Myocardial territories supplied by a significantly stenosed coronary artery have reduced perfusion or blood flow, which is accentuated during physiologic stress. For this reason, exercise treadmill testing is added to myocardial perfusion imaging to enhance the difference between normally perfused and underperfused myocardium. Stress-induced perfusion defects are used to define myocardium at risk for an ischemic and/or infarction event. The comparison of a stress-induced perfusion defect with later normal perfusion (redistribution) on delayed imaging, termed reversibility,‚ defines the imaging equivalent of myocardial ischemia. Pharmacologic agents, either dipyridamole or adenosine, can also be used to induce relative perfusion differences between normal and stenotic vascular distributions.
The comparison between stress-induced defects and resting perfusion defects may be used to define irreversibly damaged or infarcted tissue, termed a fixed defect,‚ in which no significant change in relative perfusion is noted between stress and rest. However, some of these fixed defects possess viable tissue. In hibernating‚ (viable) myocardium, metabolism is altered to conserve cellular energy at the expense of contraction resulting from severe resting ischemia. Identification of severe resting ischemia or myocardial viability may be obtained by allowing longer redistribution times or by increasing the total quantity of the radiotracer available with reinjection of additional tracer when thallium-201 imaging is performed.