European Journal of Echocardiography 2004 5(6):469-471; doi:10.1016/j.euje.2004.04.006
© 2004 by European Society of Cardiology
Copyright © 2004, The European Society of Cardiology
Acute myocardial infarction after a negative dobutamine stress echocardiogram
Abdou Elhendy*,
Wilson Ginete,
Scott Shurmur and
Thomas R. Porter
Department of Internal Medicine, Section of Cardiology, University of Nebraska Medical Center, Omaha, NE 68198-2265, United States
Received 23 February 2004; received in revised form 12 April 2004; accepted after revision 20 April 2004.
* Corresponding author. Tel.: +1-402-559-9265; fax: +1-402-559-8355. aelhendy{at}unmc.edu
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Abstract
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Acute myocardial infarction is a rare complication of dobutamine
stress echocardiography (DSE). We described angiographic findings
of a patient who developed acute inferior ST segment elevation
myocardial infarction 2 h after a normal dobutamine stress echocardiogram.
The patient failed thrombolysis and underwent coronary angiography,
which showed 60% stenosis of proximal right coronary artery
with a complex ulcerated lesion and intracoronary thrombus.
These findings suggest that myocardial infarction following
DSE does not necessarily occur in patients with severe obstructive
coronary artery disease. High shear stress may result in destabilization
of a complex plaque with subsequent thrombotic occlusion, despite
the absence of a flow-limiting lesion at the time of DSE.
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Case report
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A 52-year-old man with a history of hypertension, fibromyalgia
and rheumatoid arthritis was referred for DSE for evaluation
of atypical chest pain. The patient was receiving a diuretic
but no statins, aspirin or any cardiac medication. The patient
had a normal baseline ECG and normal left ventricular systolic
function on baseline echocardiogram. Dobutamine was infused
up to 50 µg/kg/min. The patient developed paradoxical
sinus node deceleration at a dose 30 µg/kg/min of dobutamine
and required 2 mg of atropine intravenously to achieve the target
heart rate. The patient had a hypercontractile response to dobutamine
in all myocardial segments. His ejection fraction increased
from 60% to 75%. There were no wall motion abnormalities, symptoms
or ECG changes at peak stress or at recovery. The patient drove
back home but developed acute severe chest pain 2 h after completion
of DSE. At the emergency department, his ECG showed ST segment
elevation in the inferior leads and he received intravenous
thrombolysis immediately. Subsequently, he developed ventricular
fibrillation and received electrical defibrillation. Chest pain
continued and ST segment elevation did not resolve. Therefore,
coronary angiography was performed and revealed a complex proximal
right coronary artery lesion with 60% luminal narrowing (
Fig. 1A).
The lesion was ulcerated with an overlying thrombus. Left ventriculography
revealed inferior wall hypokinesis. The patient underwent angioplasty
with successful stent placement in the right coronary artery
and no residual stenosis (
Fig. 1B). His course was uncomplicated
thereafter and was discharged in a stable condition.

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Figure 1 Right coronary artery injection: (A) prior to intervention demonstrating a 60% proximal stenosis of the right coronary artery. (B) After stent placement showing no residual stenosis with normal antegrade flow.
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Discussion
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Acute myocardial infarction is a rare complication of dobutamine
stress echocardiography (DSE).
1,2 Little is known about coronary
angiographic findings in patients with this complication. The
incidence of acute myocardial infarction during or shortly after
DSE is 1 per 2000 according to pooled safety data.
1 The maximal
reported time onset after the study was 20 min. In our case,
the onset was 2 h after the study, which is probably related
to the time required for an occlusive thrombus to develop over
a complicated plaque. The angiographic finding of non-obstructive
complicated plaque with an overlying thrombus suggests that
the shear stress during high dose DSE may have resulted in destabilization
of the plaque with subsequent triggering of the thrombotic cascade.
Nevertheless, the occurrence of plaque rupture in this patient
may have been coincidental after the DSE. Interestingly, the
patient had no signs or symptoms of ischemia during or shortly
after DSE. Previous studies have shown that the sensitivity
of DSE for diagnosis of single vessel right coronary artery
stenosis greater than 50% is as low as 40%.
3 Although DSE was
shown to predict cardiac death, the ability to predict myocardial
infarction is suboptimal. Furthermore, most of the myocardial
infarctions during follow up do not occur in the vascular distribution
that demonstrated ischemia during stress echocardiography.
4 This was explained by the fact that myocardial infarction often
occur due to acute change in an unstable intermediate lesion
that may have not been severe enough to cause flow limitation
at the time of stress test. This case report demonstrates a
clear distinction between anatomical and functional coronary
artery disease since the anatomic stenosis of this patient was
not functionally significant. The occurrence of myocardial infarction
immediately after a normal DSE represents a scenario similar
to this reported rarely after exercise or other forms of stress
testing.
Another possible explanation of our finding is that the DSE test was false negative. Although the inferior wall was well visualized in this study with good imaging quality, it is possible that the concomitant use of a perfusion technique may have detected perfusion defects5 since these occur earlier in the ischemic cascade and may be inducible with less severe stenosis.
Paradoxical sinus node deceleration at high dose dobutamine has been attributed to increased vagal tone particularly in young adults, or activation of Bezold Jarisch reflex due to inferior wall hypercontactility or ischemia.6,7 The proximal location of right coronary artery disease in this case suggests that ischemia in the sinoatrial nodal artery distribution (but not necessarily in the inferior wall) may have been the underlying mechanism of sinus node deceleration. Therefore, high-risk patients who develop sinus node deceleration with dobutamine may require closer follow up even without demonstrable ischemia in the inferior wall.
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References
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- Mathias W. Jr., Arruda A., Santos F.C., Arruda A.L., Mattos E., Osorio A., et al. Safety of dobutamine–atropine stress echocardiography: a prospective experience of 4,033 consecutive studies. J Am Soc Echocardiogr (1999) 12:785–791.[CrossRef][Web of Science][Medline]
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- Elhendy A., Geleijnse M.L., Roelandt J.R., van Domburg R.T., TenCate F.J., Cornel J.H., et al. Dobutamine-induced hypoperfusion without transient wall motion abnormalities: less severe ischemia or less severe stress? J Am Coll Cardiol (1996) 27:323–329.[Abstract]
- Attenhofer C.H., Pellikka P.A., McCully R.B., Roger V.L., Seward J.B. Paradoxical sinus deceleration during dobutamine stress echocardiography: description and angiographic correlation. J Am Coll Cardiol (1997) 29:994–999.[Abstract]
- Elhendy A., van Domburg R.T., Bax J.J., Nierop P.R., Geleijnse M.L., Ibrahim M.M., et al. The functional significance of chronotropic incompetence during dobutamine stress test. Heart (1999) 81:398–403.[Abstract/Free Full Text]

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