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* From the Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN.
Correspondence to: Ernest C. Madu, MD, FCCP, Vanderbilt University Medical Center, Division of Cardiovascular Medicine, 315 MRB II, 2220 Pierce Ave, Nashville, TN 37232-6300; e-mail: ernest.madu{at}mcmail.vanderbilt.edu
| Abstract |
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Methods and results: We prospectively evaluated 23 morbidly obese patients with chest pain using transesophageal dobutamine stress echocardiography (TE-DSE). The mean (± SD) weight was 164 ± 8 kg (range, 118 to 215 kg). We identified nine patients with abnormal TE-DSE findings. Five of these patients subsequently had cardiac catheterization with confirmation of CAD in the regions identified by TE-DSE. Over a follow-up period of 18 ± 6 months, three cardiac events (non-Q-wave myocardial infarction) occurred in the same group, including two patients without confirmatory cardiac catheterization data. Thus, seven of nine patients with positive results of TE-DSE had objective confirmatory evidence of CAD. No cardiac events were observed in the group with normal TE-DSE over the same follow-up period.
Conclusion: TE-DSE is a safe and potentially useful technique for the evaluation of suspected CAD in morbidly obese subjects.
Key Words: angiography coronary disease echocardiography obesity
| Introduction |
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Over the past several years, transesophageal echocardiography (TEE) has emerged as a reliable alternative to transthoracic cardiac ultrasound because of its safety, accessibility, and inherent ability to provide superior quality cardiac imaging in a majority of patients.9 10 In an effort to combine the advantages of pharmacologic stress testing with superior quality cardiac imaging, investigators have used TEE with dipyridamole and dobutamine in the evaluation of patients with CAD.11 12 13 The combined use of TEE with DSE in morbidly obese patients has not been reported to date. The purpose of this study, therefore, was to provide preliminary information on the safety and reliability of transesophageal dobutamine stress echocardiography (TE-DSE) in the evaluation of myocardial ischemia in morbidly obese patients.
| Materials and Methods |
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190 mm Hg), uncompensated
congestive heart failure, reactive airway disease or active
bronchospastic disease, significant supraventricular or ventricular
arrhythmias, and known or suspected congenital or significant valvular
heart disease. We report here our preliminary findings of a prospective evaluation of ischemia in 23 morbidly obese patients using a protocol for TE-DSE developed in our laboratory.
Study Patients
Twenty-three morbidly obese patients who were referred for
evaluation of suspected CAD were included in this preliminary
investigation of TE-DSE. All 23 patients were referred for evaluation
of chest pain.
There were 19 men and 4 women, with a mean age (± SD) of 48 ± 7 years (range, 36 to 58 years) and a mean weight of 164 ± 8 kg (range, 118 to 215 kg). Antianginal medications were discontinued for 72 h prior to the study. All patients were in normal sinus rhythm. All patients gave informed consent for this study.
TEE Studies
TEE studies were performed using a multiplane
transesophageal instrument (Omniplane; Hewlett-Packard; Palo Alto, CA)
composed of a 64-element phased-array transducer with color Doppler
capability and a dual-frequency feature that permits two-dimensional
imaging at 5 and 3.7 MHz. The transducer array within the tip of the
endoscope allowed electronic or mechanical rotation around the long
axis of the ultrasound beam through a 180° arc. TEE was performed
using standard technique. Lidocaine hydrochloride spray was
administered orally for topical anesthesia. Glycopyrrolate (0.2 mg), an
anticholinergic agent, was administered IV to decrease salivation.
Midazolam hydrochloride (0.5 to 10 mg; mean dose, 3.5 mg), a
benzodiazepine, was administered IV for sedation. Seven patients
received IV meperidine hydrochloride (20 to 50 mg; mean dose, 30 mg) to
reduce the gag reflex.
Images were obtained in the following sequence (Fig 1) :\
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2. Midesophageal, long-axis two-chamber view with the ultrasound array at 70 to 90°. (This view is optimal for assessing function in both the anterior and inferior walls.) We elected not to use the transgastric long-axis view at 135° due to significant foreshortening of the ventricle noted in our patients at peak dobutamine infusion;
3. Midesophageal, vertical long-axis view with the ultrasound array at 135° (this view corresponds to the transthoracic parasternal long-axis view and is optimal for assessing the anteroseptal and the posterior walls);
4. Transgastric, midpapillary short-axis view from the cardiac apex toward the base with the ultrasound array at 0° rotation and retroflexion of the probe tip at the midgastric level.
Baseline hemodynamic, ECG, and TEE data were obtained and recorded for each patient. The baseline quantitative echocardiographic data obtained included the following: LV volume, ejection fraction, LV wall thickness, and LV mass. The Doppler-derived flow velocity of the LV outflow tract was determined at baseline and during peak dobutamine infusion in all patients. LV volume measurements were obtained with the modified Simpsons rule,14 and values for the LV mass were obtained from transthoracic echocardiography measurements using the Penn convention formula, previously validated by Devereux and Reichek.15 The TEE views that were obtained, using the previously described sequence, were recorded on a 1.5-inch VHS format videotape, and selected cardiac cycles at each dose were digitally acquired in a cineloop format and stored on an optical disk. The acquired views were later reviewed off-line, and selected images were reconstructed to display side-by-side images at baseline and at peak dobutamine infusion for regional wall-motion analysis.
TE-DSE
The studies were performed with the patient in the left lateral
decubitus position. Patients were maintained at a level of sedation to
ensure comfort during the procedure but were alert enough to refer to
the presence of chest pain or any other cardiac symptoms. Dobutamine
was infused from 10 µg/kg/min for 3 min to a peak dose of 40
µg/kg/min for 3 min. Images at baseline and peak infusion were
acquired in the long-axis and midpapillary short-axis planes (Fig 1)
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All patients tolerated the procedure well. Each of the four views were
concurrently acquired, stored, and selected in a quad-screen format
using the standard stress echo imaging software (TomTec Imaging System;
Hamden, CT).
BP and a 12-lead ECG were obtained every minute during the study. Oxygen saturation, heart rate, and rhythm were continuously monitored during the study and in the immediate poststudy phase until baseline parameters were attained.
| Results |
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Significant ST-segment depression was seen in four of nine patients with regional wall motion abnormalities and in three patients without identifiable regional wall motion abnormalities. No patient developed significant supraventricular or ventricular arrhythmia or probe intolerance.
A gradual and consistent incremental rise in heart rate was noted in all patients from a baseline rate of 62 ± 12 beats per minute to a peak heart rate of 133 ± 17 beats per minute. In 10 patients, peak heart rates were recorded at doses of dobutamine that were less than the maximal dose. Only nine patients achieved 85% of the age-predicted maximal heart rate.
The test was successfully completed in all 23 patients with an esophageal intubation time of 29 ± 7 min. Adequate TEE images for analysis were obtained in 20 of 23 patients. In 9 of 20 patients (45%) with adequate images, regional wall motion abnormalities were clearly evident (Table 1 ). Except for significant hypotensive responses (ie, a 20-mm Hg drop in systolic BP at peak dobutamine infusion) in 10 of 23 patients, no significant complication or side effect was noted during the test.
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In summary, adequate TEE images for analysis were obtained in 20 of 23 patients. In 9 of 20 patients (45%) with adequate images, regional wall motion abnormalities were clearly evident (Table 1) . Five of these patients subsequently underwent cardiac catheterization and had significant CAD in the region of myocardial ischemia that was demonstrated by TE-DSE (Table 1) . Over a follow-up period of 18 ± 6 months, three cardiac events (non-Q-wave MI) occurred in the same group, including two patients without confirmatory cardiac catheterization data. Thus, seven of nine patients with positive results of TE-DSE had objective confirmatory evidence of CAD. No cardiac event was observed in the group with normal TE-DSE over the same follow-up period.
Ten of 23 patients developed significant hypotension at peak dobutamine
infusion, but in all cases, quick resolution followed the termination
of the study and did not limit image acquisition. Baseline quantitative
echocardiographic data (mean ± SEM) were calculated for the
hypotensive and nonhypotensive groups of patients. An intergroup
comparison then was performed by one-tailed unpaired t test
(
= 0.05 and
= 0.01, respectively). There were no
statistically significant differences seen between the hypotensive and
nonhypotensive groups with respect to LV volumes, ejection fractions,
and LV outflow velocity at baseline or peak dobutamine infusion.
However, when compared with the nonhypotensive group, the hypotensive
group had increased LV wall thickness and LV mass (p < 0.001).
Results are shown in Table 2
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| Discussion |
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The findings from our investigation, mirror earlier reports of transthoracic DSE for the detection of CAD3 and a previous report of TE-DSE for the evaluation of CAD in nonobese subjects.11 Even though several earlier studies have used TEE with atrial pacing or dipyridamole,12 13 we believe that dobutamine is preferable because of its close replication of the physiologic data acquired during exercise.
The infusion of dobutamine in stress doses leads to marked augmentation in heart rate, myocardial contractility, and wall stress, and to increased oxygen demand and utilization. In the presence of significant coronary artery obstruction, myocardial oxygen supply is outstripped by increasing myocardial oxygen demand and consumption, thus creating a regional supply/demand imbalance, which is manifested in regional wall motion abnormality.3 In the present study, the heart rate increased from 62 ± 12 beats per minute at rest to 133 ± 17 beats per minute with dobutamine infusion, although the majority of the study patients did not achieve 85% of their maximum predicted heart rate. We did not use atropine to augment heart rate in our patients for two reasons. (1) In an earlier study, Sawada et al2 demonstrated that the inability to achieve the target heart rate during DSE does not adversely affect the reliability of the study in identifying CAD. (2) This conclusion is supported by clinical and experimental evidence suggesting that the ischemic burden induced by dobutamine infusion is largely dependent on myocardial contractility with less of a contribution from heart rate augmentation.3 16 These observations are further strengthened by subgroup analysis of our data, which show no statistical difference in maximum attained heart rate between those patients with and without inducible ischemia. Additionally, the combined use of atropine with dobutamine in morbidly obese subjects undergoing TE-DSE raised safety concerns.
Our study shows that adequate images can be obtained during stress in morbidly obese patients with the use of multiplane TEE imaging. The use of multiplane TEE imaging allows a detailed examination of all myocardial segments in multiple planes, thus improving the diagnostic yield and accuracy.
The high quality of images obtained during TEE makes this technique quite attractive for the clinical investigation of known or suspected CAD in morbidly obese patients in whom conventional transthoracic echocardiography is not capable of producing adequate images.
Although TEE is a semi-invasive procedure, it has been shown to be extremely safe in the hands of trained and experienced operators. In our study, no major complication or side effect was observed. Ten patients (43%) in our study population experienced significant hypotension at peak dobutamine infusion. This figure is higher than the incidence of hypotension reported in prior studies of transthoracic DSE or in the TE-DSE report in nonobese subjects,11 but relatively close to the 38% incidence of hypotension reported by Rosamond and Vacek17 in a transthoracic DSE study of 112 patients. The reason for this is unclear. We speculate that the combined effect of transesophageal intubation with resultant vagal response, sedation, mild volume depletion, LV hypertrophy and ß2-receptor activation with resultant vasodilatation at high doses of dobutamine may all contribute to the observed hypotension. Based on quantitative echocardiographic data from our study, morbidly obese patients with hypertrophied ventricles appear to be particularly susceptible to hypotension during TE-DSE. (Table 2) In our study population, the LV outflow tract velocity at baseline or at peak dobutamine infusion did not predict the occurrence of hypotension at peak dobutamine infusion.
| Conclusion and Limitations |
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The present study is limited by the relatively small number of patients studied. However, the findings should encourage further investigation of this group of patients for whom no acceptable modality currently exists for adequate evaluation of known or suspected CAD.
| Footnotes |
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Presented in part at the 63rd International Scientific Assembly of the American College of Chest Physicians, New Orleans, LA, October 2630, 1997, and at the Third World Congress of Echocardiography, Rio de Janeiro, Brazil, April 2325, 1998.
Received for publication January 22, 1999. Accepted for publication August 13, 1999.
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