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• W2010035148 abstract "Background The mechanism of hypotension during dobutamine stress (DS) echocardiography is unknown. The role of left ventricular outflow tract (OT) or midcavitary (MID) obstruction provoked during stress in this process remains controversial. We hypothesized that left ventricular OT obstruction would account for hypotension as opposed to MID obstruction. Methods Multiplane DS transesophageal echocardiography (TEE) was performed in 142 adult patients who displayed no resting obstruction or DS-provoked ischemia. TEE was used to identify the precise site of obstruction. Dobutamine was infused from 5 to 40 μg/kg/min and atropine as needed. Continuous wave Doppler was performed from appropriate views to assess for obstruction. Results Ventricular obstruction was provoked at the OT in 13 patients, MID in 10 patients, and at both sites in 4 patients. A total of 115 patients without dobutamine-induced obstruction served as control subjects. Systolic blood pressure at rest was similar in all groups, but decreased to a greater magnitude from rest to peak stress in the OT (−20 ± 40 mm Hg) and MID (−29 ± 38 mm Hg) groups as compared with the control group (8 ± 30 mm Hg). A hypotensive response (ie, decrease in systolic blood pressure ≥ 20 mm Hg from baseline to peak stress) was significantly greater in OT (69%, P = .001) and MID (60%, P < .05) groups as compared with the control group (19%). Heart rate and ejection fraction at rest or peak did not differ among groups. Among clinical and hemodynamic variables, left ventricular OT (relative risk 5.9; 95% confidence interval 1.9-18; P < .002) and MID (relative risk 3.6; 95% confidence interval 1.1-12; P < .05) obstructions were the only predictors for a hypotensive response. Conclusions Hypotension during DS TEE occurs commonly when ventricular obstruction is provoked. These data support a causal relationship between a provoked ventricular obstruction and hypotension during DS TEE. The mechanism of hypotension during dobutamine stress (DS) echocardiography is unknown. The role of left ventricular outflow tract (OT) or midcavitary (MID) obstruction provoked during stress in this process remains controversial. We hypothesized that left ventricular OT obstruction would account for hypotension as opposed to MID obstruction. Multiplane DS transesophageal echocardiography (TEE) was performed in 142 adult patients who displayed no resting obstruction or DS-provoked ischemia. TEE was used to identify the precise site of obstruction. Dobutamine was infused from 5 to 40 μg/kg/min and atropine as needed. Continuous wave Doppler was performed from appropriate views to assess for obstruction. Ventricular obstruction was provoked at the OT in 13 patients, MID in 10 patients, and at both sites in 4 patients. A total of 115 patients without dobutamine-induced obstruction served as control subjects. Systolic blood pressure at rest was similar in all groups, but decreased to a greater magnitude from rest to peak stress in the OT (−20 ± 40 mm Hg) and MID (−29 ± 38 mm Hg) groups as compared with the control group (8 ± 30 mm Hg). A hypotensive response (ie, decrease in systolic blood pressure ≥ 20 mm Hg from baseline to peak stress) was significantly greater in OT (69%, P = .001) and MID (60%, P < .05) groups as compared with the control group (19%). Heart rate and ejection fraction at rest or peak did not differ among groups. Among clinical and hemodynamic variables, left ventricular OT (relative risk 5.9; 95% confidence interval 1.9-18; P < .002) and MID (relative risk 3.6; 95% confidence interval 1.1-12; P < .05) obstructions were the only predictors for a hypotensive response. Hypotension during DS TEE occurs commonly when ventricular obstruction is provoked. These data support a causal relationship between a provoked ventricular obstruction and hypotension during DS TEE." @default.
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• W2010035148 date "2006-09-01" @default.
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• W2010035148 title "Hypotension During Dobutamine Stress Transesophageal Echocardiography: Relationship with Provoked Left Ventricular Obstruction" @default.
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• W2010035148 doi "https://doi.org/10.1016/j.echo.2006.04.018" @default.
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