Download Case Report Takotsubo Cardiomyopathy and Canalith

J Am Acad Audiol 21:73–77 (2010)
Case Report
Takotsubo Cardiomyopathy and Canalith
Repositioning Procedure for Benign Paroxysmal
Positional Vertigo
DOI: 10.3766/jaaa.21.2.2
Selmin Karatayli-Ozgursoy*
Larry B. Lundy*
David A. Zapala†
Keith R. Oken‡
Abstract
Background: Takotsubo cardiomyopathy, also known as left ventricular apical ballooning syndrome,
ampulla cardiomyopathy, or transient left ventricular dysfunction is characterized by chest pain, electrocardiographic changes, transient left ventricular apical aneurysm, and normal coronary arteries. Takotsubo is a round-bottomed, narrow-necked Japanese octopus trap and lends its name to takotsubo
cardiomyopathy because of its resemblance to echocardiographic and ventricular angiographic images
of the left ventricle in this condition. This appearance takes its source from peculiar, transient regional
systolic dysfunction involving the left ventricular apex and mid-ventricle with hyperkinesis of the basal left
ventricular segments. Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo
caused by peripheral vestibular dysfunction. The symptoms of BPPV are attributed to intralabyrinthine
particles, presumed displaced otoconia. Thus, the treatment recommended for BPPV is head repositioning maneuvers.
Purpose: To present the first takotsubo cardiomyopathy case in the English literature related to BPPV
undergoing canalith repositioning procedure.
Conclusion: This report will provide additional information for physicians encountering acute-onset
chest pain and vertigo. It will also expand the spectrum of clinical correlates of the increasingly well recognized but poorly understood syndrome, takotsubo cardiomyopathy.
Key Words: Benign paroxysmal positional vertigo, canalith repositioning procedure, complication,
takotsubo cardiomyopathy, vertigo
Abbreviations: BPPV 5 benign paroxysmal positional vertigo
T
akotsubo cardiomyopathy, also known as left
ventricular apical ballooning syndrome, ampulla
cardiomyopathy, or transient left ventricular
dysfunction, is characterized by peculiar, transient
regional systolic dysfunction involving the left ventricular apex and midventricle with hyperkinesis
of the basal left ventricular segments. Takotsubo
cardiomyopathy was first described in 1991 by Dote
and colleagues (1991) in Japan and named takotsubo-like left ventricular dysfunction because of the
resemblance of the left ventricle to the appearance
of a round-bottomed, narrow-necked Japanese octopus
trap on echocardiogram. Patients with takotsubo cardiomyopathy usually present with sudden-onset chest
pain associated with ST segment elevation in the anterior electrocardiographic leads (V1–V4), relatively
*Department of Otolaryngology, Mayo Clinic Florida; †Department of Audiology, Mayo Clinic Florida; ‡Division of Cardiovascular Diseases, Mayo
Clinic Florida
Larry Lundy, M.D., Department of Otolaryngology, Mayo Clinic Florida, 4500 San Pablo Road, Jacksonville, FL 32224; E-mail: [email protected]
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Journal of the American Academy of Audiology/Volume 21, Number 2, 2010
minor elevation in cardiac enzymes, and transient apical systolic left ventricular dysfunction despite the
absence of obstructive coronary artery disease (Bybee
et al, 2004b). The majority of patients with takotsubo
cardiomyopathy are women older than 60 yr of age.
Physiological or emotional stress usually precedes
the onset of symptoms (Akashi et al, 2003b). Currently, the incidence of takotsubo cardiomyopathy in
the setting of acute coronary syndrome is reported
to be between 1.5 and 2.2% (Akashi et al, 2003a; Bybee
et al, 2004a). The pathogenesis of the syndrome has
still been unclear; however, several mechanisms including multivessel epicardial spasm, catecholamineinduced myocardial damage, microvascular coronary
spasm or dysfunction, and neurogenic myocardial
stunning have been suggested as potential causes
(Bybee et al, 2004b).
Benign paroxysmal positional vertigo (BPPV) is the
most common cause of vertigo caused by peripheral
vestibular dysfunction (Froehling et al, 2000). The
symptoms of BPPV are attributed to intralabyrinthine
particles, presumed displaced otoconia (Schuknecht,
1969). Thus, the treatment recommended for BPPV
is head repositioning maneuvers that were introduced
by Semont (Semont et al, 1988) and modified by Epley
(1992). These maneuvers include rotational head and
body movements in order to relocate the floating particles from the involved semicircular canal into the vestibule of the labyrinth. The repositioning therapies
might be repeated in recurrent or refractory cases.
We present the first case with takotsubo cardiomyopathy in the English literature that was triggered by
and presented during canalith repositioning procedures
applied for the treatment of the patient’s existing
BPPV.
CASE REPORT
A
76-yr-old female patient presented to the Department of Otolaryngology at Mayo Clinic Florida for
evaluation of her dizziness. The dizziness first started
1 yr ago with a sudden onset of hearing loss in the right
ear. Her brain MRI revealed no abnormality, and she
was diagnosed with acute right labyrinthitis with secondary BPPV. She was initially treated with oral steroids and subsequently has undergone a number of
canalith repositioning maneuver sessions with no sign
of improvement of her vertigo. Our otolaryngological
examination did not reveal any abnormality. Her audiogram showed a bilateral sensorineural hearing loss,
moderate and sloping in high frequencies on the left
and severe on the right with very poor discrimination.
Her vestibular work-up included video electronystagmography, computerized dynamic posturography, rotational testing, and vestibular evoked myogenic potentials,
which demonstrated a right posterior canal BPPV and
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no vestibulopathy otherwise. She underwent repeated
canalith repositioning procedures for the treatment
of her BPPV. Although the patient appeared to have
a classic case of right posterior canal BPPV, it seemed
to be particularly resistant to treatment with traditional repositioning procedures. One week later, the
patient underwent another trial of canalith repositioning procedure. When brought upright, she was violently dizzy and reported extreme nausea and chest
pain. As the chest pain persisted, she was taken to
the emergency room after a soft collar was placed
and phenergan (25 mg intramuscular) was given for
her nausea.
In the emergency room, the patient’s electrocardiography revealed ST segment elevation in the anterolateral leads without sign of reciprocal changes. Chest X
ray revealed a normal cardiac silhouette and no evidence of pulmonary edema. Creatinine kinase-total,
creatinine kinase-MB, and troponin-T were elevated.
Her only cardiac risk factor was hyperlipidemia, for
which she had been taking 20 mg of simvastatin per
day. Her family history was negative for cardiac diseases. With the elevated cardiac enzymes and electrocardiography implying acute myocardial infarction,
the patient was immediately referred for cardiac
catheterization. Coronary angiography revealed no significant coronary artery disease. Echocardiography revealed abnormal systolic function with anterior/septal/
apical wall motion abnormalities, with left ventricular
ejection fraction in the range of 36–49% (Fig. 1). The
constellation of an unremarkable coronary angiogram,
antero-apical hypokinesis, elevated cardiac biomarkers,
electrocardiographic changes suggestive of anterior
injury, and a precipitating stressful experience suggested a diagnosis of takotsubo cardiomyopathy secondary to her profound vestibular vertigo. The patient was
admitted to the hospital for monitoring and treated
with 3.125 mg of carvedilol po BID and aspirin; angiotensin converting enzyme inhibitor could not be started
due to hypotension. The next day, her electrocardiography revealed persistent ST–T wave elevation and prolonged QT intervals. She was discharged with 3.125 mg
carvedilol po twice a day, simvastatin, and aspirin.
In postevent fourth-month follow-up, the patient was
asymptomatic, and echocardiogram revealed no abnormality except some mild mitral regurgitation (Fig. 2).
DISCUSSION
T
akotsubo cardiomyopathy was first recognized and
described in the Japanese population (Dote et al,
1991; Kawai et al, 2000; Tsuchihashi et al, 2001; Kurisu
et al, 2002) as being characterized by chest pain, electrocardiographic changes, transient left ventricular
apical aneurysm, and normal coronary arteries. Typical
presentation is usually in postmenopausal women
Takotsubo Cardiomyopathy and BPPV/Karatayli-Ozgursoy et al
Figure 1. Echocardiographic apical four-chamber view at presentation. A. End-diastolic frame reveals normal left ventricular size and
contour. B. End systolic frame reveals apical dyskinesis and typical “tako-tsubo” configuration caused by basal hyperkinesis (arrows) and
apical akinesis/dyskinesis (arrow heads).
experiencing an inciting stressful event. In 2004, Bybee
and colleagues (2004b) proposed Mayo criteria for diagnosis of this syndrome (Table 1). Most takotsubo cardiomyopathy cases present with acute-onset chest pain,
and initial work-up reveals electrocardiographic
changes such as ST segment elevation followed by T
wave inversions and QT prolongation and a mild but
rapid increase in cardiac enzymes (Bybee et al,
2004b). The diagnosis of takotsubo cardiomyopathy is
made by the absence of significant epicardial coronary
artery stenosis despite the presence of transient apical
and left midventricular systolic dysfunction. Case
reports suggest that the vast majority of patients are
women older than 60 yr of age presenting with sudden-onset chest pain after an episode of acute emotional
or physiological stress (Bybee et al, 2004b). Reversibility of the left ventricular dysfunction is a hallmark of
the syndrome (Akashi et al, 2003a).
Our patient was a 76-yr-old woman referred to the
emergency department with acute-onset chest pain
immediately after undergoing a canalith repositioning
procedure for BPPV. Her clinical presentation and subsequent course were entirely consistent with takotsubo
cardiomyopathy. The incidence of takotsubo cardiomyopathy within patients diagnosed with acute myocardial infarction has been reported to be from 1.5 to
2.2% (Akashi et al, 2003a; Bybee et al, 2004a). Although
the exact cause of takotsubo cardiomyopathy remains
unknown, many theories about the underlying mechanisms have been proposed. Among these are abnormal
fatty acid metabolism in the apex, coronary microcirculatory dysfunction, increased catecholamine in response
to stress inducing myocardial dysfunction, and diffuse
epicardial spasm. However, neurogenic myocardial
stunning is the leading candidate mechanism (Bybee
et al, 2004b; Brenner and Powers, 2008). It is not known
Figure 2. Echocardiographic apical four-chamber view at follow-up, four months later. A. End-diastolic frame reveals normal left
ventricular size and contour. B. End systolic frame reveals normal regional and global systolic function with resolution of the apical
dyskinesis.
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Journal of the American Academy of Audiology/Volume 21, Number 2, 2010
Table 1. Proposed Mayo Criteria by Bybee and
Colleagues (2004b) for the Clinical Diagnosis of
Transient Left Ventricular Apical Ballooning Syndrome
1. Transient akinesis or dyskinesis of the left ventricular apical and
midventricular segments with regional wall-motion
abnormalities extending beyond a single epicardial vascular
distribution
2. Absence of obstructive coronary disease or angiographic
evidence of acute plaque rupture
3. New electrocardiographic abnormalities (either ST segment
elevation or T wave inversion)
4. Absence of
• Recent significant head trauma
• Intracranial bleeding
• Pheochromocytoma
• Obstructive epicardial coronary artery disease
• Myocarditis
• Hypertrophic cardiomyopathy
Note: All four criteria must be met.
why the apex of the heart is affected while the basal segments are spared. However, it may partly be explained
by increased adrenergic receptor density, increased
sympathetic innervation, or increased adrenergic sensitivity in the apical myocardium (Mori et al, 1993). The
explanation for the strong female predominance of the
syndrome is also still unclear; however, it is speculated
to be related to reduced postmenopausal estrogen levels
leading to alterations of endothelial function (Celermajer
et al, 1994) and catecholamine-mediated microvascular
reaction (Ueyama et al, 2003).
Japanese physicians identified that the predominant
and significant factor present in all cases of takotsubo
cardiomyopathy is internal (emotional) or external
(physiological) stress. They found that the death or
funeral of a family member, argument with a spouse
or partner, or intense excitation as well as medical disorders such as acute asthma and noncardiac medical
procedures are common presenting events (Park et al,
2005). In our patient, the precipitating factor was the
canalith repositioning procedure applied for her existing
BPPV. It was noted that the patient was anxious that
day because of her persisting symptoms despite repetitive canalith repositioning procedures. She expressed
skepticism that canalith repositioning would really help.
Presumably this emotional stress or the physiologic and/
or psychological stress induced by her adverse response
to the maneuver triggered the onset of takotsubo cardiomyopathy at that particular session: despite the fact
that she had undergone repetitive canalith repositioning
procedures previously without complications.
Appropriate management of takotsubo cardiomyopathy is supportive medical care with angiotensin converting enzyme inhibitor and beta-blockade, aspirin,
and intravenous diuretics as needed. Treatment should
be continued until left ventricular function returns to
normal on echocardiogram (Bybee et al, 2004b; Sealove
76
et al, 2008). Anticoagulation is generally deferred unless
apical thrombi are detected on imaging studies or embolic
events are suspected.
The short-term and long-term prognosis of patients
with takotsubo cardiomyopathy is quite favorable (Sealove
et al, 2008). However, reported in-hospital mortality
rates range from 0 to 8% (Bybee et al, 2004b). The most
frequently reported complication is left-sided heart failure with or without pulmonary edema (Bybee et al,
2004b). Infrequently reported complications include
cardiogenic shock, ventricular arrhythmias, left ventricular thrombus, mitral valve dysfunction, pulmonary
embolism, and left ventricular rupture (Tsuchihashi
et al, 2001; Bybee et al, 2004b). Our patient did not have
any immediate or late cardiac complications; at postevent fourth-month follow-up, the patient was asymptomatic, and echocardiogram revealed no abnormality
except some mild mitral regurgitation.
The misdiagnosis of takotsubo cardiomyopathy as an
acute myocardial infarction may result in unnecessary
administration of fibrinolytic medications, with their
attendant risk of bleeding complications. It is important
for emergency physicians as well as cardiologists to
recognize a suggestive clinical history of takotsubo
cardiomyopathy, especially in elderly female patients,
so that these patients may be referred for emergent
coronary angiography, which offers optimal triage
and management. However, if an emergency coronary
angiogram cannot be obtained, patients should be treated with standard acute myocardial infarction therapy.
To our knowledge this is the first takotsubo cardiomyopathy case in the English literature related to
BPPV undergoing canalith repositioning procedure. We
believe that this report will provide additional information for physicians encountering acute-onset chest pain
and vertigo. It will also expand the spectrum of clinical
correlates of the increasingly well-recognized but poorly
understood syndrome, takotsubo cardiomyopathy.
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