The development of an ischemic event, whether silent or painful, represents the cumulative impact of a sequence of pathophysiologic events. Each ischemic episode is initiated by an imbalance between myocardial oxygen supply and demand that may ultimately be manifested as angina pectoris. This sequence of events can be termed the ischemic cascade. The significance of this concept resides in the fact that it redirects the focus from the end result--angina--to the more fundamental, underlying pathophysiologic factors that precede it. Specifically, these events include diminished left ventricular compliance, decreased myocardial contractility, increased left ventricular end-diastolic pressure, ST-segment changes and, occasionally, angina pectoris.