case report

1. The Indian Practitioner q Vol.67 No.11. November 2014
Case Report
707
Introduction
T
he word ‘Takotsubo’ originates from the Japanese
term for “octopus trap” because the shape of the
ballooned cardiac apex in systole in takotsubo
cardiomyopathy appears so. Takotsubo cardiomyopathy
is also known as stress cardiomyopathy, apical balloon-
ing syndrome or broken heart syndrome.1
It is now in-
creasingly being recognised as a cause of acute transient
reversible left ventricular dysfunction. High index of
suspicion is important in order to avoid incorrect treat-
ment and because of the potential reversibility of this
condition. A case of a middle aged survivor of takotsubo
cardiomyopathy is reported here.
Case Report
A 54 year old known hypertensive and diabetic,
anatomy professor was brought with history of giddi-
ness followed by collapse during a lecture followed by
unresponsiveness 15 minutes back. She had one episode
of generalised tonic clonic seizure during transport and
another in the ICU, both lasting for 1 to 2 minutes. No
history of chest pain, breathlessness, palpitations, head-
ache, excessive sweating, missed meal, recent medication
or similar episode previously. On examination, pulse and
blood pressure were not recordable, respiratory rate was
26/min, oxygen saturation post intubation was 74% and
falling. External jugular veins did not appear engorged.
Systemic examination revealed muffled heart sounds
with bilateral diffuse coarse inspiratory crepts. Rest of
the examination was unremarkable.
The Other Great Masquerader:Takotsubo Cardiomyopathy
Bhosle D,* Adukia S,** Patil R,*** Chavan C,****
*MD (Medicine), Professor; **MBBS, Post-graduate student; ***MBBS, Post-graduate student, Department of Medicine; ****MD, DNB (Medicine), DNB (Cardiology).
Bharati HospitalAnd Research Center, Katraj, Dhankawadi, Pune-Satara Road, Pune-411043, Maharashtra.
Corresponding author:
Dr. Deepak Bhosle,AmrapaliApartment, Flat No 4, S. No 126, Plot No. 13, Katraj, Pune- 411046. Email- dgbhosle@gmail.com Mobile: +91 9960907461
Abstract
Takotsubo cardiomyopathy is a rare entity that mimics acute myocardial infarction or congestive heart fail-
ure. It is characterised by acute, transient, reversible left ventricular dysfunction that can mimic an acute
coronary event at presentation. Coronary arteries are however, often normal on cardiac catheterisation.
Patients are usually postmenopausal women who experience acute physical or emotional distress. For
years this syndrome has been mistaken for acute myocardial infarction owing to a typical presentation
with chest pain, electrocardiographic abnormalities, elevated cardiac enzymes and focal left ventricular
wall motion abnormalities. Clinical diagnosis is difficult and demands a high index of suspicion. Recently
proposed Mayo criteria might help in diagnosis. Delay in diagnosis should not result in delay in treatment.
We report a case involving a post menopausal female who had an attack of takotsubo cardiomyopathy with
a favourable outcome.
Keywords: Reversible cardiomyopathy, Mayo criteria for takotsubo cardiomyopathy, Catecholamine in-
duced ventricular dysfunction.

2. The Indian Practitioner q Vol.67 No.11. November 2014
Case Report
708
She was put on ventilatory support and inotropes.
Intravenous Frusemide was given alongwith crushed
tablets of Aspirin, Clopidogrel and Atorvastatin via
Ryle’s tube. Subcutaneous enoxaparin was given after
ruling out intracerebral bleed on CT brain. ECG showed
low voltage with sinus tachycardia and ST flattening in
V3 to V6. Serial ECG’s showed T wave inversions from
V3 to V6. Qualitative Troponin-T spot test was negative
with normal cardiac enzymes (CPK 86 U/L, CPK-MB 20
U/L), total leucocyte count 20,100 cells/cu.mm (neutro-
phils 30%). All other biochemical investigations were
normal.
X-ray chest showed bilateral diffuse haziness in bi-
lateral mid and lower zones with cardiomegaly (Cardio-
thoracic ratio > 60%). 2D echocardiography showed
mildly dilated left ventricle with akinetic ballooned apex
(Fig.1) and moderate systolic dysfunction with a left ven-
tricular ejection fraction (LVEF) of 35%. Cardiac cathe-
terisation showed normal coronary arteries and normal
renal arteries bilaterally. Ultrasound examination of ab-
domen and pelvis did not show any mass over the kid-
neys. Thyroid function tests, MRI brain and EEG were
normal.
Cardiac MRI with contrast on day 5 showed ballooned
akinetic cardiac apex (Fig.2) with fair LV systolic func-
tion (LVEF = 45%). No myocardial scarring, significant
valvular regurgitation, pericardial effusion or chamber
enlargement was noted. Repeat 2D Echo revealed similar
findings as cardiac MRI. X-ray chest showed reduction
of cardiomegaly (Cardio-thoracic ratio > 50%). Thereafter
patient remained relatively stable and was discharged by
day 10. Cardiac MRI with contrast was repeated on fol-
low up after 1 week and showed normal LV size and sys-
tolic function (LVEF = 63%) with no myocardial scarring.
She was asymptomatic on follow up and reported an un-
eventful stay at home post-discharge. Thus, a diagnosis
of takotsubo cardiomyopathy was made with evidence
of reversible left ventricular dysfunction, no residual re-
gional wall abnormalities, normal coronary arteries and
in absence of other obvious causative pathology.
Discussion
Various insults whether emotional or physical, like
status epilepticus,2
hypertensive crisis, scorpion sting
Table 1:- Proposed Mayo criteria for the clinical diag-
nosis of the transient left ventricular apical balloon-
ing syndrome1
1. Transient akinesis or dyskinesis of left ventricular
apical and mid-ventricular segments with regional
wall-motion abnormalities extending beyond a sin-
gle epicardial vascular distribution
2. Absence of obstructive coronary disease or angio-
graphic 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
● Phaeochromocytoma
● Obstructive epicardial coronary artery disease
● Myocarditis
● Hypertrophic cardiomyopathy
Fig.1: Octopus trap or “takotsubo” shaped left ventricle
(arrow) on echocardiography.
Figure 2: Ballooned apex (arrow) seen on Cardiac MRI with
contrast

3. The Indian Practitioner q Vol.67 No.11. November 2014
Case Report
envenomation, acute ischaemic stroke or sub-arachnoid
haemorrhage, thyroid storm, tachycardia induced car-
diomyopathy, sepsis, multiorgan dysfunction, postcardi-
ac arrest syndrome, physical stress like trauma, surgery
have been established as causatives of takotsubo cardio-
myopathy.3
Whatever the cause, the clinical presentation
is that of acute LV dysfunction.
Likely pathophysiological mechanisms are as below.
Epicardial coronary vasospasm
Multivessel coronary vasospasm may be responsible
for myocardial infarction like picture associated with non
obstructive coronary disease. However, urgent coronary
angiography conducted at different centres at the time of
presentation showed variability in incidence of coronary
vasospasm. This inconsistency makes multivessel coro-
nary vasospasm less likely a mechanism.4,5,6
Endothelial dysfunction
Thrombolysis in myocardial infarction (TIMI) frame
counts have demonstrated endothelial dysfunction in
all 3 major epicardial coronary arteries during the acute
phase. In addition, concomitant abnormalities of fatty
acid metabolism have also been reported causing further
endothelial damage. Microvascular ischaemia probably
contributes to LV dysfunction as opposed to myocardial
damage in transient apical ballooning.1,7,8
However, ad-
equate data on this hypothesis is lacking.
Catecholamine-induced LV dysfunction
Catecholamine excess and increased cortisol secretion
may cause myocardial stunning. It may also promote en-
dothelial dysfunction. Nonapical regional wall motion
abnormalities that do not follow a single coronary dis-
tribution can be explained by this. In patients recover-
ing from subarachnoid haemorrhage “cerebral T waves”
might reflect the transient wall motion abnormalities in
acute stress-related cardiomyopathy predominantly in-
volving the ventricular apex.9,10
Management includes non-specific therapies like ni-
trates for pulmonary oedema, intra-aortic balloon pump
for low output, combined alpha and beta blockers rather
than selective beta blockade if haemodynamically stable,
and magnesium for arrhythmias related to QT prolon-
gation. Anticoagulation is generally withheld due to the
occasional occurrence of ventricular rupture. Coronary
angiography is required to rule out acute coronary oc-
clusion.11
This report is to alert the physician to consider
takotsubo cardiomyopathy in apt clinical settings.
References
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