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International Journal of Arrhythmia 2013;14(2): 24-28.
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Introduction
Takotsubo cardiomyopathy may occur after
diagnostic or therapeutic cardiovascular procedures,
as well as following emotional and medical stress,
in susceptible patients.1-7 Patients exhibiting this
cardiomyopathy are at risk for the development of
torsades de pointes.1,8 Takotsubo cardiomyopathy
can occur in association with a complete
atrioventricular block,9,10 but its presence in a
patient with newly diagnosed sinus node dysfunction has not previously been reported. We
describe the case of a 69-year-old hypertensive
woman with sick sinus syndrome and takotsubo
cardiomyopathy in whom the electrocardiographic
and wall-motion abnormalities were reversed after
the implantation of a pacemaker.
Case
A 69-year-old woman was admitted following
progressive dyspnea over the previous month. She
reported the absence of angina, prolonged chest
pain, dizziness, and syncope. Her medical history
included chronic hepatitis C and hypertension,
which was under control with amlodipine and
ramipril; she was not taking any sympathomimetic
drugs. She had not experienced any emotional or physical stress that was likely to be related to stress
cardiomyopathy. The results of her physical
examination were unremarkable, with the
exception of bradycardia; focal neurologic
symptoms and signs were absent. A 12-lead
electrocardiogram revealed sinus arrest with a
junctional escape rhythm, a retrograde P wave, and
a repolarization abnormality (Figure 1A); her QT
and QTc intervals were 1,120 ms and 844 ms,
respectively. The patient had a creatine kinase MB
(myocardial band) isoenzyme level of 0.6 ng/mL
(upper limit of normal, 3.1 ng/mL) and a troponin I
level of 0.16 ng/mL (upper limit of normal, 0.06
ng/mL), but the levels of creatinine, sodium,
potassium, calcium, magnesium, bilirubin, and
transaminase were within normal limits. An
echocardiogram indicated akinesia of the mid- to
apical left ventricle (Figure 2A), and coronary
angiography was normal. Left ventriculography
indicated akinesia of the apex (Figure 3A and B);
Holter monitoring revealed a persistent junctional
escape rhythm and multiple episodes of sinus pause
of ＞3.0 seconds during the day.
After excluding reversible causes of bradycardia,
the patient underwent implantation of a dual
chamber pacemaker. Thereafter, her QT interval
decreased to 560 ms (Figure 1B) and focal akinesia
of the apex was observed after atrial pacing (Figure
2C and 2D). The wall-motion abnormalities in the
apex, however, normalized 2 months after the
procedure (Figure 2E and 2F). Her electrocardiogram
showed an atrial-paced rhythm of 60
bpm and a QT interval of 440 ms at 5 months after
the procedure (Figure 1C). The patient was
diagnosed with Child-Pugh class A liver cirrhosis
caused by hepatitis C at 3 years after the event.
Imaging follow-up with computed tomography and
ultrasonography did not reveal the presence of an
adrenal mass. Over a 5-year follow-up period, the
patient did not exhibit any further cardiac events.
Discussion
Takotsubo cardiomyopathy is characterized by
wall-motion abnormalities involving the apex or
mid-ventricular wall; normal coronary arteries;
electrocardiographic changes mimicking acute
myocardial infarction; and the elevation of cardiac
markers following emotional, physical, or medical
stress.1 In addition to emotional stress, medical or
surgical procedures can induce takotsubo
cardiomyopathy; catheter ablation of cardiac
arrhythmias is one of the precipitating causes of
takotsubo cardiomyopathy.2,3 Few cases of
takotsubo cardiomyopathy after the implantation
or malfunction of a pacemaker have been
reported.4-7 However, to our knowledge, this is the
first report of the occurrence of takotsubo
cardiomyopathy in a patient with newly diagnosed
sick sinus syndrome in whom wall-motion and
electrocardiographic abnormalities resolved after
atrial pacing.
Similar to a patient in a previous report, the
current patient was an elderly woman without a
history of cardiac disease.1 Given that emotional
and other medical stresses and the intake of
sympathomimetic drugs were ruled out during her
detailed history and routine examination, sick sinus
syndrome may be regarded as a trigger of
takotsubo cardiomyopathy in this patient.
Stimulation of the sympathetic nervous system is
known to play a critical role in the pathogenesis of
takotsubo cardiomyopathy.11 Therefore, reflex
stimulation of the sympathetic nervous system to
overcome bradycardia may have accounted for the
development of takotsubo cardiomyopathy in this
patient. Prolongation of a corrected QT interval is a
risk factor for the development of torsades de
pointes in patients with takotsubo cardiomyopathy.8 Considering the role of sympathetic
stimulation in the pathogenesis of takotsubo
cardiomyopathy and that detrimental effects
may occur in the presence of bradycardia upon
repolarization heterogeneity, urgent cardiac
pacing, rather than administration of
sympathomimetic drugs, may help reduce the risk
of developing torsades de pointes.12 However, no
apparent stressors were found in 11% of patients with takotsubo cardiomyopathy13,14; therefore, the
sinus node dysfunction and stress cardiomyopathy
observed in the present patient may only be a
coincidental phenomena.
Transient electrocardiographic and wall-motion
abnormalities can result from diverse causes.
Although the ergonovine provocation test was
not performed, the absence of chest pain,
gradual improvement of the electrocardiographic
abnormality, improvement of the wall-motion abnormality with pacing therapy, and the absence
of angina attacks during treatment with a beta
blocker suggested that vasospastic angina was unlikely to be the cause of the electrocardiographic
and echocardiographic abnormalities in this
patient. Spontaneous recanalization of an infarctrelated
artery may have caused the wall-motion
and electrocardiographic abnormalities. However,
the absence of a typical rise and fall in the patient’s
cardiac markers was not consistent with an acute
myocardial infarction. Acute myocarditis can be
excluded in the absence of antecedent viral illness,
the absence of elevated cardiac enzymes, and the
presence of a typical wall-motion abnormality.
Hidden pheochromocytoma is another wellknown
cause of takotsubo cardiomyopathy in the
absence of an apparent stressful condition.15 In
this case, even though a hormonal assay for
pheochromocytoma was not performed, the absence
of an intra-abdominal mass during an imaging
examination of the abdomen for cirrhosis
evaluation and the rapid resolution of clinical
manifestations following pacing treatment likely
excludes hidden pheochromocytoma as the cause of
takotsubo cardiomyopathy.
In conclusion, we report a case of takotsubo
cardiomyopathy in a patient with sick sinus
syndrome. After implantation of a permanent
pacemaker, the patient did not experience any
subsequent cardiac events during a 5-year followup
period.
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