CAN DOBUTAMINE ECHOCARDIOGRAPHY INDUCE MYOCARDIAL DAMAGE IN PATIENTS WITH DYSFUNCTIONAL BUT VIABLE MYOCARDIUM SUPPLIED BY A SEVERELY STENOTIC CORONARY-ARTERY

In animal experiments, dobutamine infusion was found to impair the oxy gen supply-demand balance in hypoperfused areas of hibernating myocard ium which may induce myocardial damage. The aim of our study was to as sess whether dobutamine echocardiography can induce myocardial damage detected by an increase in the cardiac troponin T level in blood. Twen ty seven patients with coronary artery disease and severe stenosis of at least one major coronary artery (greater than or equal to 90% of lu minal diameter narrowing) supplying dysfunctional myocardial segments underwent dobutamine echocardiography. Dobutamine was infused in 3 min dose increments of 5, 10, 20, 30, and 40 mu g per kg body weight per minute with the addition of atropine up to 1 mg if ischemia or an 85% predicted maximal heart rate were not achieved. In 15 patients the pro tocol with prolonged application of 40 mu g per kg per minute of dobut amine for 6 min and for the next 5 min with the addition of atropine w as used. To exclude minor myocardial damage, an increase in the cardia c troponin T blood level was assessed qualitatively by the TROP T sens itive Rapid Test 20 h after dobutamine echocardiography. In 20 patient s the dysfunctional segments were found to be viable with inducible is chemia exhibiting either continuous worsening in systolic thickening o r ''biphasic'' response characterised by the improvement of their syst olic thickening with a small dose and by a worsening of the thickening with a high dose of dobutamine. No patient exhibited positive TROP T sensitive Rapid Test result. In patients with coronary artery disease and severe stenosis of a major coronary artery supplying dysfunctional but viable myocardial segments, dobutamine echocardiography does not induce myocardial damage detectable by an increase in cardiac troponin T level. (C) 1997 Elsevier Science Ireland Ltd.