Coronary artery disease, the great scourge of our times, may express itself in two major
clinicopathologic forms. The chronic form is caused by progressive atherosclerotic narrowing
of the coronary arterial bed and usually presents as angina secondary to ischemia
precipitated by increased myocardial oxygen demand, i.e., “demand ischemia.” Treatment
consists of pharmacological agents and other measures to reduce oxygen demand, and
when this approach is inadequate, surgical or catheter-based revascularization. The acute
form, on the other hand, results form a sudden reduction in myocardial oxygen supply
caused, most commonly, by a thrombus on a fissured or eroded coronary atherosclerotic
plaque that previously had not caused critical obstruction. This causes “supply ischemia,”
which may result in a variety of clinical syndromes, including unstable angina, non-Q-wave
myocardial infarction, and Q-wave myocardial infarction. These acute coronary syndromes
are responsible for more than half a million deaths and a million hospitalizations each year
in the United States. The incidence is similar in other developed nations and it is rising at an alarming rate in portions of the world.