False positive ST segment elevation during dobutamine stress echocardiography due to left ventricular hypertrophy.

Abstract

The significance of ST segment elevation in dobutamine stress echocardiography (DSE) remains controversial. In patients with prior Q wave myocardial infarction (MI), it may reflect myocardial ischemia, contractile reserve in the infarct-related area, or dyskinesia of the infarcted areas of myocardium. In the nonpost-MI population, it has been attributed to vasospasm or strongly associated with coronary artery disease and ischemia. We hypothesized that ST segment elevation in the absence of inducible ischemia or prior MI is related to the presence of left ventricular hypertrophy (LVH). During DSE, dobutamine was infused from 5 microg/kg/min up to a maximum of 50 microg/kg/min. Echocardiographic images were obtained at baseline, low dose, peak dose, and recovery. Ischemia was defined as either the development of a new wall-motion abnormality or worsening wall motion at peak dose. We reviewed 682 consecutive DSE tests and found ST elevation in 42 patients (incidence = 6.1%). After excluding two patients for > 10% uninterpretable echocardiographic segments, the study population consisted of 40 patients. In 25 patients with ST elevation and without echocardiographic evidence for dobutamine-induced ischemia, 21 (84%) patients had LVH (P = 0.001). In 15 patients with inducible ischemia, only 4 (27%) patients had LVH. No other significant differences were found except that prior MI was more common in the inducible ischemia group. In the subgroup of 18 patients without prior MI, no inducible ischemia was found in 15 (83%). LVH was present in 14 (93%) of these 15 patients (P < 0.005), and all 14 had a normal baseline left ventricular ejection fraction. None of the three patients in the nonpost-MI subgroup with inducible ischemia had LVH. The 22 patients with prior MI had no significant association with LVH (P = 0.39). We conclude that ST segment elevation during DSE can occur without echocardiographic evidence for ischemia and is associated with LVH in the nonpost-MI population. This ST elevation may be related to transient electrocardiographic repolarization changes in the hypertrophied ventricle in the presence of altered loading conditions and/or altered catecholamine influences rather than true ischemia.