title: 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 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)
authors.affiliation: Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
authors.forename: A T
authors.initials: AT
authors.lastname: Weiss
authors.forename: J
authors.initials: J
authors.lastname: Maddahi
authors.forename: P K
authors.initials: PK
authors.lastname: Shah
authors.forename: A S
authors.initials: AS
authors.lastname: Lew
authors.forename: H J
authors.initials: HJ
authors.lastname: Swan
authors.forename: W
authors.initials: W
authors.lastname: Ganz
authors.forename: D S
authors.initials: DS
authors.lastname: Berman
mesh_terms: D000328:Adult; D000368:Aged; D003251:Constriction, Pathologic; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000473:pathology*; D005082:Physical Exertion; D013300:Streptokinase / Q000627:therapeutic use*
chemical_list: D013300:Streptokinase