Full Text - Research in Cardiovascular Medicine

Res Cardiovasc Med. 2015 May; 4(2): e25223.
DOI: 10.5812/cardiovascmed.4(2)2015.25223
Case Report
Published online 2015 May 23.
Mid-Ventricular Variant of Dobutamine-Induced Stress Cardiomyopathy
1,*
1
Satish Chandraprakasam ; Swapna Kanuri ; Claire Hunter
1
1Division of Cardiology, Creighton University School of Medicine, Omaha, Nebraska, USA
*Corresponding author: Satish Chandraprakasam, Division of Cardiology, Creighton University School of Medicine, Omaha, Nebraska, USA. Tel: +1-2245326843, Fax: +1-4022805967,
E-mail: sat_cp@hotmail.com
Received: November 9, 2014; Revised: January 3, 2015; Accepted: January 15, 2015
Introduction: Dobutamine stress testing is a commonly used modality in detecting and estimating the prognosis in coronary artery
disease (CAD). Although it is well tolerated by most patients, adverse events have been reported. Rarely, transient wall motion abnormalities
can occur in the absence of obstructive CAD to suggest stress cardiomyopathy.
Case Presentation: We report a 48-year-old female with intermittent chest pain. Her physical exam, cardiac enzymes and transthoracic
echocardiogram were unremarkable. She underwent dobutamine stress echocardiogram to rule out obstructive CAD. After 40 micrograms
(mcg)/kg/minute and 0.5 mg atropine, she complained of intense chest pain and became hypertensive. Stress echocardiogram
demonstrated mid-anterior and mid-septal hypokinesis. Emergent coronary angiogram demonstrated normal coronaries. Left
ventricular angiogram in the right anterior oblique projection revealed mid-ventricular ballooning during systole with apical and basal
hypercontractility. Patient demonstrated excellent recovery with expectant management.
Conclusions: The mechanism of mid-variant of Dobutamine-induced stress cardiomyopathy remains unclear. We think that multiple
mechanisms are involved and this risk should be considered in patients with comorbid psychiatric conditions and with use of centrally
acting stimulants.
Keywords: Cardiomyopathy; Takotsubo Cardiomyopathy; Echocardiography, Stress
1. Introduction
Dobutamine in combination with echocardiogram
or perfusion imaging is considered a reliable modality
of pharmacological stress testing in patients unable to
exercise, due to its safety profile, good sensitivity and
specificity (1). Common adverse effects include nausea,
palpitations, headache and anxiety. Angina can occur in
about 1 - 2% of patients. Most arrhythmias are mild and
attributable to premature atrial complex, premature
ventricular complex, and paroxysmal supraventricular
tachyarrhythmias. Rarely, hemodynamically significant
ventricular arrhythmias can occur (2). Although hypertension is expected with high doses of dobutamine infusion, especially in patients with left ventricular hypertrophy, hypotension may occur. Hypotension that occurs
due to stimulation of beta-2 receptor stimulation in peripheral vessels does not carry the same adverse prognostic significance like exercise-induced hypotension. A variety of transient wall motion abnormalities, commonly
involving the apex have been described. To the best of our
knowledge, this is the first report of an isolated mid-ventricular variant of stress cardiomyopathy occurring in a
female patient during dobutamine infusion.
2. Case Presentation
A 48-year-old Caucasian female presented for evaluation
of intermittent chest pain of 6 months duration. Past
history included asthma, schizoaffective disorder, bipolar disorder, nephrolithiasis, and diabetes insipidus. Her
medications included aspirin, lithium carbonate, methylphenidate, lurasidone, temazepam, alprazolam, desmopressin, fluticasone-salmeterol inhaler and albuterol
inhaler. She had tobacco smoking for many years. She
denied alcohol or recreational drug abuse. Her vital signs
and cardiopulmonary exam upon admission were within
normal limits. She was assessed for acute coronary syndrome with serial cardiac biomarkers and serial electrocardiograms (ECG) that were unremarkable. 2D echocardiogram demonstrated normal left ventricular ejection
fraction (LVEF) without regional wall motion abnormalities at rest. Dobutamine stress echocardiogram was performed to rule out obstructive coronary artery disease.
Her baseline blood pressure (BP) was 104/64 mmHg and
heart rate (HR) was 60 beats per minute (bpm). Peak dobutamine dose was 40 micrograms (mcg)/kg/minute.
In addition, 0.5 mg atropine was administered during
the test. After 16 minutes of dobutamine infusion, she
complained of intense chest pain. Her BP was 214/100
mmHg and HR was 107 bpm. Stress ECG demonstrated
sinus rhythm with transient left anterior fascicular block
and run of ventricular bigeminy, which resolved after
sublingual nitroglycerin and discontinuation of dobutamine infusion. Stress echocardiogram demonstrated
Copyright © 2015, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences. This is an open-access article distributed under the terms
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Chandraprakasam S et al.
Figure 1. Apical 4-Chamber View Showing the Mid-Septal Hypokinesis During Peak Stress
Figure 2. Apical 2-Chamber View Showing Mid-Anterior Hypokinesis During Peak Stress
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Res Cardiovasc Med. 2015;4(2):e25223
Chandraprakasam S et al.
Figure 3. A, Left Ventriculogram Showing Appearance of Left Ventricle During Diastole; B, Left Ventriculogram Showing Mid-Ventricular Ballooning With
Apical and Basal Segment Hypercontractility During Systole
mid-anterior and mid-septal hypokinesis with reduction
in LVEF (Figures 1 and 2, Videos 1 and 2). Peak Troponin I
(Tn I) level was 0.41 ng/mL. Emergent coronary angiogram demonstrated normal coronaries. LV angiogram in
the right anterior oblique projection revealed mid-ventricular ballooning during systole with apical and basal
hypercontractility (Figure 3A and 3 B, Video 3). Patient was
treated with metoprolol tartrate, lisinopril and methylphenidate was discontinued. Tn I level trended down
and her chest pain resolved. Follow-up echocardiogram
24 hours later demonstrated complete recovery of LV systolic function. She was discharged with beta-blockers.
3. Discussion
Dobutamine-induced stress cardiomyopathy (DiSC)
predominantly affects postmenopausal females and has
a predilection for apical region similar to the classical Takotsubo cardiomyopathy. Basal variant of DiSC has also
been reported (3). Here in, we reported a rare occurrence
of isolated mid-ventricular ballooning with apical and
basal hyperkinesis during dobutamine stress testing.
Mechanism of dobutamine induced wall motion abnormality in the absence of obstructive epicardial disease
is unclear. Several theories have been postulated including multivessel coronary vasospasm, severe systemic
hypertension, systolic anterior motion leading to mitral
regurgitation and dynamic intracavity pressure gradient
secondary to left ventricular outflow tract obstruction or
mid cavity obstruction (4, 5). In a systematic review, 90%
of study population had hypertension, hyperlipidemia
and smoking as predisposing risk factors (6). Other comorbidities known to predispose include subarachnoid
hemorrhage, following right ventricle outflow tract radiofrequency ablation and orthotopic heart transplantaRes Cardiovasc Med. 2015;4(2):e25223
tion (7-9). In our case, we believe that the following factors
contributed to the development of DiSC in our patient.
First, patient’s age, female gender and psychiatric conditions certainly predisposed her for stress cardiomyopathy (10). Second, smoking is known to increase the risk
of coronary vasospasms and microvascular dysfunction.
Third, centrally acting stimulants and beta-receptor agonists such as inhalers could lead to excessive sympathetic
activity, thereby increasing her susceptibility to stress
cardiomyopathy (11). Finally, parasympathetic withdrawal with atropine administration leads to imbalance in
sympathetic-parasympathetic activity (7). Complete recovery is the rule, as seen in this case. We suggest bearing in mind DiSC while considering options for ischemia
evaluation in patients with aforementioned risks factors,
particularly comorbid psychiatric conditions and use of
centrally acting stimulants.
Acknowledgements
We would like to thank Dr. Priya Dharishini Vejayan for
preparation and formatting of the manuscript.
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Res Cardiovasc Med. 2015;4(2):e25223