15

Takotsubo cardiomyopathy: A review

Mahdi Veillet-Chowdhury , Syed Fahad Hassan & Kathleen Stergiopoulos

Division of Cardiovascular Disease, Department of Medicine, Stony Brook University Medical Center,

Stony Brook, NY, USA

Introduction

Takotsubo cardiomyopathy (TC) or apical-ballooning syn-

drome is an increasingly recognized disorder characterized

by acute reversible apical ventricular dysfunction in the

absence of epicardial coronary disease. Th e heart takes on

the appearance of a Japanese octopus fi shing pot called a

‘ takotsubo ’ , in which there is apical ballooning with a rela-

tively narrow neck. TC is more common in post-menopausal

women and occurs soon aft er exposure to sudden, unex-

pected emotional or physical stress. Th e current thinking

behind the demographics, epidemiology, pathophysiology

and prognosis are still evolving. Th is review summarizes the

current thinking regarding this perplexing condition.

Scope of the problem

TC mimics the clinical presentation of acute myocardial

infarction. In patients undergoing cardiac catheterization for

acute myocardial infarction, there is an approximately 1%

incidence of this disorder (1). In a study of patients with

suspected acute coronary syndrome and elevated cardiac

enzymes who underwent a left heart catheterization, approx-

imately 1.2% of patients were identifi ed as having transient

Correspondence: Kathleen Stergiopoulos, Department of Medicine, Division of Cardiovascular Disease, HSC T-16 080, Stony Brook University Medical Center, Stony Brook, NY 11974 – 8167, USA. Tel: � 1 631 444 1066. Fax: � 1 631 444 1054. E-mail: kathleen.stergiopoulos@stonybrook.edu

(Received 13 September 2013; accepted 18 November 2013)

Acute Cardiac Care, March 2014; 16(1): 15–22

Copyright © 2014 Informa UK, Ltd

ISSN 1748-2941 print/ISSN 1748-295X online

DOI: 10.3109/17482941.2013.869346

Takotsubo cardiomyopathy can occur after acute mental or

physical stress, subarachnoid hemorrhage, ischemic stroke,

major head trauma, acute medical illness or acute pheochromo-

cytoma crisis. It is characterized by transient systolic dysfunction

of the apical and/or midventricular segments in patients without

epicardial coronary artery disease. The condition occurs most

commonly in postmenopausal women, and is characterized by

transient left ventricular dysfunction. The pathophysiology

of the disorder remains to be elucidated but may involve

catecholamine excess and vasospasm. Future studies, perhaps in

the form of an international registry, may clarify the incidence,

pathophysiology, clinical course, and prognosis of this disorder.

Keywords: Takotsubo cardiomyopathy , apical ballooning synd-

rome , review

cardiomyopathy that could not be otherwise explained (1).

Prevalence of TC ranges from 0.7 to 2.5% in another similar

case series (2,3). Although the majority of case series are

reported from Asia and Europe, several reports from the

United States have confi rmed similar fi ndings (4 – 6). Most

patients with TC are women (7,8). In a registry of patients

in Rhode Island, most patients were postmenopausal women

(95%) and there was suggestion of signifi cant clustering of

reported cases during the summer months (9). While the

etiology of the higher occurrence in post-menopausal women

is not completely clear, reduced estrogen levels could play an

important role in the pathogenesis by predisposing endothe-

lial cells to sympathetic myocardial stunning (6). Th e protec-

tive eff ect of estrogen in TC was suggested in oopharectomized

rats in which estrogen supplementation partially prevented

stress-induced left ventricular dysfunction (10). Th e role of

estrogen in this disorder remains to be fully elucidated.

Pathophysiology

Th e precise mechanism(s) of TC have not been fully

elucidated. Th e proposed mechanisms of this unique syn-

drome of reversible cardiomyopathy include: (1) epicardial

coronary artery vasospasm; (2) coronary microvascular

impairment; (3) direct catecholamine-induced myocyte

injury and/or (4) neurogenic stunned myocardium. Th ese

potential mechanisms may not be mutually exclusive, but

rather there is likely a strong interplay between the auto-

nomic, neurologic and cardiovascular systems. Patients

who have undergone myocardial biopsy have demonstrated

the presence of contraction bands with or without frank

myocyte necrosis, myocardial fi brosis, interstitial infi ltrates

consisting of mononuclear lymphocytes, leukocytes and

macrophages consistent with an infl ammatory response. Th e

fi ndings of contraction bands and infl ammation distinguish

TC from acute myocardial infarction, where coagulation

necrosis would predominate.

Multi-vessel epicardial coronary artery vasospasm

Several authors have proposed that multi-vessel epicardial

coronary artery vasospasm causing ischemia is responsible

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16 M. Veillet-Chowdhury et al.

Acute Cardiac Care

for reversible left ventricular dysfunction (11,12). However,

the data supporting this theory has been limited. Few patients

have demonstrable vasospasm with provocative challenges

(11,13 – 16). When no spontaneous coronary vasospasm

occurs or is observed, it has been proposed that impaired

blood fl ow may be due to vulnerable plaque rupture with

rapid endogenous thrombolysis and reperfusion. However,

multi-vessel vasospasm and regionally stunned myocardium

is inconsistent with the minimal troponin elevation that is

usually observed. Pathologically, the characteristic changes

of ischemic stunning at the cellular level are diff erent that

those observed in patients with TC (17). Electrocardio-

graphic (ECG) changes in acute coronary syndrome are

diff erent than those observed in TC, with the latter notable

for an absence of reciprocal changes (18). However, electro-

cardiographic changes are insuffi cient to make or exclude the

diagnosis. Others have proposed that short episodes of

multi-vessel vasospasms might explain the reversible nature

of the myocardial stunning and the usually large territory of

myocardium involved.

Microvascular coronary impairments

Evidence suggests that coronary microvascular impairment

plays a role in TC. In patients with transient left ventricular

dysfunction, it has been noted that coronary microcircula-

tion was impaired by the thrombolysis in myocardial infarc-

tion (TIMI) trial frame count (4,15). Diff erence in apical

myocardial fatty acid metabolism in comparison to apical

perfusion abnormalities has been demonstrated, which sup-

ports the concept of myocardial ‘ stunning ’ in the territories

of wall motion abnormalities (15). Similarly, Elesber et al.,

demonstrated abnormal myocardial perfusion in 69% of TC

patients using the TIMI myocardial perfusion grade and per-

fusion abnormalities involving multiple coronary territories

in 86% of the patients (19). Interestingly, the authors noted

a strong relationship between the severity of microvascular

dysfunction and the severity of myocardial injury.

Furthermore, coronary micovascular impairment has

been suggested using positron emission tomography (PET)

in patients with TC (20 – 22). One study by Kurowski et al.,

examining apical and mid-ventricular variants of TC patients

assessed microvascular dysfunction by scintigraphy and PET

studies (1). Th ese investigators found that myocardial glu-

cose metabolism was aff ected to a greater degree than was

the perfusion in the impaired territories, a so-called inverse

perfusion-metabolism mismatch, consistent with stunned

myocardium. It may be due to an exaggerated sympathetic

surge, which may mediate insulin resistance and inhibit the

intracellular translocation of GLUT-4 glucose transporter,

ultimately causing decreased glucose uptake (23).

Decreased coronary fl ow velocity reserve and a short

deceleration time of diastolic velocity have been observed in

the acute phase in TC patients, but returned to normal aft er

several weeks (24). Th e coronary fl ow velocity reserve and

deceleration time of diastolic velocity refl ect the degree of

coronary microvascular dysfunction under stable hemody-

namic conditions when epicardial coronary stenosis is absent

(25 – 29).

A related theory on the etiology of TC is the hypothesis

that myocardial stunning is due to rupture of an atheroscle-

rotic plaque, which temporarily occludes the left anterior

descending artery. Ibanez et al., suggested that in TC, there

is a variant left anterior descending artery that extends api-

cally and diaphragmatically (30). A plaque rupture in the

middle portion could lead to an acute coronary syndrome

with early reperfusion and, therefore, left ventricular stun-

ning and only mild cardiac biomarker elevation. However,

this theory would not explain the extensive regional wall

motion abnormalities seen in classic or variant TC.

Microcirculatory abnormalities may accompany TC;

however, it is unclear how these abnormalities result either

directly or indirectly in extensive wall motion abnormalities.

Future studies are required to address mechanistic questions

regarding this issue.

Catecholamine-induced myocyte injury

TC, oft en following emotional stress, triggers the sympa-

thetic nervous system. Both epinephrine and norepineph-

rine have been reported to be markedly elevated in TC

patients, which may contribute to the transient left ventricu-

lar myocardial stunning (1,6,7,31). Furthermore, patients

with pheochromocytoma are known to have high levels of

catecholamines and may develop a reversible cardiomyopa-

thy (32,33). Th e proposed explanation for this relationship

could be the result of increased intracellular concentrations

of calcium in cardiac myocytes and the formation of

deleterious free radicals. Endomyocardial biopsy revealed

mononuclear cell infi ltrates and contraction band necrosis,

which is consistent with fi ndings seen in other studies that

indicate catecholamine cardiotoxicity (13,34). Th ese fi ndings

may be due to calcium overload, resulting in ventricular dys-

function. In addition, elevated levels of catecholamines may

cause coronary macro- and microcirculation vasospasms

(4,35,36).

Th e diff erent morphologic left ventricular variants of TC

could be partly explained by the diff erential distribution of

adrenergic receptors and/or increased sensitivity of the recep-

tors to the circulating catecholamines in certain regions of the

heart (37,38). Murine studies have shown that high concen-

trations of epinephrine stimulates a negative inotropic eff ect

on myocyte contraction by switching the coupling of β 2

adrenoreceptors on the myocardium from G s to a G i protein

signaling, which could cause the observed wall motion abnor-

malities with the highest receptor density (39).

Neurogenic stunned myocardium

Related to the presence of excess catecholamines in TC is the

theory of neurogenic stunning of the myocardium. It has been

shown that the left ventricular dysfunction and histopatho-

logical fi ndings seen in TC are similar to that seen in suba-

rachnoid hemorrhage (40 – 42). Both problems may refl ect

activation of the central neurogenic mechanisms. However,

typically the basal segments of the left ventricle is aff ected

while the apex is spared in subarachnoid or intracranial

hemorrhage (43,44), although the reverse fi nding has also

been reported (45,46). In addition, increased catecholamine

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Takotsubo Cardiomyopathy 17

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Table I. Characteristics of patients with takotsubo cardiomyopathy from 2007 to 2012.

Author, year (ref.) n Women

(%)Age

(years)ST elevation

(%)EF(%)

Troponin(I or T)

No signifi cant CAD (%)

Akashi, 2007 (57) 10 80 70 – – 4.57 100Bybee, 2007 (58) 18 100 72 89 37.8 – 100Fujiwara, 2007 (59) 11 100 73 55 – 4.9 100Lee, 2007 (60) 10 60 55 70 40 – 100Mitchell, 2007 (61) 22 100 62 59 28 4.07 100Burgdorf, 2008 (62) 50 94 10 54 44 1.5 100Fazio, 2008 (63) 40 85 68 70 42 – – Gerbaud, 2008 (64) 15 80 68 – 43 9.9 100Meimoun, 2008 (65) 12 92 68 42 40 0.6 100Winchester, 2008 (66) 31 90 65 39 37.5 2.9 71Barker, 2009 (67) 9 89 68 67 32.7 4.91 100Eitel, 2009 (68) 38 94 73 – 48 – 100Leurent, 2009 (69) 176 95 68 – 39.3 6.04 – Regnante, 2009 (9) 70 95 67 41 37 6.9 100Sharkey, 2009 (70) 41 100 65 – 32 – 100Singh, 2010 (71) 114 93 66 21 41 0.68 100Sharkey, 2010 (8) 136 96 68 49 32 0.6 – Eitel, 2011 (72) 256 89 69 42 48 – 94Parodi, 2011 (73) 116 91 73 60 36 – 100Waldenborg, 2011 (74) 13 100 70 – 51 2.7 100Kosuge, 2012 (75) 34 85 70 – 41 – 100

Table II. Phenotypic left ventricular variants of takotsubo cardiomyopathy.

· Apical and midventricular LV dysfunction

· Isolated midventricular and basal LV dysfunction/isolated midventricular LV dysfunction (apical-sparing TC)

· Isolated basal LV dysfunction

· Global LV hypokinesis

· Other noncoronary distribution wall motion abnormalities

LV, left ventricular; TC, takotsubo cardiomyopathy (51).

increase has been linked to convulsive status epilepticus (47)

and in tonic – clonic seizures (48). Naganuma et al., discussed

the role of stimulation of the temporal lobe in the setting of

even a partial seizure as a cause of TC, possibly by proximity

of the temporal and insular cortex, and their infl uence on the

autonomic modulation on the heart (49). Th e available data

cannot defi ne the mechanism of this disorder. It may be the

result of catecholamine excess, in combination with diff eren-

tial expression and sensitivity of receptors, calcium overload,

and/or a component of vasospasm. Future studies will be

required to determine the details of the mechanism(s).

Diagnostic criteria

While no consensus on the diagnostic criteria for TC exists,

the most widely accepted diagnostic criteria have been pro-

posed by the Mayo Clinic (50). Th eir suggested diagnostic

criteria are the presence of all of the following features:

transient hypokinesis, akinesis or dyskinesis in the left ven-(1)

tricular mid segments with or without apical involvement;

regional wall motion abnormalities that extend beyond that

expected from a single epicardial vascular distribution; and

frequently but not always a stressful trigger;

the absence of obstructive coronary artery disease or (2)

angiographic evidence of acute plaque rupture;

new ECG abnormalities (ST-segment elevation and/or (3)

T-wave inversion;

the absence of pheochromocytoma and myocarditis or (4)

other reason for left ventricular dysfunction (50).

Worldwide agreement on the diagnostic criteria of TC is

required for the purposes of classifi cation, management, and

prognosis.

Clinical features and clinical course

Most reports have noted a clear gender discrepancy in

TC, with the syndrome noted to be more common in

women. Th e syndrome is usually preceded by acute physical

or emotional stressors, such as an unexpected death in the

family, abuse, a quarrel, or exhausting work. Other precipi-

tants of TC are acute intracranial events (intracranial

bleeding), head trauma, ischemic stroke, acute medical

illness including sepsis, surgical procedures, overproduction

of endogenous catecholamines as in pheochromocytoma

or administration of exogenous catecholamines agents such

as inhaled beta agonists, methylxanthines, epinephrine/

amphetamines, or cocaine (51). Th e identifi cation of a

preceding stressor ranged from 14 – 100% of cases with a

preceding emotional trigger in 11 – 100% of cases (7).

Seizures can also be associated with TC (52). In some cases,

a trigger is not clearly identifi ed. Th e most common com-

plaints of patients with TC are chest pain and dyspnea, sim-

ulating an acute myocardial infarction. Other less common

symptoms may include syncope, ventricular fi brillation

and cardiac arrest (4,19,53). Mitral regurgitation of variable

magnitude may be present, and is oft en transient (54).

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18 M. Veillet-Chowdhury et al.

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Figure 1. (A,B). Echocardiographic apical four-chamber view demonstrating the midventricular variant of takotsubo cardiomyopathy. Images were obtained with echocardiographic contrast material to enhance endocardial defi nition, in diastole (A) and systole (B). Arrows denote hypokinesis of the midventricular segments, and an ejection fraction of 35%. Th is is a 50-year-old postmenopausal woman with a past medical history of diabetes mellitus, multiple sclerosis and seizure disorder, who presented with a witnessed generalized seizure. She had a mildly elevated troponin-I level of 0.42 ng/ml (normal 0.00 – 0.04 ng/ml) and was without complaints. A 12-lead electrocardiogram showed sinus tachycardia and one premature ventricular beat (not shown), without evidence of ST-segment elevation. A CT scan of her head was normal.

Th e most common fi ndings on the admission ECG are

ST-segment elevation and T-wave inversions. ST-segment

elevation occurs in 59 – 100% of patients with ST-segment

elevation in the precordial leads are the most common

(Table I) (7). Th e presence of pathologic Q-waves ranges

from 6 – 31% of patients (2,3). Th us, distinguishing true acute

myocardial infarction from TC is diffi cult solely on the basis

of clinical and electrocardiographic data. Although diagnostic

coronary angiography is the single best tool to diagnose this

condition, this disorder remains a diagnosis of exclusion.

Not all TC strictly involves dysfunction of the apical

segments of the left ventricle. Morphologic variants are

summarized on Table II. Variants of this syndrome have

been reported that involve only the mid-ventricular or basal

segments (Figures 1 – 3) (51,55). An atypical pattern of seg-

mental dysfunction confi ned to the mid-ventricle was

reported in about one third of the patients in one small case

series with TC (1). No diff erences in the demographic, clin-

ical, impaired microcirculation in the coronary arteries, or

overall outcomes between those with more typical or atypical

variants of the syndrome (1). One possible explanation for

the variant morphologies could be related to the variable

distribution of adrenergic receptors on the myocardium.

Patients with TC oft en have elevated levels of cardiac

biomarkers. Troponin levels are usually only mildly elevated

and do not follow the typical rise and fall patterns as seen in

an acute myocardial infarction. Troponin I or T levels were

elevated in 85% of patients with TC, whereas creatine

kinase-MB fraction was elevated in 38% of patients (3). In

one study, troponin T levels inversely correlated with initial

ejection fraction. Troponin T levels greater than six or tro-

ponin I levels greater than 15 do not suggest TC (56). How-

ever, there are no generally accepted cut-off points for

troponin elevation, which would ultimately infl uence clini-

cal management. Elevations of plasma BNP (brain natri-

uretic peptide) are oft en present on admission (7).

Th e in-hospital mortality associated with TC is from

1 – 3% (51). Supportive care is usually all that is required

because left ventricular function usually recovers quickly.

However, left ventricular dysfunction may remain depressed

for weeks before recovering. In the majority of cases, the left

ventricular function returns within one-to-three months.

Associated complications of TC are not common, but may

include atrial and ventricular arrhythmias, hemodynamic

instability, heart failure and cardiogenic shock (51). Patients

with apical and midventricular variants can have associated

dynamic obstruction with functional systolic anterior motion

of the mitral valve due to the hyperdynamic basilar segments

with resultant posteriorly directed mitral regurgitation. Th is

fi nding is similar to mitral valve abnormalities associated

with hypertrophic cardiomyopathy. Treatment in this sce-

nario can be diffi cult, and may require fl uids (if the respira-

tory status allows), beta-blocker administration, and possibly

phenylephrine to increase aft erload and reduce the outfl ow

tract obstruction, which can worsen hypotension. In severe

cases, pure LV pump failure can occur and may require

intra-aortic balloon counter pulsation. Mechanical compli-

cations such as free wall rupture and ventricular septal

defects can occur, but are considered rare. Systemic embo-

lism related to acute left ventricular dysfunction can occur

and is a relatively common cause of death.

Acute and chronic management

At present, there are no clinical trial data available to guide

clinical management of TC, and treatment decisions are oft en

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Takotsubo Cardiomyopathy 19

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Figure 2. Coronary angiography demonstrates normal epicardial coronary vessels (A,B), and an ejection fraction of 55% (C,D). Angiography was performed three days aft er initial presentation. Th ese fi ndings confi rm the diagnosis of transient left ventricular dysfunction in the setting of normal coronary arteries.

Figure 3. Nuclear perfusion imaging with regadenoson stress. Regadenoson stress with technicium-99m sestamibi nuclear perfusion agent in the same patient one day prior to coronary angiography demonstrates a large reversible defect of moderate intensity of the mid to apical anterior, anteroseptal, and anterolateral segments, consistent with a partial thickness infarction with moderate ischemia. Th e calculated ejection fraction was 54%. Th is fi nding in the setting of clinical evidence of takotsubo cardiomyopathy is likely related to microvascular dysfunction.

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Bybee KA , Prasad A , Barsness GW , Lerman A , Jaff e AS , Murphy 4. JG , et al . Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome . Am J Cardiol. 2004 ; 94 : 343 – 6 . Sharkey SW , Lesser JR , Zenovich AG , Maron MS , Lindberg J , 5. Longe TF , et al . Acute and reversible cardiomyopathy provoked by stress in women from the United States . Circulation 2005 ; 111 : 472 – 9 . Wittstein IS , Th iemann DR , Lima JA , Baughman KL , Schulman 6. SP , Gerstenblith G , et al . Neurohumoral features of myocardial stunning due to sudden emotional stress . N Engl J Med. 2005 ; 352 : 539 – 48 . Akashi YJ , Goldstein DS , Barbaro G , Ueyama T . Takotsubo car-7. diomyopathy: A new form of acute, reversible heart failure . Cir-culation 2008 ; 118 : 2754 – 62 . Sharkey SW , Windenburg DC , Lesser JR , Maron MS , Hauser RG , 8. Lesser JN , et al . Natural history and expansive clinical profi le of stress (tako-tsubo) cardiomyopathy . J Am Coll Cardiol. 2010 ; 55 : 333 – 41 . Regnante RA , Zuzek RW , Weinsier SB , Latif SR , Linsky RA , Ahmed 9. HN , et al . Clinical characteristics and four-year outcomes of patients in the Rhode Island Takotsubo Cardiomyopathy Registry . Am J Cardiol. 2009 ; 103 : 1015 – 9 . Ueyama T , Ishikura F , Matsuda A , Asanuma T , Ueda K , Ichinose 10. M , et al . Chronic estrogen supplementation following ovariec-tomy improves the emotional stress-induced cardiovascular responses by indirect action on the nervous system and by direct action on the heart . Circ J. 2007 ; 71 : 565 – 73 . Dote K , Sato H , Tateishi H , Uchida T , Ishihara M . Myocardial 11. stunning due to simultaneous multivessel coronary spasms: A review of 5 cases . J Cardiol. 1991 ; 21 : 203 – 14 . Sato H , Taiteishi H , Uchida T . Takotsubo-type cardiomyopathy 12. due to multivessel spasm . In: Kodama K , Haze K , Hon M , eds. Clinical aspect of myocardial injury: From ischemia to heart fail-ure . Tokyo: Kagakuhyouronsha , 1990 . pp. 56 . Abe Y , Kondo M , Matsuoka R , Araki M , Dohyama K , Tanio H . 13. Assessment of clinical features in transient left ventricular apical ballooning . J Am Coll Cardiol. 2003 ; 41 : 737 – 42 . Kawai S , Suzuki H , Yamaguchi H , Tanaka K , Sawada H , Aizawa 14. T , et al . Ampulla cardiomyopathy ( ‘ takotsubo ’ cardiomyopathy) — reversible left ventricular dysfunction: With ST segment eleva-tion . Jpn Circ J . 2000 ; 64 : 156 – 9 . Kurisu S , Inoue I , Kawagoe T , Ishihara M , Shimatani Y , Nishioka 15. K , et al . Myocardial perfusion and fatty acid metabolism in patients with tako-tsubo-like left ventricular dysfunction . J Am Coll Cardiol. 2003 ; 41 : 743 – 8 . Tsuchihashi K , Ueshima K , Uchida T , Oh-mura N , Kimura K , 16. Owa M , et al . Transient left ventricular apical ballooning without coronary artery stenosis: A novel heart syndrome mimicking acute myocardial infarction . Angina pectoris-myocardial infarc-tion investigations in Japan. J Am Coll Cardiol. 2001 ; 38 : 11 – 8 . Nef HM , Mollmann H , Weber M , Deetjen A , Brandt R , Hamm 17. CW , et al . Release pattern of cardiac biomarkers in left ventricu-lar apical ballooning . Int J Cardiol. 2007 ; 115 : 128 – 9 . Inoue M , Shimizu M , Ino H , Yamaguchi M , Terai H , Fujino N , 18. et al . Diff erentiation between patients with takotsubo cardiomy-opathy and those with anterior acute myocardial infarction . Circ J. 2005 ; 69 : 89 – 94 . Elesber A , Lerman A , Bybee KA , Murphy JG , Barsness G , Singh 19. M , et al . Myocardial perfusion in apical ballooning syndrome cor-relate of myocardial injury . Am Heart J. 2006 ; 152 : 469 e9 – 13 . Ito K , Sugihara H , Kawasaki T , Yuba T , Doue T , Tanabe T , et al . 20. Assessment of ampulla (Takotsubo) cardiomyopathy with coro-nary angiography, two-dimensional echocardiography and 99mTc-tetrofosmin myocardial single photon emission computed tomography . Ann Nucl Med. 2001 ; 15 : 351 – 5 . Nishikawa S , Ito K , Adachi Y , Katoh S , Azuma A , Matsubara H . 21. Ampulla ( ‘ takotsubo ’ ) cardiomyopathy of both ventricles: evaluation

Table III. Management of patients with takotsubo cardiomyopathy.

· Monitor in hospital on telemetry

· Perform echocardiography or magnetic resonance imaging to assess left ventricular function, mitral regurgitation, LV mural thrombus, right ventricular function, dynamic LV outfl ow tract obstruction

· Consider anticoagulation with heparin to prevent LV thrombus in patients with apical involvement if there are no contraindications to anticoagulation

· Consider anticoagulation with warfarin in patients with persistent apical LV dysfunction at time of hospital discharge

· Standard therapy for LV dysfunction including beta-blockers, angiotensin converting enzyme inhibition or other adrenergic blocking agent

· Repeat echocardiography prior to hospital discharge to reassess LV systolic function

· Consider repeat echocardiography at one-to-three months, to assess for LV recovery

LV, left ventricular (51).

individualized. In the absence of consensus guidelines,

Table III lists some general principles of management. Since

sympathetic activation is thought to contribute to the patho-

genesis of TC, it is reasonable to consider long-term beta-blocker

therapy with the goal of preventing recurrence (31). Diuretics

are administered as needed, but may worsen dynamic obstruc-

tion if present. Th e use of angiotensin-converting enzyme

inhibition should be considered at least until left ventricular

function recovers. Th e prognosis of patients with TC appears

to be favorable, but long-term registry data is lacking.

Risk of recurrence

Recurrence of TC has been reported. Little evidence exists

on the incidence and risk of recurrence aft er an initial epi-

sode (5). However, some data suggests the risk of recurrence

in the fi rst few years aft er an initial episode may be in the

range of 2 – 10% (2,5). It is thought that recurrence rates may

be low in patients who are maintained on comprehensive

beta adrenergic blockade. More information is needed in this

arena to guide patients and clinicians.

Declaration of interest: Th e authors report no confl icts of

interest. Th e authors alone are responsible for the content

and writing of the paper.

References

Kurowski V , Kaiser A , von Hof K , Killermann DP , Mayer B , 1. Hartmann F , et al . Apical and midventricular transient left ventricular dysfunction syndrome (tako-tsubo cardiomyopathy): Frequency, mechanisms, and prognosis . Chest 2007 ; 132 : 809 – 16 . Bybee KA , Kara T , Prasad A , Lerman A , Barsness GW , Wright RS , 2. et al . Systematic review: Transient left ventricular apical balloon-ing: A syndrome that mimics ST-segment elevation myocardial infarction . Ann Intern Med . 2004 ; 141 : 858 – 65 . Pilgrim TM , Wyss TR . Takotsubo cardiomyopathy or transient left 3. ventricular apical ballooning syndrome: A systematic review . Int J Cardiol , 2008 ; 124 : 283 – 92 .

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Takotsubo Cardiomyopathy 21

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22 M. Veillet-Chowdhury et al.

Acute Cardiac Care

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