9 for Evaluation of Myocardial Ischemia
1989
Myocardial ischemia is caused by decreased oxygen supply, increased demand, or a combi nation of the two. The episodes of ischemia may be silent (painless) or with pain. The con cept of "total ischemic burden" was intro duced to represent the sum of all episodes of ischemia. l The painful episodes, which may be due to increased workload on the heart or an increase in vasoconstrictor tone with de creased supply, and the painless episodes con stitute the total ischemia burden. It is one of the frustrations of the clinician to quantify ischemia with coronary anatomy, be cause coronary anatomy does not necessarily translate the physiologic status and the ten dency of the patient to develop ischemic epi sodes. The development of an ischemic event causes an imbalance in myocardial oxygen supply and demand which in turn sets off a chain of events with left ventricular dysfunc tion, electrocardiographic, and hemodynamic changes culminating in angina. This patho physiologic sequence of events is termed the "ischemic cascade."2 Repeated episodes of "ischemic cascade" can disrupt myocardial function at the cellular level. Prolonged peri ods of ischemia may result in stunning of the myocardium. 3 One has to consider the total ischemic burden, taking into account the se quence of ischemic cascade resulting in stunned myocardium and ischemic left ven tricular dysfunction. For prognostication, diagnosis, and treat ment of total ischemic burden, we may need new tests or a combination of the existing tests and interventions because visual quantitation of coronary obstructions by conventional an giographic approaches will not provide physi ologic and functional assessment of angio graphically documented coronary artery obstruction.4 There are shortcomings, even in the proper interpretation of coronary angiograms, due to interobserver and intraobserver variability;5,6 hence the need for interventions to evaluate myocardial ischemia, for provocation of coro nary artery spasm, and assessment of viable myocardium in the postinfarct state. There are several technical methods for evaluating ischemia in a semiquantitative manner. Stressing the heart by atrial pacing and measuring various parameters to docu ment ischemia and ischemic cascade are well established. One can measure a number of pa rameters using different techniques, such as thallium myocardial scintigraphy, echocardio graphy, radio nuclide ventriculography, meta bolic studies, and scanning. We briefly describe technical aspects and indications for the various tests. We know that vasomotor tone effects changes in epi cardial and intramyocardial vessels, and it can cause segmental or generalized reduction in luminal diameter, and the dynamic shifts in the luminal diameter are unpredictable; hence the sensitivity. specificity, and predic tive accuracy of any of these tests is de creased.
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