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Intractable Ventricular Tachycardia Associated With Stress Cardiomyopathy

경희대학교 의과대학 내과학교실 진 은 선

Eun-Sun Jin, MD, PhDCardiovascular Center, Kyung Hee University Hospital at Gangdong, Seoul, Korea

Introduction

Stresscardiomyopathy(SCM)—alsoknownas

Takotsubocardiomyopathy—isacommonclini-

cal condition with a clinical presentation that

similartoacutemyocardialinfarction.Suchpa-

tientsmaypresentwithchestpain,STchanges

on electrocardiography (ECG), elevated cardiac

enzymelevels,andregionalwallmotionabnor-

malities of the left ventricularwall.However,

the coronary arteries appear normal in such

casesandtheprognosisisgood.Patientswith

SCMalsopresentwithQTprolongationonECG.

However,onlya fewcasesofSCMpresenting

withventriculartachycardia(VT)associatedwith

longQThavebeenreported.Inthepresentre-

port,wedescribeacaseofa75-year-oldpatient

withmedicallyintractablemonomorphicVTas-

sociatedwithSCM.

Case

A75-year-oldwomanwastransferredtothe

emergencyroomofourhospitalforchestdis-

Received: 14 August, 2014 Revision Received: September 11, 2014accepted: September 14, 2014Correspondence: Eun-Sun Jin, MD, PhD, cardiovascular center, Kyung Hee University Hospital at Gangdong, 892, Dongnam-ro, Gangdong-gu, Seoul, Korea. Tel: +82-2-440-6109, Fax: +82-2-440-7242 E-mail: esjin@khu.ac.krm-suk Ko, MD, PhD, Division of cardiology

ABSTRACT

A 75-year-old woman presented with medically intractable wide QRS tachycardia. She had experienced chest discomfort during a vertebral procedure and was transferred to our hospital. Electrocardiography showed sustained wide QRS tachycardia, which persisted in various QRS axes despite the repeated administration of electrical shock. Through amiodarone infusion and repeated shock delivery, the cardiac rhythm was stabilized to a sinus rhythm. Thereafter, the sustained ventricular tachycardia, for which electrical shock was necessary, occurred repeatedly for 12 hours, but then decreased in frequency and disappeared in 3 days. Echocardiog-raphy revealed akinesia of the entire left ventricular apical segment, and coronary angiography showed mini-mal coronary disease, which was compatible with a diagnosis of stress-induced cardiomyopathy. The patient recovered with general supportive care. Follow-up echocardiography revealed normalized left ventricular wall

motion and systolic function.

Key Words: ■ Takotsubo cardiomyopathy ■ tachycardia ■ ventricular

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comfort that developed during neuroplasty for

lumbarspinalstenosis.Shewasreceivingmedi-

cation for diabetes mellitus and hypertension.

Uponarrival to theemergencyroom,herECG

showedasustainedwideQRStachycardiaof150

bpm.Herbloodpressurewas90/50mmHg.We

suspectedthepresenceofmonomorphicVT,and

hence,electricalshockwasdelivered.Afterre-

peated administration of electrical shock, the

QRSaxischanged,butthewideQRStachycardia

persisted(Figure1).MostoftheVTsweremono-

morphic,butoccasionally,theQRSaxischanged

spontaneously(Figure2).Thepatientunderwent

electrical shockmore than 30 times within 12

hourstoterminatetherecurrentVT.Becausethe

QTintervalofthesinusrhythmwasnormal(Fig-

ure3),amiodaronewasinfusedfortherecurrent

VT.Subsequently,VTchanged to thenonsus-

Figure 1. Sustained wide QRS tachycardia even after an electrical shock. Occasionally, the QRS axis changed after an electrical shock.

Figure 2. Spontaneous QRS axis changes during wide QRS tachycardia.

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Figure 3. Electrocardiography in sinus rhythm showed no QT prolongation (A). 1 month later, ECG showed better R wave progression and T wave change without QT prolongation in precordial leads (B).

Figure 4. Coronary angiography showing no significant stenosis.

A

B

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tainedformandthengraduallyresolved.

Thereafter,echocardiographyshowedakinesia

of the middle and apical wholesegments. Ex-

tensiveischemiaoftheleftanteriordescending

arterywassuspected,butthefindingswerealso

compatiblewithstress-inducedcardiomyopathy.

In addition, coronaryangiography indicatedno

significantstenosis(Figure4).

Amiodarone administration was discontinued

becauseofthedevelopmentofQTprolongation

duringdruginfusion.Withsupportivetreatment,

theleftventricularfunctionandwallmotionnor-

malized,andVTdidnotrecur.Thepatientwas

dischargedwithoutanymedication.ECGwhich

wastaken1monthafterdischargeshowedbetter

RwaveprogressionwithTwavechangewithout

QTprolongationinprecordialleads(Figure3B).

Discussion

SCMisacommonlyencountereddisease,char-

acterizedbyitsinitiallyseverepresentation,fol-

lowedbyamildclinicalcourse.Onpresentation,

itisoftenmisdiagnosedasmyocardialinfarction.

Themostdistinguishableclinicalaspectsofthis

diseasearetheabsenceofcoronaryarteryste-

nosisandagoodprognosis.Althoughmyocardial

infarctionisthemostcommoncauseofsudden

cardiacdeath,themortalityrateofSCMinhos-

pitalsrangesfrom1%to2%.1,2

A potentially dangerous clinical presentation

of SCM is torsades de pointes coinciding with

QTprolongation,whichisoftenaccompaniedby

hypokalemia.3 However, cases of sustained VT

causingcardiacdeathareuncommon.

Inthepresentcase,thepatientshowedrecur-

rent,sustainedVTofboththemonomorphicand

polymorphicforms,withthemonomorphicform

occurringmorefrequently.Inthesinusrhythm,

QTwasnotprolongedandtheserumpotassium

levelwas 3.5mmol/L.Although prolongedQT

withpolymorphicVTisacommonECGfinding

incasesofSCM,monomorphicVTmayalsode-

velop.BecausetheproposedmechanismofSCM

involvesmicrovascularmyocardialischemia.4,5

MedicaltreatmentforsustainedVTcanbead-

justedaccording to theVTmechanism.Amio-

daroneinfusionisnotusedfortreatingcasesof

torsadesdepointeswithlongQT,butcanbeused

fortreatingcasesofmonomorphicVTwithnoQT

prolongationthatmaybeassociatedwithmicro-

vascularmyocardialischemia.

Althoughapatientmayexperiencelife-threat-

ening sustained VT resulting from SCM, place-

ment of an implantable cardioverter-defibrillator

isnotrecommendedbecauseSCMisconsidereda

reversible, self-limiteddisease.Nevertheless, 11%

ofpatientsexperiencesymptomrecurrenceaftera

4-yearfollow-upperiod.6Thus,large-scale,long-

termfollow-updataareneededtoestimatethere-

currenceoflife-threateningVTcausedbySCM.

References

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2. Dib C, Prasad A, Friedman PA, Ahmad E, Rihal CS, Hammill SC, Asir-vatham SJ. Malignant arrhythmia in apical ballooning syndrome: risk factors and outcomes. Indian Pacing Electrophysiol J. 2008;1;8:182-192.

3. Kawano H1, Matsumoto Y, Arakawa S, Satoh O, Hayano M. Premature atrial contraction induces torsades de pointes in a patient of Takotsubo cardiomyopathy with QT prolongation. Intern Med. 2010;49:1767-1773.

4. Galiuto L, De Caterina AR, Porfidia A, Paraggio L, Barchetta S, Locoro-tondo G, Rebuzzi AG, Crea F. Reversible coronary microvascular dys-function: a common pathogenetic mechanism in Apical Ballooning or Takotsubo Syndrome. Eur Heart J. 2010;31:1319-1327.

5. Afonso L, Bachour K, Awad K, Sandidge G. Takotsubo cardiomyopathy: pathogenetic insights and myocardial perfusion kinetics using myocar-dial contrast echocardiography. Eur J Echocardiogr. 2008;9:849-854.

6. Elesber AA, Prasad A, Lennon RJ, Wright RS, Lerman A, Rihal CS. Four-year recurrence rate and prognosis of the apical ballooning syndrome. J Am Coll Cardiol. 2007;50:448-452.