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42 (2009) 353–357.e1www.jecgonline.com

Journal of Electrocardiology

Takotsubo cardiomyopathy and QT interval prolongation:who are the patients at risk for torsades de pointes?☆

Liat Samuelov-Kinori, MD,a Michael Kinori, MD,a Yevgeni Kogan, MD,b

Michael Swartzon, MD,c Hadas Shalev, BSc,c Daniel Guy, BSc,c Fotini Ferenidou, MD,d

Noa Mashav, BSc,c Ben Sadeh, BSc,c Lihi Atzmony, BSc,c Orit Kliuk-Ben-Basat, MD,a

Arie Steinvil, MD,a Dan Justo, MDa,⁎aDepartment of Internal Medicine D, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel

bDepartment of Cardiology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, IsraelcSackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

dAristotle University of Thessaloniki and Papa Georgiou General Hospital, Thessaloniki, Greece

Received 26 November 2008

Abstract Objectives: QT interval prolongation is prevalent among patients with Takotsubo cardiomyopathy

☆ A suggested rejecgonline.com.

⁎ Corresponding aSourasky Medical Cen

E-mail address: ju

0022-0736/$ – see frodoi:10.1016/j.jelectroc

(TC), whereas torsades de pointes (TdP) has rarely been reported in these patients. We studied allpeer-reviewed reports on TC-associated QT interval prolongation and all peer-reviewed reports onTC-associated TdP to characterize the clinical circumstances leading to TdP in patients with TC.Methods: The literature search yielded 14 reports on TC-associated TdP and 26 reports on TC-associated QT interval prolongation. Overall, 15 patients with TC-associated TdP and 86 patientswith TC-associated QT interval prolongation were reported. We systematically reviewed each reportand recorded the risk factors for TdP as well as the clinical circumstances of TC.Results: The prevalence of the male sex was higher among patients with TC-associated TdP relativeto patients with TC-associated QT interval prolongation (26.7% vs 5.8%; P = .01). There was a trendin the mean maximal corrected QT interval being longer among patients with TC-associated TdPrelative to patients with TC-associated QT interval prolongation (679.9 ± 230.6 vs 555.9 ± 63.8milliseconds; P = .06). There were no differences between patients with TC-associated TdP andpatients with TC-associated QT interval prolongation in mean age, maximal troponin levels, andlowest ejection fraction. Overall, 12 (80.0%) patients with TC-associated TdP had risk factors forTdP other than the female sex and systolic dysfunction, including suspicion of congenital long QTsyndrome, bradycardia, hypokalemia, recent conversion from atrial fibrillation to sinus rhythm, andusing QT prolonging agents.Conclusions: Men with TC-associated QT interval prolongation are at risk for TdP. Most patientswith TC-associated TdP have risk factors for TdP other than the female sex and systolic dysfunction.© 2009 Elsevier Inc. All rights reserved.

Keywords: QT prolongation; Takotsubo; Torsade de pointes

Introduction

QT interval prolongation might precede torsade depointes (TdP)—a polymorphic ventricular tachycardia thatmight lead to ventricular fibrillation and sudden death. This

ading list accompanies this article online at www.

uthor. Department of Internal Medicine D, Tel-Avivter, 6 Weitzman Street, Tel-Aviv 64239, Israel.sto1@bezeqint.net

nt matter © 2009 Elsevier Inc. All rights reserved.ard.2009.01.005

potentially fatal arrhythmia is associated with administrationof QT prolonging agents, hypokalemia, hypomagnesaemia,and congenital long QT syndrome.1

Takotsubo cardiomyopathy (TC) is a rare acquired diseasecharacterized by acute transient left ventricular dysfunction inthe absence of significant obstructive coronary artery disease.Ventriculography or echocardiography might demonstrateapical dyskinesia in patients with TC, also termed apicalballooning (Fig. 1). The precise pathophysiologic mechan-ism of TC is unknown, though emotional or physical stress is

Fig. 1. Left ventriculography in diastole (left panel) and systole (right panel)of a patient with TC. There is an apical ballooning during systole. Takenfrom Furushima et al. Europace 2008;10:1112-5. With permission from theauthors and Oxford University Press.

354 L. Samuelov-Kinori et al. / Journal of Electrocardiology 42 (2009) 353–357.e1

believed to be the main triggers by causing adrenergic-basedmyocardial impairment.2

The prevalence of QT interval prolongation among TCpatients is high, ranging from 50% to 100% according todifferent case series.3-6 This is probably because systolicdysfunction is associated with both TC and QT intervalprolongation.1,7 Although QT interval prolongation isprevalent among TC patients and might precede TdP(Fig. 2), the later has rarely been reported in TC patients;Denney et al8 first reported TdP occurring in a patient withTC in 2005. Since then, 13 more reports on 14 patients werepublished.9-21 It is of great importance to study the clinicalcircumstances leading to TdP in patients with TC-associatedQT interval prolongation because TdP can be fatal, whereasthe prognosis of TC is usually good. Hence, we studied all

Fig. 2. A, Corrected QT interval prolongation (740 milliseconds) in a 61-year-oldlater (B) and 6 months later (C), the QTc interval gradually decreased (590 and 42008;10:1112-5. With permission from the authors and Oxford University Press

reports on TC-associated QT interval prolongation with TdPand all reports on TC-associated QT interval prolongationalone to characterize the clinical circumstances leading tothis potentially fatal complication.

Material and methods

Retrieval of reports

We performed a literature search for all peer-reviewedin all languages reports on TC patients diagnosed ashaving QT interval prolongation and/or TdP, untilDecember 2008, by using the following keywords:“Takotsubo,” “apical ballooning,” “stress cardiomyopathy,”“torsades de pointes,” “QT,” “arrhythmia,” “syncope,” and“sudden death.” The references in each report were furtherreviewed for additional publications. Only full-lengthreports were reviewed.

Definitions

Takotsubo cardiomyopathywas defined as a dyskinesia orakinesia of the left ventricular apical segments documentedby echocardiography or ventriculography that resolved in afollowing imaging.2 QT interval prolongation was definedas corrected QT interval (QTc) more than 430 millisecondsfor male patients and QTc more than 450 milliseconds forfemale patients according to the formula by Bazett.22 Weused the QTc that was mentioned in the text of each casereport by the authors. In several cases, we measured the QTinterval length in lead II and calculated the QTc according tothe electrocardiogram (ECG) strip enclosed in the case. In

woman with TC. B, The following day, the patient had TdP. Two month70 milliseconds, respectively) (D). Taken from Furushima et al. Europace.

s

Table 1Clinical characteristics of reported patients

Groups No. (%) ofcases withavailable data

Mean ± SD P

Age (y) QT prolongation 86 (100) 64.7 ± 10.7 .44TdP 15 (100) 64.8 ± 17.9

Baseline QTcinterval (ms)

QT prolongation 13 (15.1) 442.7 ± 15.8 .95TdP 9 (60.0) 470.8 ± 80.7

Maximal QTcinterval (ms)

QT prolongation 58 (67.4) 555.9 ± 63.8 .06TdP 14 (93.3) 679.9 ± 230.6

Lowest EF (%) QT prolongation 50 (58.1) 36.5 ± 10.2 .41TdP 7 (46.7) 40.1 ± 14.9

Peak troponinlevels (ng/mL)a

QT prolongation 39 (45.3) 5.6 ± 15.9 .89TdP 5 (38.5) 3.1 ± 4.4

Peak CPKlevels (U/L)

QT prolongation 42 (48.8) 304.5 ± 493.1 .002TdP 5 (15.3) 82.0 ± 28.3

EF indicates ejection fraction.a In 36 patients, troponin I was measured, whereas in 7 patients

troponin T was measured. In 3 patients, troponin type was not available.

355L. Samuelov-Kinori et al. / Journal of Electrocardiology 42 (2009) 353–357.e1

case of a U wave, the QT interval was measured in leadswithout a U wave.

Exclusion of reports

The following reports were excluded: reports on TC withmonomorphic ventricular tachycardia,23,24 reports without adetailed description of the patient,25 and reports that did notmeet the definitions of TC.26

Table 2Clinical characteristics of reported patients with TC-associated TdP

First author Age/sex

Stressor Admission TdP

Rh HR(b/m)

QTc(ms)

T EF (%) Rh

Denney8 32♂ NA Sinus 91 416 − NA Sinu

Ghosh9 59♀ Emotional& alcohol

Sinus 97 NA − 25 Sinu

Furushima10 61♀ NA Sinus 62 740 − NA NAFinsterer11 75♀ Tracheal

operationAF NA NA + NA Sinu

Okada12 77♂ Pneumonia Sinus 75 450 + NA SinuBoulouffe13 68♀ Emotional Sinus NA NA + 15 NA

Sasaki14 22♀ NA Sinus NA 730 − NA Sinu

Patel15 72♀ COPDexacerbation

AF NA NA + NA Sinu

Akashi16 67♀ NA Sinus 68 394 + NA SinuNault17 76♂ Fall &

ImmobilitySinus NA 630 + NA Sinu

Kurisu18 87♀ NA 2:1AVB

46 735 + NA 2:1AVB

Kurisu18 78♂ NA CompAVB

46 735 + NA ComAVB

Hirose19 63♀ Respiratoryfailure

Sinus NA 549 + NA NA

Inoue20 82♀ Emotional CompAVB

38 630 − 45 ComAVB

Mahida21 55♀ Emotional Sinus NA 510 − NA Sinubrad

NA indicates not available; EF, ejection fraction; AVB, atrioventricular block; Coleads; COPD, chronic obstructive pulmonary disease; AF, atrial fibrillation; TnI, t

Risk factors for TdP

Each report was analyzed for the presence of risk factorsforTdPother than female sexand systolic dysfunction,1whichare also common among TC patients.2 Risk factors for TdPincluded recent conversion of atrial fibrillation to sinusrhythm,1 administering QT prolonging agents,1,27 hypokale-miadefinedaspotassiumserumlevelsof less than3.5mmol/L,hypocalcemia defined as calcium serum levels of less than 8.5mg/dL, severehypomagnesemiadefined asmagnesiumserumlevels of less than 1 mg/dL, and bradycardia defined as heartrate of 60 beats perminute or lower.1 Because genetic analysiswas not available for all the patients, suspicion of congenitallong QT syndrome was also included as a risk factor and wasdefined as QT interval prolongation in the baseline ECGrecorded before TC appearance or after its resolution.

Clinical aspects of TC

Each report was analyzed for the presence of the followingclinical aspects of TC: presumable mechanism or trigger ofthe syndrome, peak troponin levels, peak creatine phospho-kinase (CPK) levels, lowest ejection fraction, highest ejectionfraction, and coronary angiography findings.2

Statistical analysis

Continuous variables were expressed as mean ± SD. TheMann-Whitney test was used to compare the mean para-

day TdP timingafteradmission

Peak TnI(g/mL)

Outcome

HR(b/m)

QTc(ms)

T EF (%)

s 91 416 − NA TdP atadmission

0.75 Live

s 97 669 − 2 Few hours 1.3 Live

NA NA − NA 1 d NA Lives NA 375 + 30 1 d NA Live

s 54 851 − NA 3 d NA LiveNA NA NA NA Few hours 1.9 (Tn

type NA)Live

s NA 730 − NA TdP atadmission

NA Live

s 100 674 − NA 6 h 0.8 Live

s NA NA − 41 6 h NA Lives NA 786 − NA 27 h 10.86 Live

42 1060 − 62 6 d NA Live

p 40 1135 − 38 2 d NA Live

NA NA − NA 8 h NA Live(died 69days later

p 38 630 − 45 TdP atadmission

NA Live

sy

NA 510 − NA 1 d NA Live

mp, complete; Rh, rhythm; HR, heart rate; T, T-wave polarity in precordiaroponin I; brady, bradycardia.

)

l

356 L. Samuelov-Kinori et al. / Journal of Electrocardiology 42 (2009) 353–357.e1

metric variables between TC patients with QT intervalprolongation and TC patients with TdP. The χ2 test was usedto compare the prevalence of nonparametric variablesbetween TC patients with QT interval prolongation and TCpatients with TdP. P ≤ .05 was considered statisticallysignificant throughout. Version 15.0 of the SPSS statisticalpackage (SSPS Inc, Chicago, IL) was used to perform allstatistical evaluations.

Results

The literature search yielded 14 reports on 15 patientswith TC-associated TdP8-21 and 26 reports on 86 patientswith TC-associated QT interval prolongation (5,15,17, and1-23 in the suggested reading list online). Overall, 101reports were reviewed on 93 (92.1%) female patients and 9(8.9%) male patients. The prevalence of the male sex washigher among patients with TC-associated TdP relative topatients with TC-associated QT interval prolongation(26.7% vs 5.8%; P = .01).

Mean peak CPK levels were higher among patients withTC-associated QT interval prolongation relative to patientswith TC-associated TdP. There were no statistical differencesbetween patients with TC-associated TdP relative to patientswith TC-associated QT interval prolongation in mean age,mean baseline QT interval length, mean lowest ejectionfraction, and mean peak troponin levels (Table 1). There wasa trend in the mean maximal corrected QT interval beinglonger among patients with TC-associated TdP relative topatients with TC-associated QT interval prolongation (679.9± 230.6 vs 555.9 ± 63.8 milliseconds; P = .06), although inmost cases it was observed after TdP and not duringadmission. Torsades de pointes was presented at admissionin 3 patients, but in the others, it appeared between few hoursand 6 days after admission. All patients survived thearrhythmia, although one patient died 69 days later ofother complications (Table 2).

Overall, 12 (80.0%) patients with TC-associated TdP hadone or more risk factors for TdP other than female sex andsystolic dysfunction, compared with 2 (2.3%) patients withTC-associated QT interval prolongation (P = .002). Amongpatients with TC-associated TdP, risk factors for TdPincluded bradycardia with or without atrioventricular block(n = 4), suspicion of congenital long QT syndrome (n = 3),hypokalemia (n = 1), recent conversion from atrial fibrilla-tion to sinus rhythm (n = 1), recent conversion from atrialfibrillation to sinus rhythm and the use of amiodarone (n =1), suspicion of congenital long QT syndrome andhypokalemia (n = 1), and hypokalemia and the use ofdisopyramide (n = 1).

Discussion

We studied all reports on TC-associated QT intervalprolongation and all peer-reviewed reports on TC-associatedTdP to characterize the clinical circumstances leading toTdP in patients with TC. Our main finding was that menwith TC-associated QT interval prolongation were at higherrisk for TdP compared with women, although TC was much

more prevalent among women.2 This finding is consistentwith a well-known paradox—women have longer QTccompared with men28 but lower incidence of sudden death.The mechanism for the longer corrected QT interval inwomen is unknown but might be related to the effects ofhormones or differences in autonomic innervations.29

One may assume that markers of severe TC, such as highCPK levels, prolonged QT interval, or low ejection fraction,are associated with increased risk for TdP. However, CPKlevels were higher among TC-associated QT intervalprolongation, the maximal corrected QT interval was higheramong TC-associated TdP only after the arrhythmia most ofthe times, and the mean lowest ejection fraction was notdifferent between TC-associated QT interval prolongationand TdP patients. For this reason, markers of TC severitywere not predictive of TdP. On the other hand, known riskfactors for TdP such as congenital long QT syndrome,bradycardia, hypokalemia, using QT prolonging agents, andrecent conversion from atrial fibrillation to sinus rhythmwereobserved among patients with TC-associated TdP.We believethis finding has a great clinical implication (see below).

Limitations

Our study was based on published case reports. Weassume that there are more incidents of TdP in patients withTC that have not been published, for example, when a reportis rejected from publication because TdP is attributed to earlymultiple risk factors for TdP rather than to TC or whenphysicians are reluctant to report on their deceased patients.Indeed, in all the cases we studied, the patients survived thearrhythmia. Patients with sudden death without documenta-tion of an arrhythmia would also go unrecorded. Hence, webelieve that our results are more likely an underestimation ofthe true prevalence of the clinical circumstances that mightlead to TdP in TC patients.

Risk factors for TdP were not reported in all cases of TC-associated QT interval prolongation, probably because theauthors considered TC itself as a cause for QT intervalprolongation or because QT interval prolongation was notthe main issue in these reports. Hence, we could not performa multivariate analysis of the different risk factors for TdPand their weight in predicting TdP. Still, 80% of patients withTC-associated TdP had one ore more risk factors for TdPother than the female sex, and systolic dysfunction is ofclinical importance.

In several cases, the authors did not mention the QTcinterval length. Hence, we measured the QT interval lengthin lead II and calculated the QTc according to the ECG stripenclosed in the case. Measuring the QT interval in theoriginal ECG strips might have been more accurate, but webelieve these differences are minor.

Clinical implications

We believe that previous recommendations regardingtaking measures before prescribing any QT prolonging agentare particularly relevant to patients with TC. It is alsoadvisable to monitor the potassium serum levels frequently,especially in TC patients treated with diuretics. QT intervalmight be prolonged for a while in TC patients,2 and they

357L. Samuelov-Kinori et al. / Journal of Electrocardiology 42 (2009) 353–357.e1

might be discharged before the ECG has returned to normal.Hence, these recommendations are also relevant to thepatients' general practitioner. Finally, in patients with TC andatrioventricular block and bradycardia, it is advisable toimplant a temporary pacemaker not only for hemodynamicstability purposes but also to prevent pause-dependent TdP.All of the above are particularly relevant to men with TC.

Conclusions

Men with TC-associated QT interval prolongation areat risk for TdP. Most patients with TC-associated TdPhave risk factors for TdP other than female sex andsystolic dysfunction. We wish to raise the awareness levelsof risk factors for TdP in patients with TC-associated QTinterval prolongation.

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3. Dundon BK, Puri R, Leong DP, Worthley MI. Takotsubo cardiomyo-pathy following lightning strike. Emerg Med J 2008;25:460.

4. Gavish D, Rozenman Y, Hafner R, Bartov E, Ezri T. Takotsubocardiomyopathy after general anesthesia for eye surgery. Anesthesiology2006;105:621fs.

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8. Saeki S, Matsuse H, Nakata H, Fukahori S, Miyahara Y, Kohno S. Caseof bronchial asthma complicated with Takotsubo cardiomyopathy afterfrequent epinephrine medication. Nihon Kokyuki Gakkai Zasshi2006;44:701.

9. Seth PS, Aurigemma GP, Krasnow JM, Tighe DA, Untereker WJ, MeyerTE. A syndrome of transient left ventricular apical wall motionabnormality in the absence of coronary disease: a perspective from theUnited States. Cardiology 2003;100:61.

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16. Metzl MD, Altman EJ, Spevack DM, Doddamani S, Travin MI, OstfeldRJ. A case of Takotsubo cardiomyopathy mimicking an acute coronarysyndrome. Nat Clin Pract Cardiovasc Med 2006;3:53.

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