Assessment of Myocardial Viability After Thrombolysis

T he time course of absolute myocardial ischemia is rapid. With the interruption of blood flow to the myocardium, aerobic metabolism ceases within 10 seconds,1 and soon even anaerobic metabolism is inhibited due to the accumulation of H', lactate, and other metabolites. To preserve limited in situ stores of preformed high-energy phosphate, systolic contraction is markedly inhibited, generally ceasing within 10 to 15 seconds, but ATP is gradually depleted by the ongoing activity of membrane proteins.2 By 40 minutes of ischemia, membrane chemogradients can no longer be maintained, and the resulting influx of calcium and sodium causes cellular and subcellular edema, which, along with accumulation of toxic metabolites, leads to cell death. However, as critical as the issue of myocardial viability is, our ability to distinguish reversibly from irreversibly damaged tissue remains imperfect. Even with electron microscopy, the precise boundary of irreversibility is not obvious. Clinically, such complete coronary occlusion produces a wave front of necrotic tissue, beginning in the subendocardium within about 40 minutes and spreading outward, so that by 6 hours the maximal infarct size is achieved. However, the presence of even a small amount of perfusion to the infarct bed, from either antegrade or collateral flow, will significantly delay necrosis and limit infarct size. In general, the likelihood that myocardium downstream from a coronary occlusion will remain viable depends on many factors, including the duration of coronary occlusion, presence of collateral vessels, and timeliness and extent of reperfusion. Interpretation of the clinical results of myocardial reperfusion therapy often hinges on the definition of regional viability. It is of importance that previous studies have demonstrated how difficult accurate assessment of viability can be after thrombolytic therapy.3