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Transient Left Bundle Branch Block
Case Report
Acta Cardiol Sin 2010;26:193-7
Transient Left Bundle Branch Block:
An Unusual Electrocardiogram in
Takotsubo Cardiomyopathy
Cheng-Kang Chen and Chen-Tung Hsu
Transient mid-ventricular ballooning syndrome is a variant form of Takotsubo cardiomyopathy (TTC). The
precipitating factors and clinical course are similar, and the clinical manifestations mimic those of acute coronary
syndrome, which are characterized by transient left ventricular dysfunction without significant coronary artery
disease. Takotsubo cardiomyopathy with transient left bundle branch block (LBBB) is rare. Herein, we describe the
case of a 64-year-old woman who had a transient mid-ventricular apical ballooning syndrome. Electrocardiography
(ECG) revealed a transient LBBB.
Key Words:
Mid-ventricular ballooning · Takotsubo · Transient left bundle branch block
INTRODUCTION
cal presentation mimics acute myocardial infarction but
without evidence of coronary artery stenosis on angiography, and the left ventricular (LV) dysfunction can
completely regress.
The main electrocardiographic finding at presentation is ST-segment elevation followed by T-wave inversion. In a minority of cases, left bundle branch block
(LBBB) may be the ECG pattern of TTC presentation.8
We herein describe such a case with transient mid-ventricular ballooning syndrome and transient LBBB at
presentation.
Takotsubo cardiomyopathy (TTC), also known as
transient left ventricular apical ballooning syndrome,
was first described in the Japanese literature in 1991 by
Dote et al.1 TTC accounts for 0.7 to 2.5% of admissions
for suspected acute coronary syndrome.2 Transient midventricular ballooning syndrome is a variant form of
TTC. The precipitating factors and clinical course of the
nonapical type are mostly similar to those of the apical
type.3,4 However, TTC has been rarely reported in Taiwan.4-7
The syndrome is characterized by the abrupt onset of
angina-like chest pain, mild creatine kinase and troponin
I elevations, ischemic electrocardiogram (ECG) changes
and transient wall motion abnormalities in the absence of
obstructive epicardial coronary artery disease. The clini-
CASE REPORT
A 64-year-old woman with a history of type 2 diabetes mellitus was brought to our emergency room with
severe dyspnea for 2 hours. She had developed chest
tightness and dyspnea for 5 days after receiving news of
her son’s death. Her blood pressure was 148/87 mmHg,
pulse 98 beats per minute, respirations 22 per minute,
and temperature 36 °C. The heart rhythm was regular,
and other physical examinations were unremarkable. Her
chest roentgenogram showed mild cardiomegaly with
pulmonary edema. The ECG showed sinus rhythm with
Received: December 20, 2009 Accepted: March 25, 2010
Division of Cardiology, Department of Internal Medicine, Chia-Yi
Christian Hospital, Chia-Yi, Taiwan.
Address correspondence and reprint requests to: Dr. Chen-Tung Hsu,
Division of Cardiology, Department of Medicine, Chia-Yi Christian
Hospital, No. 539 Jung-Shiau Road, Chia-Yi 600, Taiwan. Tel:
886-5-276-5041 ext. 7354; Fax: 886-5-276-5041 ext. 5023; E-mail:
[email protected]
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Cheng-Kang Chen et al.
distribution; (2) absence of significant coronary stenosis
(more than 50% of the luminal diameter) or angiographic
evidence of acute plaque rupture; (3) new ECG abnormalities (ST-segment elevation and/or T-wave inversion);
and (4) absence of pheochromocytoma or myocarditis.
Due to its clinical characteristics, TTC is frequently
misdiagnosed as acute coronary syndrome (ACS), or
myocarditis. Since the ECG and symptoms cannot reliably distinguish TTC from ACS, identification of TTC requires diligence on the part of the diagnosing physician
and sound clinical judgment. Differentiating from TTC
from ACS is important, because of different treatment
strategies and prognoses. If TTC is suspected, fibrinolytic
therapy should be avoided and emergency coronary
angiography should be performed in any patient presenting with ST-segment elevation. Furthermore, patients
with ACS benefit from secondary preventive pharmacotherapy, whereas in patients with TTC, the LV wall motion abnormalities usually resolve without any specific
treatment. Cardiac magnetic resonance seems to be a useful technique to differentiate TTC (characterized by the
absence of delayed gadolinium hyperenhancement) from
myocardial infarction and myocarditis, in which delayed
hyperenhancement is present. Therefore, cardiac magnetic resonance can add valuable information for all patients with suspected TTC for further differential diagnosis and guidance of medical therapy.10
The underlying pathophysiology, which is often preceded by a recent stress inducing event (physical or
emotional) in many cases, is still not well understood.
However, several mechanisms for reversible cardiomyopathy have been proposed, including multivessel
epicardial spasm, 1 microvascular dysfunction and catecholamine-induced myocardial stunning.2
Several reports have suggested that wall motion abnormalities associated with TTC might not exclusively
be located in apical segments, but may also occur in
midventricular segments of the LV.3,4,11 Kurowski et al.
reported that transient midventricular LV ballooning was
observed in 40% of patients with transient LV dysfunction; no differences in demographic, clinical, angiographic, laboratory parameters, or outcome were found
between these patients and patients with apical ballooning. 3 The presentation, clinical features, and transient
nature of the midventricular LV ballooning cases are
similar to those of transient LV apical ballooning and
left bundle branch block pattern (Figure 1A). The patient’s creatine kinase and creatine kinase, muscle and
brain (CKMB) levels were 132 and 2.8 IU/L respectively, and troponin I 0.318 ng/ml (normal range < 0.5
ng/ml). The white-cell count was 8430 per cubic millimeter, hematocrit 42%, blood sugar 241 mg/dl, and the
prothrombin and partial-thromboplastin times and the
values for nitrogen, creatine, and electrolytes were normal. Intravenous diuretics and supplemental oxygen
were administered, and the patient’s dyspnea improved a
little. A cardiologic consult was obtained, and echocardiography showed hypokinesis over the mid-portion
of the LV and an ejection fraction of 38%. A cardiac
catheterization was done immediately and revealed no
evidence of coronary artery stenosis (Figures 2A, B).
The contrast left ventriculography demonstrated hypokinesis over the mid portion of the anterior wall and normal contractility of the basal and apical portions (Figures 2C, D). No LV outflow pressure gradient was apparent. The patient was diagnosed with stress cardiomyopathy. Follow-up creatine kinase and CKMB levels
were 100 and 3 IU/L respectively, and troponin I was
measured 0.183 ng/ml 12 hrs later. A repeat ECG performed 2 days later (Figure 1B) demonstrated resolution
of the LBBB, and the appearance of T-wave inversion in
I, aVL, and V3-6 leads. The patient remained stable and
was transferred to the general ward on admission day 3.
She was discharged on admission day 4 and remained
well without chest pain or dyspnea. Two weeks later, repeat echocardiography showed complete resolution of
the LV wall motion abnormalities, and the ejection fraction had improved to 65%.
DISCUSSION
One review of relevant studies has suggested that
TTC accounts for 0.7 to 2.5% of patients presenting with
a suspected ACS. Over the last decade, there have been
many articles published on the topic of TTC. A modified
version of the Mayo Clinical Criteria for the clinical diagnosis of transient LV apical ballooning syndrome has
been made. 9 This includes (1) transient hypokinesis,
akinesis, or dyskinesis of the LV and mid-segments with
or without apical involvement; the regional wall motion
abnormalities extend beyond a single epicardial vascular
Acta Cardiol Sin 2010;26:193-7
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Transient Left Bundle Branch Block
A
B
Figure 1. (A) A 12-lead ECG showed left bundle branch block. (B) ECG demonstrating resolution of left bundle branch block with T-wave
inversion in leads I, aVL, and V3-6 leads.
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Cheng-Kang Chen et al.
A
B
C
D
Figure 2. Coronary angiography (A: left coronary artery; B: right coronary artery), No coronary artery stenosis was seen. A left ventriculogram
showed hypokinesis of the mid-portion of the left ventricle and normal contraction of the basal and apical portions (C: end-diastole and D:
end-systole).
suggest a shared pathophysiologic etiology.11
The ECG findings associated with TTC are numerous, but the most common abnormality is ST-segment
elevation. Typically, the elevation is present in the
precordial leads, but it may be seen in the inferior or
lateral leads, nonspecific T-wave abnormality, or new
bundle branch block, and in some cases, a normal ECG
may be the finding at presentation.8 A recent study by Dib
et al. showed that new onset of LBBB was found in 1 of
105 patients with TTC.8 They also concluded that the
ECG features at presentation do not correlate with the
magnitude of ventricular dysfunction or long-term outcomes. Thus, the ECG in patients with TTC does not provide significant prognostic information. The presence of
new onset of LBBB is associated with adverse outcome in
patients with acute myocardial infarction. However, when
adjusted for age, baseline characteristics, and concomitant
Acta Cardiol Sin 2010;26:193-7
diseases, LBBB does not appear to be an independent
predictor of poor outcome in patients with TTC.12
Transient LBBB has not been reported in mid-ventricular ballooning syndrome. Our patient had normal coronary arteries, despite the appearance of LBBB and concomitant chest pain at heart rate of 96 bpm and disappearance of LBBB at heart rate of 78 bpm. This finding indicated that this was not a heart rate-dependent LBBB. A
likely explanation for the appearance of LBBB in this
case is that the deterioration of the coronary flow reserve
resulted in myocardial ischemia. Several studies have
suggested that microvascular dysfunction may be a potential cause for stress cardiomyopathy. Reduced coronary flow reserve in Doppler flow-wire measurements,
and higher thrombolysis in myocardial infarction (TIMI)
frame counts in all three major epicardial coronary vessels after onset of TTC, indicate the presence of impaired
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Transient Left Bundle Branch Block
microvascular flow.2 Several nuclear studies have been
performed recently, and the investigators interpreted the
nuclear imaging findings of reduced myocardial perfusion
in the absence of obstructive coronary lesions as direct
evidence for impaired coronary microcirculation as a
causative mechanism of the syndrome.2,3
4.
5.
6.
CONCLUSION
7.
Although new-onset LBBB is usually associated
with myocardial ischemia, this case suggests that TTC
should also be considered in the differential diagnosis of
patients with acute coronary syndrome and transient
LBBB.
8.
9.
REFERENCES
10.
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2. Pilgrim TM, Wyss TR. Takotsubo cardiomyopathy or transient
left ventricular apical ballooning syndrome: a systemic review.
Int J Cardiol 2008;283-92.
3. Kurowski V, Kaiser A, von Hof K, et al. Apical and midventricular transient left ventricular dysfunction syndrome (tako-
11.
12.
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Chang NC, Kawai S. Takotsubo (ampulla) cardiomyopathy is not
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Hsu CT, Chen CY, Chang RY, et al. Prevalence and clinical features of Takotsubo cardiomyopathy in Taiwanese patients presenting with acute coronary syndrome. Acta Cardiol Sin 2010;
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Prasad A, Lerman A, Rihal CS, et al. Apical ballooning syndrome
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Eitel I, Behrendt F, Schindler K, et al. Differential diagnosis of
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magnetic resonance imaging. Eur Heart J 2008;21:2651-9.
Hurst RT, Askew JW, Reuss CS, et al. Transient midventricular
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