Can dobutamine echocardiography induce myocardial damage in patients with dysfunctional but viable myocardium supplied by a severely stenotic coronary artery?

Abstract

In animal experiments, dobutamine infusion was found to impair the oxygen supply-demand balance in hypoperfused areas of hibernating myocardium which may induce myocardial damage. The aim of our study was to assess whether dobutamine echocardiography can induce myocardial damage detected by an increase in the cardiac troponin T level in blood. Twenty seven patients with coronary artery disease and severe stenosis of at least one major coronary artery (90% of luminal diameter narrowing) supplying dysfunctional myocardial segments underwent dobutamine echocardiography. Dobutamine was infused in 3 min dose increments of 5, 10, 20, 30, and 40 μg 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 protocol with prolonged application of 40 μg per kg per minute of dobutamine for 6 min and for the next 5 min with the addition of atropine was used. To exclude minor myocardial damage, an increase in the cardiac troponin T blood level was assessed qualitatively by the TROP T sensitive Rapid Test 20 h after dobutamine echocardiography. In 20 patients the dysfunctional segments were found to be viable with inducible ischemia exhibiting either continuous worsening in systolic thickening or “biphasic” response characterised by the improvement of their systolic thickening with a small dome 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.