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[Early echocardiographic identification of viable myocardium after acute myocardial infarct using inotropic agents: comparison of dobutamine and enoximone].

BACKGROUND
The reversibility of regional dysfunction early after acute myocardial infarction may be obtained with inotropic adrenergic stimulation, in particular during low dose dobutamine infusion, suggesting the presence of viable myocardium. The aim of this study was to determine whether viable myocardium can be identified by two-dimensional echocardiography after an i.v. bolus of enoximone-positive inotropic non-adrenergic drug, phosphodiesterase III inhibitor as well as during dobutamine infusion, in patients with acute myocardial infarction.


METHODS
Twelve male patients, aged 57 +/- 10 years and treated with rtPA (100 mg i.v. in 180 minutes) within the first 6 hours of a first anterior myocardial infarction were studied. All patients underwent a dobutamine infusion (5 and 10 mcg/kg/min, 5 minutes per dose) 4 +/- 1 days after entrance, followed by an enoximone bolus (1 mg/kg over 5 minutes) 1 hour later. Echocardiography was performed before dobutamine and enoximone, during dobutamine, 10 minutes after enoximone and at 6 +/- 2 months follow-up. A Wall Motion Score Index (WMSI) was calculated as recommended by the American Society of Echocardiography. All patients underwent coronarography on days 9-11 post-infarction.


RESULTS
Improvement in regional function of basally asynergic segments occurred in 8 patients during dobutamine infusion, as well as after enoximone i.v. bolus, and in 1 patient only during dobutamine infusion. Both dobutamine and enoximone tests were found to be negative in the other 3 patients. A decrease of WMSI was observed with both dobutamine and enoximone tests (from 1.84 +/- 0.32 to 1.73 +/- 0.31; p = .002 with dobutamine; from 1.84 +/- 0.32 to 1.70 +/- 0.27; p = .0132 with enoximone) with concordant wall motion changes between two tests in 73/84 (87%; K = 0.61) basally asynergic segments. There were no complications occurred during the study. Of 8 patients with positive response for viable myocardium to both tests, 6 had a patent and 2 an occluded infarct-related artery. However, in the latter a collateral circulation toward necrotic area was present. At follow-up improvement in regional function of basally asynergic segments, with a decrease of WMSI (from 1.74 +/- 0.23 to 1.59 +/- 0.24; p < .05), was observed in 4 of 8 patients with viable myocardium detected by either dobutamine or enoximone.


CONCLUSIONS
1) Viable asynergic myocardium may be identified early after acute myocardial infarction by enoximone bolus, as carefully and safely as by dobutamine infusion; 2) transient recovery of post-ischemic myocardial dysfunction may be obtained independently of beta-receptor stimulation.