Exercise-induced ischemia in the streptokinase-reperfused myocardium: Relationship to extent of salvaged myocardium and degree of residual coronary stenosis

Abstract To assess the functional significance of residual stenosis at the site of the thrombolysed infarct-related coronary artery, 37 patients underwent exercise radionuclide ventriculography or stress-redistribution thallium-201 scintigraphy at an average of 7 weeks following streptokinase therapy during evolving myocardial infarction. The size of the initially jeopardized myocardium and the salvaged myocardium were quantitated on thallium-201 studies obtained immediately before and 10 days after streptokinase infusion. Exercise-induced ischemia (defined by reversible thallium-201 perfusion defects or stress-induced deterioration of regional wall motion) in the reperfused myocardium was absent in 46% of patients and was present in different degrees in the remaining 54%. A significantly lower proportion of patients, however, showed exercise-induced chest pain and/or ST segment depression (10% and 20%, respectively). By stepwise multiple logistic regression analysis, the quantitatively determined size of the salvaged myocardium (398 units versus 65 units, p p p = NS), incidence of ≥99% coronary stenosis (37% versus 46%, p = NS), and ischemic time (160 versus 196 minutes, p = NS) did not provide additional predictive information. We conclude that exercise-induced ischemia, which is frequently present in the streptokinase-reperfused myocardium, cannot be detected accurately by exercise-induced chest pain or ST segment depression, nor can it be predicted by the severity of residual coronary stenosis. The extent of salvaged myocardium by itself or proportionate to the size of initially jeopardized myocardium are the main determinants of exercise-induced ischemia in the reperfused myocardium. The functional significance of residual coronary stenosis following acute streptokinase coronary thrombolysis can be assessed by radionuclide evaluation of the extents of salvaged myocardium and exercise-induced ischemia.