Dynamic left ventricular outflow tract obstruction causing myocardial ischemia.
BACKGROUND Hypotension has been found to occur in more than one-third of patients during DBSE. Unlike traditional treadmill exercise stress testing, hypotension does not appear to be associated with significant coronary artery disease or left ventricular (LV) dysfunction. Several ischemic and nonischemic mechanisms such as dynamic LV intracavitary obstruction have been implicated in the pathogenesis of hypotension and the induction of symptoms during DBSE. HYPOTHESIS The purpose of this study was the prospective evaluation of patients referred for dobutamine stress echocardiography (DBSE) to determine (1) the frequency of hypotension during DBSE, (2) the underlying mechanisms responsible for the induction of hypotension, and (3) to describe the cardiac chamber sizes and mass of patients in whom hypotension occurs. METHODS Seventy-eight consecutive patients were studied during DBSE. Pulsed and continuous-wave Doppler echocardiography were performed at baseline and at each dobutamine infusion stage. Maximum velocities were recorded. Cardiac output was determined noninvasively at each stage in patients who developed an outflow tract gradient. Echocardiography was used to characterize LV dimensions and mass. RESULTS During dobutamine infusion, 14 of 78 (18%) patients developed a left ventricular outflow tract (LVOT) velocity > or = 2.5 m/s. Pulsed Doppler echocardiography verified that the maximal velocity originated in the LVOT. Of the patients who developed an LVOT gradient, 57% had a concomitant hypotensive response to dobutamine compared with 33% of patients without a gradient (not significant). Four of nine patients had a simultaneous fall in cardiac output. Patients who developed an LVOT gradient had smaller LV dimensions and increased wall thicknesses compared with those who did not develop a gradient. CONCLUSIONS Dobutamine stress echocardiography precipitates LVOT obstruction in certain patients. The development of a gradient corresponded with a fall in blood pressure and a decline in cardiac output in nearly half of the patients. These findings suggest that stress-induced LVOT obstruction may be responsible in part for the hemodynamic changes and symptoms experienced by these patients during exercise.