The aim of this study was to identify post-thrombolysis
stunned myocardium using low dose (10 micrograms/kg/min)
dobutamine echocardiography, and to elucidate the role of the residual
stenosis in the
infarction artery in wall motion recovery. Forty-seven consecutive patients treated with
thrombolytic agents for a first non-complicated
myocardial infarction were included. An early
dobutamine echocardiogram was performed 7 +/- 2 days after thrombolysis to calculate a wall motion score index at baseline and with
dobutamine. A late resting echocardiogram 36 +/- 7 days and a coronariography 41 +/- 8 days after thrombolysis were also performed. In 12 patients no baseline regional dysfunction was observed in the early echocardiogram (Group I), whereas 35 patients (Group II) presented regional dysfunction which improved with
dobutamine in 11 cases (Group IIA), but not in 24 (Group IIB). Maximum
creatine kinase peak was smaller in Group I (458 +/- 162, P < or = 0.01) and in Group IIA (931 +/- 593, P < or = 0.05) than in Group IIB (1547 +/- 886). Late resting echocardiogram was performed in 44 patients: all 12 from Group I, 10 from Group IIA and 22 from Group IIB; all patients from Group I persisted with normal wall motion, while the baseline score index improved in seven patients (70%) from Group IIA vs. three patients (14%) from Group IIB (P < or = 0.01). Quantitative angiographic parameters in the
infarction artery failed to differentiate the subgroup of patients in whom wall motion improved in the late echocardiogram. By simple regression, smaller
creatine kinase peak (P < or = 0.05) and a positive response to
dobutamine in the early echocardiogram (P < or = 0.001) correlated with wall motion recovery, but the minimum lumen diameter in the
infarction artery did not correlate; by multiple logistic regression, only a positive response to
dobutamine in the early echocardiogram independently predicted late wall motion improvement (P < or = 0.001).
CONCLUSIONS: