LEFT-VENTRICULAR OUTFLOW TRACT OBSTRUCTION AS A CAUSE FOR HYPOTENSIONAND SYMPTOMS DURING DOBUTAMINE STRESS ECHOCARDIOGRAPHY

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 significan t coronary artery disease or left ventricular (LV) dysfunction. Severa l ischemic and nonischemic mechanisms such as dynamic LV intracavitary obstruction have been implicated in the pathogenesis of hypotension a nd the induction of symptoms during DBSE. Hypothesis: The purpose of t his study was the prospective evaluation of patients referred for dobu tamine stress echocardiography (DBSE) to determine (1) the frequency o f hypotension during DBSE, (2) the underlying mechanisms responsible f or the induction of hypotension, and (3) to describe the cardiac chamb er sizes and mass of patients in whom hypotension occurs. Methods: Sev enty-eight consecutive patients were studied during DBSE. Pulsed and c ontinuous-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 infusi on, 14 of 78 (18%) patients developed a left ventricular outflow tract (LVOT) velocity greater than or equal to 2.5 m/s. Pulsed Doppler echo cardiography verified that the maximal velocity originated in the LVOT . Of the patients who developed an LVOT gradient, 57% had a concomitan t hypotensive response to dobutamine compared with 33% of patients wit hout a gradient (not significant). Four of nine patients had a simulta neous 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. Th e 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 responsi ble in part for the hemodynamic changes and symptoms experienced by th ese patients during exercise.