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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