sindrome de takotsubo

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doi: 10.4037/ccn2009451 2009;29:49-57Crit Care Nurse Dawn DerrickThe''Broken Heart Syndrome'': Understanding Takotsubo Cardiomyopathy

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The damaging effects ofstress on the cardiovas-cular system are widelydocumented andaccepted by the general

public and the medical community.A specific syndrome of stress-relatedreversible cardiomyopathy, however,has recently been observed withgreater frequency. Increasingly referredto as the “broken heart syndrome,”this condition mimics myocardialinfarction in patients without obstruc-tive coronary artery disease. Initialsigns and symptoms resemble thoseof acute coronary syndrome; chestpain, dyspnea, electrocardiographic(ECG) changes, and elevated levels ofcardiac biomarkers are common.1

Clinical Article

The“Broken Heart Syndrome”:Understanding TakotsuboCardiomyopathy

This article has been designated for CE credit. Aclosed-book, multiple-choice examination fol-lows this article, which tests your knowledge ofthe following objectives:

1. Describe the clinical manifestations of takotsubo cardiomyopath.

2. Recognize the importance of prompt diagnosis and management of takotsubo cardiomyopathy

3. Understand the proposed pathological mechanisms associated with takotsubo cardiomyopathy

CEContinuing Education

www.ccnonline.org CRITICALCARENURSE Vol 29, No. 1, FEBRUARY 2009 49

It is important for critical carenurses to be aware of this syndromeand what differentiates it from classicacute myocardial infarction. Properunderstanding will guide appropri-ate assessment, monitoring, man-agement, and education of patients.

The hallmark of the syndromeis a characteristic transient contrac-tile abnormality of the left ventriclecausing a balloonlike morphologythat can be detected with left ven-tricular angiography or contrastechocardiography. Damage of theleft ventricle causes a contractiledefect of the apex of the heart. Dur-ing systole, or ventricular contrac-tion, ventricular imaging shows arounded, hypokinetic apex with anarrow, hypercontracted base (Fig-ure 1). This phenomenon was firstdescribed in 1991 by Dote et al,2 whonamed the syndrome “takotsubo-like cardiomyopathy” because theappearance resembles a pot histori-cally used in Japan to catch octopus(tako in Japanese means octopus;tsubo means pot). The cardiac dys-function is transient, and the leftventricle returns to normal and con-tractile function is restored withindays to weeks.2

Dawn Derrick, MSN

PRIME POINTS

• “Broken heart syndrome,”or takotsubo cardiomyopa-thy, is a spontaneouslyreversible form of cardio -myopathy that is ofteninduced by emotional orphysical stress.

• Signs and symptomsinclude chest pain, dyspnea,electrocardiographicchanges, and elevated levelsof cardiac biomarkers.

• Patients often have signsand symptoms of fluidoverload and can haveacute pulmonary edema.

• Most patients are post-menopausal women, manywith no risk factors forcoronary artery disease.

• The left ventricularabnor mality reverses spon-taneously in days or weeks.

©2009 American Association of Critical-Care Nurses doi: 10.4037/ccn2009451



50 CRITICALCARENURSE Vol 29, No. 1, FEBRUARY 2009 www.ccnonline.org

Terms used to describe thissyndrome in published reportsinclude transient left ventricular

apical ballooning, stress cardiomy-opathy, and ampulla cardiomyopa-thy.3 In this article, I use the term

takotsubo [tah-ku-su-bu] cardiomy-opathy. I describe the pathophysiol-ogy of takotsubo cardiomyopathy,signs and symptoms, diagnosis,treatment, and prognosis. A casereport is included.

IncidenceThe National Heart, Lung, and

Blood Institute estimated that in2007 in the United States, about1.2 million people would have amyocardial infarction.4 Akashi et al5

reported that takotsubo cardiomy-opathy may account for about 1% ofall acute myocardial infarctions,suggesting that about 12 000 Amer-icans might have had the syndromein 2007. Bybee et al,6 in a review ofthe literature, reported that the syn-drome accounted for 1.5% and 2.2%of Q-wave and ST-segment acutecoronary syndrome, respectively, inthe patients studied.

Most patients who have takotsubocardiomyopathy are postmenopausalwomen.1,7 Gianni et al1 reviewed 14studies and found that of 286 patientswith the syndrome, 254 (89%) werefemale. The mean age of the patientswas 68.5 years. Of the 14 studies, 11included data on risk factors forcoronary disease. Figure 2 comparesthe presence of risk factors in patientswith takotsubo cardiomyopathy andpatients with coronary artery disease.Cardiovascular risk factors are gen-erally present to a lesser degree inpatients with takotsubo cardiomy-opathy than in patients with coro-nary artery disease.1,8

EtiologySevere reversible left ventricular

dysfunction (myocardial stunning)in patients without marked coronarydisease is thought to be caused by

Dawn Derrick is an advanced practice nurse certified nurse practitioner at NorthShoreUniversity Health System in Evanston, Illinois.

Corresponding author: Dawn Derrick, MSN, Department of Cardiology, Evanston Hospital, Walgreens Building,Third Floor, 2650 Ridge Avenue, Evanston, IL 60201 (e-mail: [email protected]).

To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

Author

Figure 1 A, Angiogram of normal left ventricle in systole shows contraction of allmyocardial segments. B, Angiogram of left ventricle with takotsubo defect showscontraction of the base with akinesis of the apex.

A B

Figure 2 Occurrence of risk factors for coronary artery disease in patients withtakotsubo cardiomyopathy and patients with coronary artery disease.Based on data in Gianni et al1 and Khot et al.8

60

50

40

30

20

10

0Smoking Diabetes Dyslipidemia

Takotsubo cardiomyopathy, Coronary artery Coronary arteryboth sexes disease, men disease, women

Hypertension

Risk factor

Prev

alen

ce, %



excessive exposure to catecholaminesmediated by exaggerated sympa-thetic stimulation.7 Although thissituation is known to occur in criti-cally ill patients in the absence ofcoronary artery disease9 (Table 1),the takotsubo variant involvespatients in their usual state ofhealth, often after an episode ofemotional or physical distress.

PathophysiologyThe pathophysiological mecha-

nisms associated with takotsubocardiomyopathy remain unclear,although broadly speculated on.The most accepted theory is cate-chol amine excess due to activationof sympathetic tone. Other theoriesconsidered include ischemia frommultivessel coronary spasm or atransient atherosclerotic plaque.

Role of CatecholaminesPatients with takotsubo cardiomy-

opathy can have abnormally highserum levels of circulating cate-cholamines.7 Wittstein et al7 moni-tored plasma levels of epinephrine,norepinephrine, and dopamine inpatients with takotsubo cardiomy-opathy on hospital days 1 and 2.Levels were also measured in patientshospitalized with classic myocardialinfarction. Patients with takotsubocardiomyopathy had levels 7 to 34times as high as published normalvalues and 2 to 3 times as high asthe levels in patients with classicmyocardial infarction.7

Histological examination ofbiopsy samples from the affectedleft ventricle of patients with takot-subo cardiomyopathy have showncontraction band necrosis, which isassociated with clinical states of cat-echolamine excess.4 Catecholamine

excess has reversible toxic effects onmyocardium that have been docu-mented in cases of pheochromocy-toma (a catecholamine-secretingtumor).10 In takotsubo cardiomy-opathy, the apex of the left ventricleappears to be selectively vulnerableto these effects. The basal segmentsare spared, suggesting a difference

in sympathetic innervation orandrenergic receptor sensitivity inthe apex.6 The exact mechanism ofcatecholamine-induced damageand selective apical involvement isnot yet understood.

Coronary Artery SpasmOne of the first theories for the

cause of takotsubo cardiomyopathywas multivessel coronary spasm.3

Coronary spasm can cause ischemiain the absence of obstructive coro-nary artery disease, and occlusivespasm causes transmural ischemiawith ST-segment elevation.11(p1160)

Feasibly, multivessel coronaryartery spasm could account for thediffuse takotsubo defect. Manyresearchers5,6,7,12,13 have tested thespasm theory by performing angio-graphy during persistent ST-segmentelevation and did not observe orprovoke any spasm. Bybee et al,6 ina systematic review of 7 studies,identified 3 studies in which provo-cable multivessel spasm occurred in13 of 73 patients (18%) with the syn-drome who were tested. This resultsuggests that although spasm mayplay a role in takotsubo cardiomy-opathy, it does not explain most cases.

Transient Occlusion by Atherosclerotic Plaque

Although obstructive coronaryartery disease (>50% narrowing) isruled out by angiography, someresearchers hypothesize that a rup-tured coronary plaque could be theunderlying cause of takotsubo car-diomyopathy.14 Spontaneous inter-mittent occlusion and recanalizationof coronary arteries due to a combi-nation of thrombosis and vasocon-striction are common during earlyacute coronary syndrome.14 Can a


Table 1 Causes of reversiblemyocardial dysfunction described incritically ill patients with no cardiacpathologya

Neurogenic stunned myocardiumSubarachnoid hemorrhageStrokeSubdural hematomaCranial traumaElectroconvulsive therapy

Acute respiratory failureUpper airway obstructionAsthmaPulmonary embolismAcute lung injuryAcute respiratory distress syndrome

Anaphylaxis

Trauma injuriesPulmonary contusionMultiple traumaHemorrhagic shockBlast injuryBurn injuries

Postsurgical pathology transplant

Sepsis

Systemic inflammatory response syndrome

Pancreatitis

Cardiac arrest

Poisoning

Rhabdomyolysis

Episodes of arterial hypertension/pheochromocytoma

Thyroid disease

Arrhythmias

Hyperthermia/hypothermia

Obstructive jaundice

Emotional stress

Nutritiona Reprinted from Ruiz Balién,9 with permission.



ruptured plaque cause severe ortotal coronary occlusion that thenundergoes spontaneous recanaliza-tion before angiography?

In classic myocardial infarction,the size of the infarct corresponds tothe amount of myocardium suppliedby the obstructed artery. In takot-subo cardiomyopathy, the area ofaffected myocardium is much largerthan the normal distribution of asingle coronary artery. Involvementof more myocardium than could besupplied by a single artery seems tonegate the possibility of transientcoronary occlusion. Ibanez et al14

used intravascular ultrasound toimage the LAD in 5 patients withtakotsubo cardiomyopathy. Althoughall patients had less than 50% steno-sis on angiograms, intravascularultrasound showed ulcerated ather-

osclerotic lesions in each patient’sLAD. Further evaluation of the LADin these patients showed that theartery bent around the apex andextended along the diaphragmatic leftventricle. Ibanez et al14 proposed thatin patients with a “well-developed”LAD such as those studied, wide-spread apical akinesis can be causedby transient occlusion; implyingthat takotsubo cardiomyopathy inthese patients is essentially anaborted myocardial infarction.

Higher Prevalence in WomenAnother confounding variable

is that takotsubo cardiomyopathyoccurs predominantly in post-menopausal women. Does a differ-ence exist between the sexes in thepsychological response to stress thattriggers an abnormal physiological

change? Is the cardiovascular systemof women physiologically or anatom-ically more sensitive than that of mento catecholamines? Sex hormonesmay influence the sympatheticnervous system and may affectcoronary vasoreactivity or the ten-dency to spasm. Perhaps endothelialdysfunction, known to worsen aftermenopause (because of loweredestrogen levels) further increasesvulnerability to sympatheticallymediated myocardial stunning.1

Clinical FeaturesPatients with takotsubo cardio -

myopathy have signs and symptomssuggestive of acute coronary syn-drome, usually chest pain, dyspnea,ST-segment changes on ECGs, andelevated levels of cardiac biomark-ers.3,6,15,16 Degree of symptom severity


CASE STUDY

A65-year-old woman with no significant medicalhistory was brought to the emergency department

because of a sudden onset of substernal chest pressure.She had been riding in a car after the funeral of a childwho was a close friend of her family. The chest pressureprogressed to pain reported as severe (8 on a 10-pointpain scale) and constant and was associated with short-ness of breath. The pain did not radiate, and she couldidentify no aggravating or alleviating factors.

Blood pressure was 106/50 mm Hg and oxygen sat-uration was 89% on room air. The patient was visiblytachypneic (respiratory rate, 32/min) and diaphoretic.Results of a physical examination were consistent withmild pulmonary edema, including jugular venous dis-tension and crackles in the basilar lung fields. An ECGshowed sinus tachycardia with a heart rate of 112/minand ST-segment elevation in leads V2 through V6. She was given oxygen by nasal cannula, aspirin, andsublingual nitroglycerin along with metoprolol, furosemide,and an infusion of heparin. Her pain improved to 4 (ona 10-point scale). She was taken urgently to the cardiac

catheterization laboratory approximately 1 hour afterarrival in the emergency department. In the catheterizationlaboratory, she report dizziness, and her blood pressurewas 69/30 mm Hg. A dopamine infusion was started.

Cardiac catheterization and coronary angiographywere performed. All coronary arteries were patent withno marked obstruction. The left anterior descendingartery (LAD) tapered at the apex but did not circumnavi-gate the apex (Figure 3). The left ventricle had a large,severely hypokinetic to akinetic segment involving theanterolateral, apical, and distal diaphragmatic walls. All other myocardial segments contracted normally. The estimated ejection fraction was 25%.

Hemodynamic measurements revealed an aorticpressure of 68/32 mm Hg, left ventricular pressure of76/18 mm Hg, pulmonary capillary wedge pressure of 19mm Hg, pulmonary artery pressure of 34/20 mm Hgwith a mean of 25 mm Hg, right ventricular pressure of41/11 mm Hg, and right atrial pressure of 9 mm Hg.

Takotsubo cardiomyopathy was diagnosed. Anintra-aortic balloon pump was placed to mechanicallysupport the left ventricle. The dopamine was discontin-ued to avoid further catecholamine stimulation. The



varies widely. Because of acute leftventricular dysfunction, some patientshave pulmonary edema or cardio-genic shock.1,3,7 Onset of signs andsymptoms is usually sudden andusually occurs after an emotionalstressor such as the death of a lovedone or a physical stressor such as anasthma attack (Table 2). A system-atic review1 of 254 patients withtakotsubo cardiomyopathy indicatedthat 27% had an emotional stressor,39% had a physical stressor, and34% could not identify a stressor.

ECG FindingsThe most common ECG finding

in takotsubo cardiomyopathy is ST-segment elevation, typically in theprecordial leads5 (Figure 4), but ECGscan have normal findings or showT-wave abnormalities or Q waves5

(Figure 5). Evolutionary changessometimes occur in the first fewdays, including resolution of theST-segment elevation with develop-ment of diffuse and often deep T-waveinversion that involves most leads.15

Cardiac BiomarkersMost patients with takotsubo

cardiomyopathy have elevated levelsof cardiac biomarkers, althoughusually not to the extent associatedwith classic myocardial infarction.6

In the Global Use of Strategies toOpen Occluded Arteries in AcuteCoronary Syndromes (GUSTO IIa)troponin substudy,17 222 patientswith classic myocardial infarctionassociated with ECG changes werestudied. Their levels of CKMB andtroponin and the degrees of elevationabove the upper limit of normal

Table 2 Emotional and physicalstressors associated with takotsubocardiomyopathy

Emotional stressorsUnexpected death of relative or friend1,7

Domestic abuse1

Confrontational argument1,7

Catastrophic medical diagnosis1

Devastating business1

Armed robbery7

Gambling losses1

Surprise party7

Surprise reunion7

Car accident7

Fear of procedure7

Fear of choking7

Court appearance7

Public performance7

Physical stressorsExacerbated systemic disorders1

Noncardiac invasive procedures1,13

Exhausting physical effort1,5

Asthma attack1

Pneumothorax5

Ventricular fibrillation5

Cold exposure5


patient required 48 hours of support with the pump. Shewas monitored in the intensive care unit, where she contin-ued to receive intravenous furosemide and had good diure-sis. She had no further chest pain. Her levels of cardiacbiomarkers were monitored and showed a pattern of eleva-tion consistent with myocardial infarction. Peak levels ofcardiac biomarkers occurred approximately 24 hours afterher arrival in the emergency department: troponin I, 3.31ng/mL; creatine kinase–MB fraction (CKMB), 28.3 ng/mL;myoglobin, 902 ng/mL. On the third day, she was weaned

off of the intra-aortic balloon pump.On the fourth day, she was transferredout of the intensive care unit. Hermedications were changed to oralfurose mide, and a β-blocker wasadded to her medication regimen,and when she tolerated that withouthypotension, an angiotensin-convertingenzyme inhibitor was added.

On the fifth day after admission,an echocardiogram showed a leftventricular ejection fraction greaterthan 55% with normal systolic func-

tion. The previous contractile abnormalities were notdetected, suggesting that the left ventricle had made acomplete recovery. On physical examination, the patientappeared euvolemic with no clinical indications of fluidoverload. Use of the diuretic and the angiotensin-con-verting enzyme inhibitor were stopped. The β-blockerwas continued to attenuate her intrinsic catecholamineactivity. After discharge from the hospital, she continuedto recover and returned to her former lifestyle with nopermanent limitations.

Figure 3 Angiograms of left (A) and right (B) coronary arteries in a patient withtakotsubo cardiomyopathy show no obstructive coronary disease.

A B



were examined. Among these patients,95% had more than a 2-fold increasein CKMB level and more than a 3- to11-fold increase in troponin level.17

Gianni et al,1 in a review of 14 studieson patients with takotsubo cardiomy-opathy, found 6 studies in which tro-ponin levels were measured and 3studies in which CKMB levels weremeasured. The troponin level waselevated in 106 of 123 patients (86.2%),and the CKMB level was elevated in17 of 23 (73.9%),1 well below theexpected 95% elevation that occursin patients with classic myocardialinfarction. Kazuki et al13 compared10 patients who had takotsubo car-diomyopathy with 16 patients whohad classic acute coronary syndrome.The mean elevation of levels of cardiac

biomarkers in acute coronary syn-drome was 10 times that in thepatients with takotsubo cardiomy-opathy. The mean level of CKMB(normal, 25 IU/L) in patients withtakotsubo cardiomyopathy was 34IU/L (SD, 23) compared with a meanof 326 IU/L (SD, 98) in patientswith acute coronary syndrome.13

DiagnosisNo way currently exists to imme-

diately distinguish the signs andsymptoms of takotsubo cardiomy-opathy from those of myocardialinfarction caused by acute coronarythrombosis. Urgent cardiac catheter-ization is often performed. A diag-nosis of takotsubo cardiomyopathyis suspected when obstructive coro-

nary disease is not present to explainthe patient’s degree of left ventriculardysfunction. Diagnosis is confirmedby observation of the typical octopuspot morphology of the left ventricle.Identification of a triggering emo-tional or physical stressor is consid-ered supportive of but not necessaryto the diagnosis.15 An echocardio-gram must be obtained within daysor weeks after the acute phase toconfirm that abnormalities havereversed. Table 3 summarizes theclinical findings that lead to a diag-nosis of takotsubo cardiomyopathy.

TreatmentBecause takotsubo cardiomyopa-

thy is initially indistinguishablefrom classic acute coronary syn-drome, immediate treatment shouldinclude management of coronaryischemia and pulmonary edema.This management includes continu-ous telemetry monitoring andadministration of aspirin, anticoag-ulants with direct thrombin inhibi-tion and or glycoprotein IIb/IIareceptor inhibition, nitrates, β-blockers, and diuretics. Once takot-subo cardiomyopathy is diagnosed,treatment is primarily supportive.Akashi et al5 noted complete reversal

Figure 4 Electrocardiograms of 2 different patients with takotsubo cardiomyopathy show variations of ST-segment elevations. A,Convex upward elevation of the ST segment in the anteroseptal leads (V2 through V5) and to a lesser degree in the inferior leads(I, II, AVF). B, Concave upward elevation of ST segment in the anterolateral leads (V3 through V6) and to a lesser degree in theinferior leads. Note the lack of reciprocal ST-segment depression in both electrocardiograms.

I

II

III

V1

II

V5

I

II

III

V1

II

V5

V1

V2

V3

V4

V5

V6

V1

V2

V3

V4

V5

V6aVF

aVL

aVR

aVF

aVL

aVR

BA

Figure 5 Electrocardiographic features in takotsubo cardiomyopathy.Based on data in Gianni et al.1

Q waves

T-wave abnormalities

ST-segment elevation

0 20 40 60 80 100

Percentage of cases




of contractile abnormalities andrecovery with no treatment. Aspirincan be discontinued unless coronarydisease or peripheral vascular dis-ease is concomitant. β-Blockers maybe continued long-term to protectagainst catecholamine sensitivity,which may predispose to this syn-drome. Heparin and coumadinshould be used if apical thrombus ispresent, or a severe apical defectmakes thrombus formation likely.6

ComplicationsMost complications of takotsubo

cardiomyopathy occur during theacute phase of illness. Late compli-cations are rare because the syndromeis reversible and the damage is notpermanent. The reported complica-tion rate is about 19%.16 Heart failureand pulmonary edema occur in 3%to 46% of patients, and mortality ratesare 1%6,17 to approximately 3%.16

Reported complications are sum-marized in Table 4.

Heart FailurePatients with left-ventricular

failure can require mechanical sup-port with intra-aortic counterpulsa-tion by balloon pump during theacute phase. Adrenergic agents areusually avoided to prevent additionalcatecholamine stimulation. Diuretics

are often helpful for pulmonaryedema and fluid overload. Standardtherapy for left ventricular dysfunc-tion should be initiated, includinguse of angiotensin-converting enzymeinhibitors and β-blockers.

Thrombus FormationHeparin and warfarin may be

used to treat or prevent left ventric-ular apical thrombus, which is a riskof significant left ventricular dysfunc-tion. Apical thrombi form becauseof stasis of blood in the akinetic seg-ments. This same protocol is usedto prevent thrombus in patients withventricular aneurysms as a compli-cation of classic myocardial infarc-tion.19 Warfarin can be discontinuedonce ventricular function has returnedto normal.6

Left Ventricular Outflow TractObstruction

Patients with takotsubo car-diomyopathy are at risk for obstruc-tion of the left ventricular outflowtract (LVOT).1 The LVOT is the paththat blood takes along the septalwall as the blood is being ejectedfrom the left ventricle through theaortic valve. Obstruction of thispathway is caused by exaggeratedcontraction of the base of the ventri-cle when hypokinesis of the apexoccurs. The unbalanced contractionof the ventricle reduces the size ofthe outflow tract, resulting in accel-eration of blood flow through thispathway during systole. Acceleratedflow decreases the pressure abovethe neighboring mitral valve, caus-ing a suctioning effect of the ante-rior mitral valve leaflet toward theseptum. This “systolic anteriormotion” of the mitral valve towardthe septum causes further LVOTobstruction,20 which can causehypotension. Echocardiography orcatheterization of the left side of theheart is used to diagnose this com-plication. The hypotension of LVOTobstruction can be managed in sev-eral ways. β-Blockers can reducethe hypercontractility of the base

and lessen thedegree ofobstruction.β-Blockers alsoincrease ven-tricular fillingduring diastole.Reduction inpressure gradi-ent between theleft ventricularapex and out-flow tract hasbeen observed

Table 4 Reported complications in takotsubo cardiomyopathy

Left ventricular failure with or without pulmonary edema1,6,16

Cardiogenic shock6,16

Left ventricular outflow tract obstruction1,6

Mitral regurgitation from “systolic anterior motion”6

Ventricular arrythmias6

Transient complete atrioventricular block18

Left ventricular mural thrombus6,16

Left ventricular free wall rupture6

Death6

Table 3 Clinical findings in takotsubo cardiomyopathy

Sudden onset of chest pain or shortness of breath

Precipitant physical or emotional stressor

Electrocardiographic changes suggestive of acute myocardial infarction

Mild to moderate elevation of cardiac biomarkers

Typical octopus pot morphology on echocardiogram or left ventriculogram

No evidence of obstructive coronary artery disease on cardiac catheterization

Complete resolution of left ventricular dysfunction weeks after event




after intravenous injection of pro-pranolol.3 Increased blood volumeincreases the functional size of theoutflow tract and reduces the obstruc-tion.20 Intravenous fluids can be usedto increase volume if the patientdoes not have pulmonary edema.

PrognosisOverall, without significant

comorbid diseases, prognosis forpatients with takotsubo cardiomy-opathy is good once the acute phasehas passed. Recommendations forfollow-up include echocardiographyat approximately 4 to 6 weeks afterdischarge to document normalizationof left ventricular function. Completeresolution of contractile abnormali-ties within weeks is characteristic ofthis syndrome, so another diagnosisshould be considered for patients withpersistent contractile abnormalities.

Reoccurrence of takotsubo car-diomyopathy is considered rare andhas been reported in no more than10% of cases.15 Gianni et al1 identi-fied 4 studies documenting a meanrecurrence rate of 3.5%. However,the syndrome has been documentedfor a relatively short time, and sothe natural history remains largelyunknown. Patients should be fol-lowed up regularly as outpatients.

Nursing ImplicationsTakotsubo cardiomyopathy is

an important health issue involvingpostmenopausal women without

severe coronary artery disease andoften without classic risk factors forcoronary artery disease. Patientsare affected suddenly, with nowarning, often at a time of crisis intheir life. Health care providersshould be prepared to provide edu-cation and counseling to patientswith this unique diagnosis. Takot-subo cardiomyopathy should beconsidered when patients havesigns and symptoms of acute coro-nary syndrome and appear to beat low risk for coronary artery dis-ease, especially if a stressful eventoccurred before the onset of thesigns and symptoms.

Nursing care of patients withtakotsubo cardiomyopathy involvesmonitoring hemodynamic status,providing supportive measures, andwatching for complications. Nursesneed a thorough understanding ofthe nature of the syndrome andwhat distinguishes it from classicmyocardial infarction. Education ofpatients and their families aboutthe nature of the syndrome, includ-ing its reversibility and low rate ofrecurrence, is imperative. Expecta-tion for a full recovery will be reas-suring to patients and their families.Assessing effective coping is impor-tant, especially if a major emotionalstressor was the precipitant of thesyndrome. The added stress ofbeing ill and hospitalized requirescontinued psychological support.Patients must be educated on theimportance of outpatient follow-upfor repeat echocardiography toconfirm resolution.

If mild or moderate coronarydisease was detected during angio-graphy, the patient should also becounseled on risk-factor modifica-tion for coronary artery disease.

Implications for FutureResearch

Further research is needed toclarify the pathophysiology of takot-subo cardiomyopathy, especially inrelationship to women. Also impor-tant is distinguishing any potentiallymodifiable risk factors. Additionally,future research should focus ontechniques for differentiating takot-subo cardiomyopathy from classicacute coronary syndrome and onestablishing standardized criteriafor diagnosis and clinical guidelinesfor treatment and follow-up. CCN

Financial DisclosuresNone reported.

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d•tmore�

To learn more about takotsubo cardiomyopa-thy, read “Transient Left Ventricular ApicalBallooning,” by Brenda McCulloch in CriticalCare Nurse 2007;27(6):20-27. Available atwww.ccnonline.org.

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15. Prasad A. Apical ballooning syndrome: an important differential diag-nosis of acute myocardial infarction. Circulation. 2007;115(5):56-59.

16. Donohue D, Movahed M. Clinical characteristics, demographics, andprognosis of transient left ventricular apical ballooning syndrome.Heart Fail Rev. 2005;10(4):311-316.

17. Bahit MC, Criger DA, Ohman EM, Granger CB, Wagner GS. Thresh-olds for the electrocardiographic change range of biochemical mark-ers of acute myocardial infarction (GUSTO-IIa data). Am J Cardiol.2002; 90(3):233-237.

18. Lee WL, Miao LF, Chan HW, Chen MZ. Takotsubo syndrome withtransient complete atrioventricular block. Chin Med J (Engl). 2006;119:73-76.

19. Akashi YJ, Tejima T, Sakurada H, et al. Left ventricular rupture associ-ated with takotsubo cardiomyopathy. Mayo Clin Proc. 2004;79(6):821-824.

20. Haley J, Sinak LJ, Tajik J, et al. Dynamic left ventricular outflow tractobstruction in acute coronary syndromes: an important cause ofnew systolic murmur and cardiogenic shock. Mayo Clin Proc. 1999;74(9):901-906.




CE Test Test ID C0913: The “Broken Heart Syndrome”: Understanding Takotsubo CardiomyopathyLearning objectives: 1. Describe the clinical manifestations of takotsubo cardiomyopath 2. Recognize the importance of prompt diagnosis and management oftakotsubo cardiomyopathy 3. Understand the proposed pathological mechanisms associated with takotsubo cardiomyopathy

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Test answers: Mark only one box for your answer to each question. You may photocopy this form.

1. How is takotsubo cardiomyopathy best described?a. Stress-related reversible cardiomyopathyb. Ventricular dilatation and grossly impaired systolic functionc. Asymmetrical septal hypertrophic cardiomyopathyd. Reduced diastolic compliance of the left ventricle

2. What do the initial signs and symptoms of takotsubo cardiomyopathy most closely resemble?a. Pulmonary embolismb. Thoracic aortic aneurysmc. Acute coronary syndromed. Pericarditis

3. What does systolic ventricular imaging demonstrate in a patient with takotsubo cardiomyopathy?a. Rounded, hypokinetic apex with a narrow, hypercontracted baseb. Rounded, hyperkinetic apex with a narrow, hypocontracted basec. Narrow, hypokinetic apex with a rounded, hypercontracted based. Narrow, hyperkinetic apex with a rounded, hypocontracted base

4. What is another name for takotsubo cardiomyopathy?a. Dilated cardiomyopathyb. Hypertrophic cardiomyopathyc. Restrictive cardiomyopathyd. Ampulla cardiomyopathy

5. Which group of patients has the greatest incidence of takotsubo cardiomyopathy?a. Postmenopausal womenb. Adolescent girlsc. Perimenopausal womend. Pregnant women

6. What is the leading source of morbidity, cost, and legal ramifications after cardiac catherization?a. Multivessel coronary artery spasmb. Catecholamine excessc. Transient atherosclerotic plaqued. Obstructive coronary artery disease

7. Which of the following is correct about takotsubo cardiomyopathy?a. The onset of signs and symptoms is usually insidious.b. Electrocardiographic changes typically involve limb leads.c. Signs and symptoms usually occur after an emotional stressor.d. Cardiac biomarkers are usually normal.

8. What is the most common electrocardiography finding in takotsubo cardiomyopathy?a. ST-segment depressionb. T-wave inversionc. ST-segment elevationd. Pathological Q waves

9. What drug may be continued long term to protect against catecholaminesensitivity?a. Alpha adrenergic blockersb. Calcium channel blockersc. Angiotensin-converting enzyme inhibitorsd. Beta adrenergic blockers

10. What is correct about the complications of takotsubo cardiomyopathy?a. Late complications are frequent.b. Most complications occur during the acute phase of illness.c. The reported complication rate is about 3%.d. Pulmonary edema occurs in 64% of patients.

11. Accelerated blood flow through the left ventricular outflow tract decreases the pressure above which valve?a. Tricuspidb. Mitral c. Pulmonicd. Aortic

12. What is recommended at approximately 4 to 6 weeks after discharge todocument normalization of left ventricular function in a patient diagnosedwith takotsubo cardiomyopathy?a. A multigated acquisition scanb. Coronary angiographyc. Exercise stress testingd. Echocardiography

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Test ID: C0913 Form expires: February 1, 2011 Contact hours: 1.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%) Category: A, Synergy CERP ATest writer: Denise Hayes, RN, MSN, CRNP

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sindrome de takotsubo

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