Takotsubo cardiomyopathy, also known as stress cardiomyopathy, is a
type of non-ischemic cardiomyopathy in which there is a sudden
temporary weakening of the muscular portion of the heart. This
weakening may be triggered by emotional stress, such as the death of a
loved one, a break-up, rejection from a partner or constant anxiety.
This leads to one of the common names, broken heart syndrome.
Stress cardiomyopathy is now a well-recognized cause of acute heart
failure, lethal ventricular arrhythmias, and ventricular rupture.
The name "takotsubo syndrome" comes from the Japanese word
takotsubo (ja) "octopus trap," because the left ventricle takes
on a shape resembling a fishing pot.
1 Signs and symptoms
4.1 Heart failure
4.2 Low blood pressure
8 Cultural references
10 External links
Signs and symptoms
The typical presentation of takotsubo cardiomyopathy is a sudden onset
of chest pain associated with
ECG changes mimicking a myocardial
infarction of the anterior wall. During the course of evaluation of
the patient, a bulging out of the left ventricular apex with a
hypercontractile base of the left ventricle is often noted. It is the
hallmark bulging-out of the apex of the heart with preserved function
of the base that earned the syndrome its name takotsubo (ja)
"octopus trap," in Japan, where it was first described.
Stress is the main factor in takotsubo cardiomyopathy, with more than
85% of cases set in motion by either a physically or emotionally
stressful event that prefaces the start of symptoms. Examples of
emotional stressors include grief from the death of a loved one, fear
of public speaking, arguing with a spouse, relationship disagreements,
betrayal, and financial problems. Acute asthma, surgery,
chemotherapy, and stroke are examples of physical stressors. In a
few cases, the stress may be a happy event, such as a wedding, winning
a jackpot, a sporting triumph, or a birthday.
Takotsubo cardiomyopathy is more commonly seen in postmenopausal
women. Often there is a history of a recent severe (usually
negative, sometimes happy) emotional or physical stress.
The cause of takotsubo cardiomyopathy is not fully understood, but
several mechanisms have been proposed.
Transient vasospasm: Some of the original researchers of takotsubo
suggested that multiple simultaneous spasms of coronary arteries could
cause enough loss of blood flow to cause transient stunning of the
myocardium. Other researchers have shown that vasospasm is much
less common than initially thought. It has been noted that
when there are vasospasms, even in multiple arteries, that they do not
correlate with the areas of myocardium that are not contracting.
Microvascular dysfunction: The theory gaining the most traction is
that there is dysfunction of the coronary arteries at the level where
they are no longer visible by coronary angiography. This could include
microvascular vasospasm, however, it may well have some similarities
to diseases such as diabetes mellitus. In such disease conditions the
microvascular arteries fail to provide adequate oxygen to the
Mid-ventricular obstruction, apical stunning: It has been suggested
that a mid-ventricular wall thickening with outflow obstruction is
important in the pathophysiology.
Catecholamine-induced myocyte injury: It has been suggested that the
response to catecholamines (such as epinephrine and norepinephrine,
released in response to stress) leads to heart muscle dysfunction that
contributes to takotsubo cardiomyopathy.
It is likely that there are multiple factors at play that could
include some amount of vasospasm and a failure of the
microvasculature Case series looking at large groups of patients
report that some patients develop takotsubo cardiomyopathy after an
emotional stress, while others have a preceding clinical stressor
(such as an asthma attack or sudden illness). Roughly one-third of
patients have no preceding stressful event. A 2009 large case
series from Europe found that takotsubo cardiomyopathy was slightly
more frequent during the winter season. This may be related to two
possible/suspected pathophysiological causes: coronary spasms of
microvessels, which are more prevalent in cold weather, and viral
infections – such as
Parvovirus B19 – which occur more frequently
during the winter.
Transient apical ballooning syndrome or takotsubo cardiomyopathy is
found in 1.7–2.2% of patients presenting with acute coronary
syndrome. While the original case studies reported on individuals
in Japan, takotsubo cardiomyopathy has been noted more recently in the
United States and Western Europe. It is likely that the syndrome
previously went undiagnosed before it was described in detail in the
Japanese literature. Evaluation of individuals with takotsubo
cardiomyopathy typically includes a coronary angiogram to rule out
occlusion of the left anterior descending artery, which will not
reveal any significant blockages that would cause the left ventricular
dysfunction. Provided that the individual survives their initial
presentation, the left ventricular function improves within two
The diagnosis of takotsubo cardiomyopathy may be difficult upon
ECG findings often are confused with those found
during an acute anterior wall myocardial infarction. It
classically mimics ST-segment elevation myocardial infarction, and is
characterised by acute onset of transient ventricular apical wall
motion abnormalities (ballooning) accompanied by chest pain, shortness
of breath, ST-segment elevation, T-wave inversion or QT-interval
prolongation on ECG. Cardiac enzymes are usually negative and are
moderate at worst, and cardiac catheterization usually shows absence
of significant coronary artery disease.
The diagnosis is made by the pathognomonic wall motion abnormalities,
in which the base of the left ventricle is contracting normally or is
hyperkinetic while the remainder of the left ventricle is akinetic or
dyskinetic. This is accompanied by the lack of significant coronary
artery disease that would explain the wall motion abnormalities.
Although apical ballooning has been described classically as the
angiographic manifestation of takotsubo, it has been shown that left
ventricular dysfunction in this syndrome includes not only the classic
apical ballooning, but also different angiographic morphologies such
as mid-ventricular ballooning and, rarely, local ballooning of other
The ballooning patterns were classified by Shimizu et al. as takotsubo
type for apical akinesia and basal hyperkinesia, reverse takotsubo for
basal akinesia and apical hyperkinesia, mid-ventricular type for
mid-ventricular ballooning accompanied by basal and apical
hyperkinesia, and localised type for any other segmental left
ventricular ballooning with clinical characteristics of takotsubo-like
left ventricular dysfunction.
In short, the main criteria for the diagnosis of takotsubo
cardiomyopathy are: the patient must have experienced a stressor
before the symptoms began to arise; the patient’s
ECG reading must
show abnormalities from a normal heart; the patient must not show
signs of coronary blockage or other common causes of heart troubles;
the levels of cardiac enzymes in the heart must be elevated or
irregular; and the patient must recover complete contraction and be
functioning normally in a short amount of time.
Left ventriculography during systole showing apical ballooning
akinesis with basal hyperkinesis in a characteristic takotsubo
Left ventriculogram during systole displaying the characteristic
apical ballooning with apical motionlessness in a patient with
(A) Echocardiogram showing dilatation of the left ventricle in the
acute phase (B) Resolution of left ventricular function on repeat
echocardiogram six days later
ECG showing sinus tachycardia and non-specific ST and
T wave changes
from a person with confirmed takotsubo cardiomyopathy
Echocardiogram showing the effects of the disease
The treatment of takotsubo cardiomyopathy is generally supportive in
nature, for it is considered a transient disorder. Treatment is
dependent on whether patients experience heart failure or acute
hypotension and shock. In many individuals, left ventricular function
normalizes within two months.
Aspirin and other heart drugs
also appear to help in the treatment of this disease, even in extreme
cases. After the patient has been diagnosed, and myocardial
infarction (heart attack) ruled out, the aspirin regimen may be
discontinued, and treatment becomes that of supporting the
While medical treatments are important to address the acute symptoms
of takotsubo cardiomyopathy, further treatment includes lifestyle
changes. It is important that the individual stay physically
healthy while learning and maintaining methods to manage stress, and
to cope with future difficult situations.
Although the symptoms of takotsubo cardiomyopathy usually go away on
their own and the condition completely resolves itself within a few
weeks, some serious complications can happen that must be treated.
These most commonly include congestive heart failure and very low
blood pressure, and less commonly include blood clotting in the apex
of the left ventricle, irregular heart beat, and tearing of the heart
For patients in acute heart failure, ACE inhibitors, angiotensin
receptor blockers, and beta blockers, are considered mainstays of
heart failure treatment. But use of beta blockers specifically for
takotsubo cardiomyopathy is controversial, because they may confer no
Low blood pressure
For people with cardiogenic shock, medical treatment is based on
whether a left ventricular outflow tract (LVOT) obstruction is
present. Therefore, early echocardiography is necessary to
determine proper management. For those with obstructed LVOTs inotropic
agents should not be used, but instead should be managed like patients
with hypertrophic cardiomyopathy, (e.g. phenylephrine and fluid
resuscitation). For cases in which the LVOT is not obstructed,
inotropic therapy (e.g. dobutamine and dopamine) may be used, but with
the consideration that takotsubo is caused by excess
Furthermore, mechanical support with an intra-aortic balloon pump
(IABP) is well-established as supportive treatment.
Despite the grave initial presentation in some of the patients, most
of the patients survive the initial acute event, with a very low rate
of in-hospital mortality or complications. Once a patient has
recovered from the acute stage of the syndrome, they can expect a
favorable outcome and the long-term prognosis is excellent.
Even when ventricular systolic function is heavily compromised at
presentation, it typically improves within the first few days and
normalises within the first few months. Although
infrequent, recurrence of the syndrome has been reported and seems to
be associated with the nature of the trigger.
Takotsubo cardiomyopathy is rare, affecting between 1.2% and 2.2% of
Japan and 2% to 3% in western countries who suffer a
myocardial infarction. It also affects far more women than men with
90% of cases being women, most postmenopausal. Scientists believe one
reason is that estrogen causes the release of catecholamine and
glucocorticoid in response to mental stress. It is not likely for the
same recovered patient to experience the syndrome twice, although it
has happened in rare cases. The average ages at onset are between
58 and 75 years. Less than 3% of cases occurred in patients under age
The Japanese octopus traps after which this disease is named
Although the first scientific description of takotsubo cardiomyopathy
was not until the 1990s, Cebelin and Hirsch wrote about human stress
cardiomyopathy in 1980. The two looked at homicidal assaults that had
happened in Cuyahoga County, Ohio the past 30 years, specifically
those with autopsies who had no internal injury, but had died of
physical assault. They found that 11 of 15 had myofibrillar
degeneration similar to animal stress studies. In the end, they
concluded their data supported "the theory of catecholamine mediation
of these myocardial changes in man and of the lethal potential of
stress through its effect on the heart".
The first studied case of takotsubo cardiomyopathy was in
1991 by Sato et al. More cases of the syndrome appeared in Japan
within the next decade, although western medicine had still not
acknowledged it. The syndrome finally occurred in 1997 when Pavin et
al. wrote about two cases of "reversible LV dysfunction precipitated
by acute emotional stress." The western world had not heard of such a
thing at the time, as it was incredibly rare and often misdiagnosed.
The Japanese at last reported about the syndrome to the west in 2001
under the name "transient LV apical ballooning" though at this point
the west had already heard of numerous cases. The syndrome reached
international audiences through the media in 2005 when the New England
Journal of Medicine wrote about the syndrome.
A case of what is evidently, takotsubo syndrome is a central motif of
the end of the novel Blossoms in Autumn (Slovene: Cvetje v jeseni:
1917) by Slovene writer
Ivan Tavčar and the film Blossoms in Autumn
(1973) shot after it. A village girl named Meta suddenly dies after
she had been asked by Janez, a lawyer from Ljubljana that she had
spent summer with, to marry him. At her funeral, her father states
that she was never very healthy, and that she had a heart defect. Her
mother states: "She has died from happiness."
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