients, with reversal of the normal dilator response to acetylcholine and paradoxical constriction of stenoses. This evidence of endothelial dysfunction in humans could be central to the problems of atheromatous narrowing, thrombus, and disturbed vasomotion.