S Intractable Ventricular Tachycardia Associated With Stress...
Transcript of S Intractable Ventricular Tachycardia Associated With Stress...
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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: [email protected] 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
1. Sharkey SW, Windenburg DC, Lesser JR, Maron MS, Hauser RG, Lesser JN, Haas TS, Hodges JS, Maron BJ. Natural history and expansive clini-cal profile of stress (takotsubo) cardiomyopathy. J Am Coll Cardiol. 2010;26;55:333-341.
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.