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

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 less than 0.01) and the ratio of the salvaged myocardium/extent of initially jeopardized myocardium (70% versus 28%, p less than 0.01) were both independent predictors of stress-induced ischemia, whereas the extent of initially jeopardized myocardium (585 units versus 407 units, p = NS), incidence of greater than or equal to 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.(ABSTRACT TRUNCATED AT 250 WORDS)