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Abstract
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.
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© 1987 Published by Elsevier Inc.