Korean Heart Rhythm Society Room 805, Masters Tower #553, Dohwa-dong, Mapo-gu, Seoul 121-040, Korea Phone 82-2-3275-5411 Fax 82-2-3275-5412 E-mail [email protected]http://www.k-hrs.org The Official Journal of Korean Heart Rhythm Society Arrhythmia The Official Journal of Korean Heart Rhythm Society 부정맥 Vol.14 No.3 September 2013 ISSN 2005-9728 Main Topic Reviews 심실조기수축 특발성 심실빈맥 허혈성 심근증 환자에서 심실빈맥 확장성 심근증 환자에서 심실빈맥 Article Review 브루가다 증후군에서 milrinone 그리고 cilostazol이 부정맥 발생을 억제하는 세포 기전 ECG & EP Cases Ventricular Tachycardia Originating from the Right Ventricular Outflow Tract Terminated by Steam Pop A case of left bundle branch block-shaped wide QRS complex Tachycardia with diagnostic Ambiguity on a Surface electrocardiogram Vol.14 No.3 ● 통권 46호 ● September 2013 부정맥 심실빈맥(I)
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브루가다 증후군에서 milrinone 그리고 cilostazol이 부정맥 발생을 억제하는 세포 기전 ······ 차태준 ········· 26
ECG & EP Cases
Ventricular Tachycardia Originating from the Righ Ventricular Outflow Tract
Terminated by Steam Pop ···························· 김기훈 ········· 28
A case of left bundle branch block-shaped wide QRS complex Tachycardia
with diagnostic Ambiguity on a Surface electrocardiogram ·········· 안민수 ········· 34
자율 학습 문제 ·················································· 40
The Official Journal of Korean Heart Rhythm Society
Vol.14 No.3●통권46호●September 2013
Contents
Cover: Electrocardiograms of various premature ventricular contraction patterns (page 9).
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건국대학교 의과대학 내과학교실 박 경 민
Kyoung-Min Park, MD, PhDDivision of Cardiology, Department of Internal Medicine, Konkuk University Hospital, Konkuk University School of Medicine, Seoul, Korea
서론
심실조기수축(prematureventricularcontraction,
PVC)은심실에서기원하는조기심장박동이다.PVC는
규칙적인심장박동전조기에발생하기때문에정상
맥박보다 이르게 발생하며, 이로 인해 증상이
나타나기도한다.PVC가일어나는동안동방결절(SA
node)로부터정상적으로전기적신호가도달되기전에
심실은정상보다이른신호를보낸다.이러한조기
신호는심실근의전기적인과민성때문이라고알려져
있으며심근경색,전해질의불균형,산소부족또는
약물에의해생길수있다.심실조기수축후심장의
전기적시스템은즉시 reset된다.이 resetting은
심장박동에서짧은휴지를일으키고,몇몇환자들은
PVC후에심장이짧은순간멈추는것을느낀다고
보고한다.
PVC의발생
PVC는 건강한 성인에서 흔하게 발견되는
부정맥이다.PVC가있지만증상이전혀없는경우도
많다. PVC는고령환자,고혈압환자,심장질환
환자에서더일반적이다.또한심장질환이나고혈압이
없는젊고건강한사람에서도발생한다.그러나최근의
여러보고에서는증상이없어도PVC가하루동안24%
이상발생할경우심근기능저하에이를수있다고
심실조기수축
Received: May 17, 2013Revision Received: September 2, 2013Accepted: September 28, 2013Correspondence: Kyoung-Min Park, MD, PhD, Department of Internal Medicine, Konkuk University Hospital, Konkuk University School of Medicine, Seoul 143-729, Republic of KoreaE-mail: [email protected]
Premature ventricular contraction
AbSTRACT
Premature ventricular contraction (PVC), also known as premature ventricular complex, ventricular
premature contraction/complex, ventricular premature beat, or ventricular extrasystole, is a relatively
common event where the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the
sinoatrial node, the normal heartbeat initiator. The electrical events of the heart detected by an
electrocardiogram allow PVC to be easily distinguished from a normal heartbeat. This paper provides useful
information about PVC to physicians for understanding and managing clinical PVC
8 The Official Journal of Korean Heart Rhythm Society
이유로사망한다.
많은의사들은PVC가심실빈맥이나심실세동을
항상일으키는것은아니라고여긴다.대신PVC는
심근경색으로부터진행되고있는심장손상과같은
심각한상태,저칼륨혈증,저산소증및 digoxin,
aminophylline독성상태의간접적이지만중요한
지표가될수있다.많은PVC가무해하고양성이라고
말할수있으려면우선구조적인심장질환이PVC
발생과연관이없음이확인되어야한다.만약근본적인
심장질환에대한이상소견이없다면PVC의예후가
좋다는것을확신할수있다.그러나최근PVC의
빈도가많은경우(›24%/24hrs)1,2그리고PVC의
넓이가넓은경우(›156msec)3에는심근기능을
저하시키는위험인자및예측인자가될수있다고
보고된바있다.
PVC의치료
PVC자체가양성부정맥이라하더라도치료를해야
하는이유는다음과같다.
•두근거리는증상완화
•PVC를발생시키는질환들은잠재적으로생명을
위협하기때문에해당질환치료
•심실빈맥과돌연사의발생을예방
심장질환이없는건강한사람에게있어증상이없는
PVC는 적극적으로 치료할 필요가 없다. 그러나
두근거림의완화를위해다음의방법을고려하는것이
좋다.
•음주,카페인섭취중단
•Pseudoephedrine을포함하는약물처럼
adrenaline을함유할가능성이있는비염완화제를
과다사용하지않을것(체중감소를위한보조제는
PVC를악화시킬가능성이있다)4
•Amphetamines,cocaine같은약물의남용을
줄일것
•금연
PVC를유발하는질환들은또한생명을위협할수
있다.이러한질환들이있는경우종종병원에서
사용되는telemetry로PVC,심실빈맥등을발견할수
있다.이러한질환과대처법을예로들면다음과같다.
•저칼슘혈증과저마그네슘혈증:칼슘과
마그네슘은정맥주사로투여할수있다.
•Digoxin,aminophylline의독성:약물을투여할
수있다.
•급성심근경색:약물,관상동맥조영술,
관상동맥중재술(percutaneous
transluminal coronary angioplasty)은
막힌관상동맥을개방하여심근에혈액공급을
회복시키기위하여응급으로사용할수있다.
•저산소증:산소를코로공급하고,근본적인
폐질환을치료하기위해약물을투여할수있다.
항부정맥제
항부정맥제는심실빈맥,심방세동,PVC를제어하는
데사용된다.예를들면베타차단제,procainamide,
flecainide/propafenone,amiodarone그리고몇몇
다른약제들이있다.그러나일부항부정맥제는실제로
심장의이상리듬을일으킬수있다는단점이있다.
따라서항부정맥제는심실빈맥과심실세동의고위험
환자에게만신중하게처방해야한다.잦은PVC와
심실성부정맥을유발하는중요한심장질환을가진
경우또는실신등중증의증상이있는환자들에게는
전기생리학검사를권고한다.전기생리학검사는
생명을위협하는심실성부정맥이있는지알아보기
위해하는검사이며,그결과악성부정맥이유발될
가능성이있다면항부정맥제또는이식형제세동기
(implantablecardioverterdefibrillator,ICD)로돌연사
예방치료를한다.
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전극도자절제술
일반적으로부정맥은약물치료를통하여억제할수
있지만,이는근본적인치료라기보다는임시로부정맥의
활동을억제하는것이며약물을중단하면재발될
가능성이있다.또한약물부작용이나타나는경우는
약물을지속적으로사용할수없으며,활동적인젊은
연령에서는약물을평생지속적으로복용하는것이
번거롭고경제적으로도상당한부담이된다.최근에는
심실조기수축을포함한심실성부정맥의경우에도
상심실성빈맥의시술처럼도관을이용한절제술(고주파
전극도자절제술,radiofrequencycatheterablation)을
할수있다.이는심도자검사와같은방법으로심장
내에여러개의전극도자를넣어심실조기수축발생
위치를정확하게찾아내고,전극도자를통해고주파
전류(radiofrequencyenergy)를주어그자리에열을
발생시켜심실조기수축의원인이되는병소를완전히
제거함으로써완치하는방법이다.
References
1. Bogun F, Crawford T, Reich S, Koelling TM, Armstrong W, Good E, Jongnarangsin K, Marine JE, Chugh A, Pelosi F, Oral H, Morady F. Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: Comparison with a control group without intervention. Heart Rhythm. 2007;4:863–867.2. Baman TS, Lange DC, Ilg KJ, Gupta SK, Liu TY, Alguire C, Armstrong W, Good E, Chugh A, Jongnarangsin K, Pelosi F Jr, Crawford T, Ebinger M, Oral H, Morady F, Bogun F. Relationship between burden of premature ventricular complexes and left ventricular function. Heart Rhythm. 2010;7:865-869. 3. Deyell MW, Park KM, Han Y, Frankel DS, Dixit S, Cooper JM, Hutchinson MD, Lin D, Garcia F, Bala R, Riley MP, Gerstenfeld E, Callans DJ, Marchlinski FE. Predictors of recovery of left ventricular dysfunction after ablation of frequent ventricular premature depolarizations. Heart Rhythm. 2012;9:1465-1472.4. Upadhyay S, Afaq M, Upadhyay S, Zarich S, McPherson C. Weight loss supplement provoked idiopathic ventricular tachycardia. Indian Heart J. 2007;59(6):494-496.
Ventricular bigeminy
Ventricular trigeminy
Ventricular couplet
Ventricular triplet
Figure 1. Electrocardiograms of various premature ventricular contraction patterns.
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차의과학대학교 내과학교실 성 정 훈
Jung-Hoon Sung, MD, PhDDivision of Cardiology, Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Gyeonggi-do, Korea
특발성 심실빈맥
서론
특발성심실빈맥(idiopathicventriculartachycardia)
은심실빈맥(ventriculartachycardia,VT)이구조적으
로정상이며반흔이없는심장에서발생하는것이다.유
출로심실빈맥(outflowtractVT,OT-VT),섬유속심실
빈맥(fascicularVT),유두근심실빈맥(papillarymuscle
VT),윤상심실빈맥(annularVT),기타(miscellaneous)
로분류할수있다.1
유출로심실빈맥
1.유출로심실빈맥
1)메카니즘
유출로심실빈맥은catecholamine에의한delayed
afterdepolarization에의해이루어진다.이메카니즘에
의한tachycardia는adenosine,베타차단제,칼슘차단
제로종료시킬수있다.2
2)유출로의해부학적특징
우심실 유출로(right ventricular outflow tract,
RVOT)는좌심실유출로(leftventricularoutflowtract,
LVOT)에비해좌측및앞쪽방향으로위치한다.그리
고pulmonicvalve는aorticvalve의위쪽에위치한다.
Received: June 21, 2013Revision Received: September 2, 2013Accepted: September 28, 2013Correspondence: Jung-Hoon Sung, MD, PhD, Division of Cardiology, Department of Internal Medicine, CHA Bundang Medical Center, CHA University, 351 Yatap-dong, Bundang-gu, Seongnam-si, Gyeonggi-do 463-712, KoreaTel: 82-31-780-4864, Fax : 82-31-780-5584E-mail: [email protected]
Idiopathic ventricular tachycardia
AbSTRACTVentricular arrhythmias (VAs) in structurally normal hearts can be broadly considered under non-life-
threatening monomorphic and life-threatening polymorphic rhythms. VAs are commonly seen in young
patients and typically have a benign course. Monomorphic VAs are classified on the basis of the site of origin
in the heart, and the most common areas are the ventricular outflow tracts and left ventricular fascicles. The
morphology of the QRS complexes on an electrocardiogram is an excellent tool to identify the site of origin
of the rhythm. Treatment options include reassurance, medical therapy, and catheter ablation. Very frequent
ventricular ectopy may result in cardiomyopathy in a minority of patients.
VT transition earlier than sinusV2 transition ratio ≥ 0.60
Broader R-wave duration and greater R/S-wave amplitude ratio in V1 and V2
Notch (qRS) in V1 or V2
Table 1. Electrocardiographic classification of right ventricular outflow tract ventricular tachycardia (RVOT-VT) versus left ventricular outflow tract (LVOT)/aortic cusp ventricular tachycardia (VT)
맥의발생은거의없다.좌우의판첨이심실과바로닿아
있고좌심실근섬유(musclefiber)는대동맥근부로뻗
어있어심실조기수축(prematureventricularcontrac-
tion,PVC)을만들수있다.1
대동맥판첨에서발생하는빈맥은좌판첨이가장
많고그다음이우판첨그리고좌우의판첨의접합부
(junction)에서많이발생한다.
2)심전도특징
LVOT또는대동맥판첨에서발생하는심실빈맥은좌
각차단패턴QRS에하향축을갖지만,RVOT위치보
다precordialtransition이좀더빠르다.Precordial의
R파는V3또는이보다먼저transition된다.좌판첨의
VT는V1/V2에서transition이있고우판첨은V2/3에
서나타난다.대동맥판첨에서발생하는심실빈맥은R
파가›0.5ms로좀더넓고V1,V2에서R/S파가좀더
크게나타난다.LVOT-VT는또한aorticvalve아래쪽
의LVendocardium에서도나타날수있다.빈도가낮
은LVOT-VT는aortomitralcontinuity에서나타난다
(Table1).2
4.심외막유출로심실빈맥
심실빈맥은심외막(epicardial)에서거의발생하지않
는다.MDI(maximumdeflectionindex,최초의QRS
시작에서흉부유도에서최대편향까지의시간을총
QRS기간으로나눈값)로정량화해서delayedinitial
precordialQRSactivation이0.55보다크면심외막
심실빈맥을제안한다.2LeadI의하향축인QS도심외
막임을가리킨다.Transition또는patternbreak라
해서V1toV2의R파가없어지는것(QS또는rS)이보
이고V3의R파가잘보이는것은aorticroot의앞쪽의
anteriorLV를가리킨다.이것이leadI의QS와같이보
이면심실간정맥(interventricularvein)근처의심외막
(epicardialorigin)을가리킨다.
5.예후
Outflowtract의VT는주로양성이며대부분은예후
가좋다.하지만두가지예외가있다.Shortcoupled
PVC가polymorphicVT를유발하거나죄심실기능장애
(LVdysfunction)가빈맥에의해일어나는경우이다.이
런환자들은전기생리학검사가필요하다.3
6.검사및치료
환자가전형적인monomorphicoutflowtractPVC를
보이면홀터와심초음파로진단이충분하다.만약mul-
tiplePVC가있거나위치가특이하면(freewall)MRI같
은검사를통해구조적인심장문제인 arrhythmo-
genic right ventricular dysplasia/cardiomyopathy
(ARVD/C)등이있는지고려해야한다.RVOT는be-
nign이나ARVD/C가있는경우는돌연심장사(sudden
cardiacdeath)의위험도및가족력을살펴봐야한다.4,5
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1)약물요법
증상이있는outflowtractVT에는베타차단제를일
차적으로쓴다.베타차단제를못쓰면non-dihydro-
pyridine칼슘차단제(verapamil또는diltiazem)를쓸
수있다.
2)전극도자절제술
전극도자절제술(catheterablation)은비교적안전하
고믿을만한치료방법이다.심전도localization이절제
술을시행하는데도움이되나,환자에게는위험도와치
료효과를설명해야한다.수면치료는심실빈맥을줄일
수있어서삼가야한다.Isoproterenol을이용한pacing
은심실빈맥을유발하는데도움이된다.3Dmapping
이절제술에도움이된다.Activationmapping은환자
에서PVC나VT가잘나오면사용할수있고,bipolar
electrogram의earliestactivation이surfaceQRS보다
20-40ms앞설때성공적인절제부위로고려할수있
다.Bipolarelectrogram으로는일반적으로날카로운신
속한초기편향을가지고있으며,sinusrhythm동안후
반편향의역전(reversalofalatecomponentpresent)
을보일수있다.Unipolarelectrogram은주로QS패턴
이뾰족하고아래로향하면서surfaceQRS앞에위치하
면고려할수있다.6
Pacemapping은PVC/VT가잘나오지않을때시도
할수있다.빈맥의속도와비슷하게mappingcatheter
를pacing한다.Pacemapping의surface12심전도를
임상의VT/PVC와비교하는것이중요하다.6LVOT에
서는intracardiacechocardiography(ICE)가도움이된
다.1전극도자절제술의부작용은다른부위의절제술
과비슷하다.혈관으로접근하면서발생할수있는합
병증,심장천공(cardiacperforation),심낭압전(cardiac
tamponade),뇌졸중,심근경색등이있다.
섬유속심실빈맥
특발성좌심실빈맥(idiopathicleftVT)또는섬유속
심실빈맥은좌각(leftbundlebranch)의섬유속(fasci-
cles)에서주로발생한다.이것은심전도모양및해당
되는섬유속(correspondingfascicles)에따라left
posteriorfascicularVT,leftanteriorfascicularVT,
leftupperseptalVT로나눈다.Leftposteriorfascicu-
larVT가가장흔하고그다음이leftanterior,leftup-
perseptal순이다.
1.메카니즘
VerapamilsensitiveleftVT는reentry에의한것으
로이는심실또는심방자극에의해유도,종결된다.
2.심전도특징
Fascicular VT는 우각 차단(right bundle branch
block,RBBB)패턴QRS에leftsuperioraxis를보인다.
이것은상대적으로좁아져SVT가BBB패턴QRS와같
이있을때와혼돈될수있다.Leftposteriorfascicular
VT는우각차단패턴QRS에좌향편위(leftaxisde-
viation,LAD)가관찰되며,leftanteriorfascicularVT
의경우는우각차단패턴QRS에우향편위(rightaxis
deviation,RAD)가관찰된다.중격(septal)심실빈맥은
불완전한우각차단패턴QRS에normalaxis를보인다.
3.약물치료
Verapamil이빨리종결시키는데효과적이다.만성적
인verapamil치료는전극도자절제술을원하지않을때
사용하며,베타차단제또한효과적이다.
4.전극도자절제술
전극도자절제술은성공률이높아90%이상효과가
있다.Fascicularpotential이PVC/VTwithF-F(fas-
cicularpotential-fascicularpotential)보다앞서는것
이중요하다.EarliestPurkinjepotential이심실빈맥동
안QRS앞에나오면성공적인절제부위로고려할수
있다.
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Table 2. Specific locations and electrocardiographic features2
Left cusp “M” or “W” pattern in V1Monophasic R by V1/2Tall R-wave amplitude in inferior leadsGreater R-wave II/III ratio or III/IILead I QS or rS
Right cusp Monophasic R by V2/3Larger R-wave amplitude in lead I
R/L cusp junction QRS in lead V1-V2 (notched downstroke), QS in lead V1 (notched downstroke)
Aortomitral continuity
qR in lead V1Rs/rs complex in lead IR-wave ratio < 1 in II/IIIqR in lead V1Rs/rs complex in lead IR-wave ratio < 1 in II/III
Epicardial MDI > 55%QS in lead IQS in II, III, avF (MCV)A Q-wave ratio in avL/avR >1.4 or an S-wave amplitude >1.2 mVA “transition break,” specifically a loss of R from leads V1 to V2 (QS or rS) with prominent R by V3 (AIV);
MDI >55%QS in lead IQS in II, III, avF (MCV)A Q-wave ratio in avL/avR >1.4 or an S-wave amplitude >1.2 mVA “transition or pattern break,” specifically a loss of R from leads V1 to V2 S or rS) with prominent R by V3 (AIV)
Pulmonary artery Tall R-wave in the inferior leadsLarger Q-wave ratio in avL/avR
Larger R/S amplitude in lead V2, larger R-wave amplitude in the inferior leadsLarger Q-wave ratio in avL/avRLarger R/S amplitude in lead V2
Tricuspid annular R- or r-wave lead IR or r with overall positive polarity in aVL or r-wave IR or r with overall positive polarity in aVL
Tricuspid inflow or para-Hisian
Large R-wave in I, R-wave or flat in aVL, large R-wave in I,R-wave or flat in aVL
MDI (maximum deflection index): measured as the time from the earliest QRS onset to the maximum deflection in precordial leads, divided by the total QRS duration.QRS duration.
유두근심실빈맥
유두근심실빈맥은주로운동에의해서일어나고,
catecholamine에민감해isoproterenol또는epineph-
rine에의해유도된다.발생기전은국소성이며회귀하
지는않는다.종종multipleQRS를보이고자연히바뀌
거나절제를통해바뀐다.3
윤상심실빈맥
승모판과 삼첨판륜(tricuspid annulus)에서도 심실
빈맥이발생한다.각각의발생률은비슷하여삼첨판은
5-8%,승모판은약5%이다.
승모판륜(mitralannular)심실빈맥
승모판륜심실빈맥은해부학적으로구분된다.주로
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anteriormitralannulus에서나오며posteriororpos-
teroseptalannulus는드물다.심전도는우각전도차단
패턴의monophasicR또는RsinleadV2-V6가보인
다.전극도자절제술은매우성공적이고이는earliest
ventricularactivation또는12/12pacemapmatch를
통해된다.
삼첨판륜심실빈맥
삼첨판륜심실빈맥은8%에서나타나며우측심실빈
맥의5%에서보인다.Septalsite는자유벽보다더많다
고보고되었지만,다른결과를보인연구도있다.
기타
1.우심실에서발생하는부정맥
ARVD/C는다른심실빈맥과감별이중요하다.
2.CruxoftheHeart
이곳은중간심장정맥(middle cardiac vein)과관상
부비동(coronarysinus)의교차점에가깝게위치한심
외막지점이다.심전도는leftsuperioraxis및early
precordial transition과 delayed deflection을보인다
(Table2).2
결론
특발성심실빈맥은심실빈맥이구조적으로정상이며
반흔이없는심장에서발생하는경우이다.분류하면유
출로심실빈맥,다발성심실빈맥,유두근심실빈맥,윤
상심실빈맥,기타등으로구분된다.이런심실빈맥은주
로젊은환자에서비교적좋은예후를보인다.12-lead
심전도로일반적인발생위치를확인할수있고,특이한
유형의경우결정적으로구별하는데에도도움이된다.2
심실빈맥의기전을이해하고약물치료를하거나전극
도자절제술을시행하는것이도움이된다.
References
1. Prystowsky EN, Padanilam BJ, Joshi S, Fogel RI. Ventricular arrhythmias in the absence of structural heart disease. J Am Col Cardiol. 2012;59:1733–1744.2. Hoffmayer KS, Gerstenfeld EP. Diagnosis and management of idiopathic ventricular tachycardia. Curr Probl Cardiol. 2013;38: 131-158.3. European Heart Rhythm Association; Heart Rhythm Society,
Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, Gregoratos G, Klein G, Moss AJ, Myerburg RJ, Priori SG, Quinones MA, Roden DM, Silka MJ, Tracy C, Smith SC Jr, Jacobs AK, Adams CD, Antman EM, Anderson JL, Hunt SA, Halperin JL, Nishimura R, Ornato JP, Page RL, Riegel B, Priori SG, Blanc JJ, Budaj A, Camm AJ, Dean V, Deckers JW, Despres C, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Tamargo JL, Zamorano JL; American College of Cardiology; American Heart Association Task Force; European Society of Cardiology Committee for Practice Guidelines. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guide lines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol. 2006;48:e247-346.
4. Kiès P, Bootsma M, Bax JJ, Zeppenfeld K, van Erven L, Wijffels MC, van der Wall EE, Schalij MJ. Serial reevaluation for ARVD/C is indicated in patients presenting with left bundle branch block ventricular tachycardia and minor ECG abnormalities. J Cardiovasc Electrophysiol. 2006;17:586-593.
5. Lee HW, Kim JB, Joung B, Lee MH, Kim SS. Successful catheter ablation of focal automatic left ventricular tachycardia presentedwith tachycardia-mediated cardiomyopathy. Yonsei Med J.2011;52:1022-1024.
6. Takemoto M, Yoshimura H, Ohba Y, et al. Radiofrequency catheter ablation of premature ventricular complexes from right ventricular outflow tract improves left ventricular dilation and clinical status in patients without structural heart disease. J Am Coll Cardiol. 2005;45:1259-1265.
7. Hasdemir C, Ulucan C, Yavuzgil O, Yuksel A, Kartal Y, Simsek E, Musayev O, Kayikcioglu M, Payzin S, Kultursay H, Aydin M, Can LH. Tachycardia-induced cardiomyopathy in patients with idiopathic ventricular arrhythmias: the incidence, clinical and electrophysiologic characteristics, and the predictors. J Cardiovasc Electrophysiol. 2011;22:663-668.
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서론
심장질환에서대표적인심근경색은심장에반흔(scar)
을형성하여이와관련한심실부정맥을유발한다.이러
한심근경색후발생하는심실빈맥(post-infarctven-
triculartachycardia)은발생시기에따라급성기와만
성기로나눠볼수있는데,심근경색의급성기에는심실
세동(ventricularfibrillation)으로이어지는다형성심실
빈맥(polymorphicventriculartachycardia)이흔하다.
경색후수주가지나면서경색부위에구조적인변화가
발생하는데,경색후발생되는섬유화는전도차단을일
으키고경색주위의경계부위(borderzone)에서는전
도속도가느려지는현상이일어나면서이로인한회귀
성경로가형성되는것으로알려져있다1.최근심근경색
에대한치료가발전하면서이에따라심근경색이후발
생하는심실빈맥의빈도가감소하게되었는데,경색초
경희대학교 의과대학 내과학교실 김 진 배
Jin-Bae Kim, MD, PhDCardiology Division, Department of Internal Medicine, Kyung Hee University College of Medicine, #1, Hoegi-dong, Dongdaemun-gu, Seoul, Korea
허혈성 심근증 환자에서 심실빈맥
Received: May 27, 2013Accepted: September 28, 2013Correspondence: Jin-Bae Kim, MD, PhD, Cardiology Division, Department of Internal Medicine, Kyung Hee University College of Medicine, #1, Hoegi-dong, Dongdaemun-gu, Seoul, Korea 130-702Tel: 82-2-958-8200, Fax: 82-2-968-1848E-mail: [email protected]
Ventricular tachycardia in ischemic cardiomyopathy
AbSTRACTDespite the decreased incidence of coronary artery disease, several studies showed that the
ischemic ventricular tachycardia (VT) are most common type of ventricular tachycardia. Ischemic
VTs have been known to arise in the ventricular scar or border zone, consisting of the reentry
circuit. Therefore, reentry has been accepted as the principal mechanism of ischemic VT. However,
recent studies showed a different background of the mechanism. In treatment, antiarrhythmic
agents and implantable cardioverter defibrillator (ICD) are the first line of therapy. However, some
cases require a more invasive approach, such as catheter ablation or cardiac surgery. The
techniques of these treatments have evolved for several decades, showing better clinical outcome
than before. Therefore, the management for ischemic VT should be tailored in patients with broad-
Outer loop systolic absent <Egm-QRS >0.7 =TCL Different <Egm-QRS
Entrance site
early diastolic present* =Egm-QRS <0.7 =TCL Different <Egm-QRS
Exit site late diastolic present >Egm-QRS >0.7 >TCL Same =Egm-QRS
Bystander 1 mid-diastolic* present >Egm-QRS >0.7 >TCL Same >Egm-QRS
Bystander 2 late diastolic* present >Egm-QRS >0.7 >TCL Same >Egm-QRS
Bystander 3 early diastolic* present* >Egm-QRS >0.7 >TCL Same† >Egm-QRS
*variable †depends on whether captured orthodromically or antidromically
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반면,혈역학적으로불안정한경우는빈맥에대한자세
한지도화가불가능하기때문에빈맥의발생과유지에
결정적역할을하는심실의기질에대한지도화및이
에대한절제술이진행된다.회귀기전에대한이해와
반흔사이의잠재적회귀로를확인하는방법등이발전
함에따라여러다른회귀로에의한심실빈맥이나불
안정형심실빈맥에대한전극도자절제술에의한치료
가확대되기에이르렀다(Figure1,Table1).9,10특히삼
차원입체전기해부학적지도화(3Delectroanatomical
mapping)는전기생리학적자료를3차원으로구현된
해부학적자료와결부함으로써,경색으로인한반흔의
부위와정상부위,경계부위를시술자에게직관적으로
Figure 2. Voltage mapping of substrate with 3D electroanatomic mapping system (CARTO®) not published data)
V1
MAPp
MAPd
V1
MAPp
MAPd
V1
MAPp
MAPd
V1
MAPp
MAPd
V1
MAPp
MAPd
V1
MAPp
MAPd
V1
MAPp
MAPd
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제공하여시술이더욱용이하게되었다(Figure2).최
근Michigan그룹에서발표한24명의심근경색환자를
대상으로하는후향적연구에의하면반흔사이의채널
이모두심실빈맥과관련되어있지않고,latepotential
과함께존재하는채널이심실빈맥과연결된결정적경
로(criticalpathway)임을확인하였다.13이보고는기존
의구조적질환과동반된심실빈맥의전극도자절제술
의연구와일관된결과를보여주고있다.예를들면부
정맥유발형우심실이형성증(arrhythmogenicright
ventriculardysplasia)이나브루가다증후군에서도
비슷한결과를보여주고있다.14-16또하나심내막뿐아
니라심외막에서도심실빈맥의유발이가능하기에동시
에두부위에접근할필요가있는경우도고려해야한다.
최근증례보고에서심장이식수술을받은심실빈맥환
자의전극도자절제술후심장병리소견을보면lesion
size를증폭시키는irrigationtipcatheter를사용했음에
도transmurallesion을얻지못하였음을알수있다.이
는심실빈맥치료시심내막으로의접근으로심외막에
서유래하는심실빈맥이나심외막을결정적경로로이
용하는심실빈맥을치료할수없음을반증하며,반드시
심외막에대한접근도고려해야함을시사한다.17또한
2013년UCLA의Tung등이발표한자료를보면비허혈
성심실빈맥환자에비해허혈성심실빈맥의경우심내
막,심외막양쪽으로모두전극도자절제술을시행한환
자군에서심실빈맥의재발이의미있게적었음을알수
있었다.이는허혈성심실빈맥의전극도자절제술을시
행하는경우반드시심내막과더불어심외막으로접근
하는것도함께고려해야함을뒷받침한다.18
3.심실빈맥의수술치료
심근경색후발생하는심근의재형성과심실류(ven-
tricular aneurysm)와관련하여발생하는심실부정
맥의치료목적으로수술적교정(surgical correction
or left ventricular aneurysmectomy)이시도되었다.
1970~1980년대초기성적은항부정맥제치료성적에
비해좋았으나수술후조기사망률이문제가되었고,
1990년대Dor등이수술법을변형한subtotalendo-
cardiectomy를시행하여좋은결과를얻었으며,이후
cryoablation이도입되면서수술후심기능향상및심실
부정맥을줄이는결과를얻을수있었다.19-22하지만수
술적응증에해당하지않는환자들에게는도움이되지
않고,수술경험이많은기관과적은기관의성적차이
가커치료법이확대되지는못하였다.현재에는관상동
맥질환에심한심근재형성이동반되어수술치료를고
려할때부가적인치료로받아들여지고있는실정이다.
결론
허혈성심실빈맥은관상동맥치료가발전함에따라
그발생빈도가줄었지만,아직도가장많은형태의심실
빈맥이며예후가좋지않아적극적인치료가필요하다.
현재ICD의보편화로허혈성심실빈맥으로인한사망률
은줄었으나이로인해더많은부정맥이발견되고ICD
shock으로인해환자불편감이증가한경우전극도자절
제술이부가적인의미로중요한치료법이될수있다.
현재시행되고있는전극도자절제술에대한이론적
발전과기술의발전으로인하여시술에대한성적이향
상되고있고,아직도많은부분에서발전할여지가있기
에보다더좋은결과가나올것으로예상된다.또한카
테터를이용한치료외에도국한된환자군에서는수술
적치료도고려해야할것이다.
References
1. Wit A, Janse MJ. The ventricular arrhythmia of ischemia and infarction: Electrophysiological mechanisms. Mount Kisco, NY: Futura; 1993.
2. Andresen D, Steinbeck G, Brüggemann T, Müller D, Haberl R, Behrens S, Hoffmann E, Wegscheider K, Dissmann R, Ehlers HC. Risk stratification following myocardial infarction in the thrombolytic era. J Am Coll Cardiol.1999;33:131–138.
3. Das MK, Scott LR, Miller JM. Focal mechanism of ventricular tachycardia in coronary artery disease. Heart Rhythm. 2010;7:305–311.
4. Johnson CM, Pogwizd SM. Focal initiation of sustained and nonsustained ventricular tachycardia in a canine model of ischemic cardiomyopathy. J Cardiovasc Electrophysiol. 2012;23: 543–552.
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5. The ESVEM investigators. Determinants of predicted efficacy ofantiarrhythmic drugs in the electrophysiologic study versus electrocar diographic monitoring trial. Circulation. 1993;87:323–329.
6. The Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implanable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med. 1997;337:1576–1583.
7. Connolly SJ, Gent M, Roberts RS, Dorian P, Roy D, Sheldon RS,Mitchell LB, Green MS, Klein GJ, O'Brien B. Canadian implantable defibrillator study (CIDS); a randomized trial of the implantable cardioverter defibrillator against amiodarone. Circulation. 2000;101:1297–1302.
8. Kuck KH, Cappato R, Siebels J, Rüppel R. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest. The cardiac arrest study Hamburg (CASH). Circulation. 2000;102:748–754.
9. Marchlinski FE, Callans DJ, Gottlieb CD, Zado E. Linear ablationlesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation. 2000;101:1288–1296.
10. Soejima K, Suzuki M, Maisel WH, Brunckhorst CB, Delacretaz E, Blier L, Tung S, Khan H, Stevenson WG. Catheter ablation in patients with multiple and unstable ventricular tachycardias after myocardial infarction: short ablation lines guided by reentry circuit isthmuses and sinus rhythm mapping. Circulation. 2001;104:664–669.
11. Stevenson WG, Friedman PL, Sweeney MO. Catheter ablation as an adjunct to ICD therapy. Circulation. 1997;96:1378–1380.
12. Strickberger SA, Man KC, Daoud EG, Goyal R, Brinkman K, Hasse C, Bogun F, Knight BP, Weiss R, Bahu M, Morady F. A prospective evaluation of catheter ablation of ventricular tachycardia as adjuvant therapy in patients with coronary artery disease and implantable cardioverter-defibrillator. Circulation.1997;96:1525–1531.
13. Mountantonakis SE, Park RE, Frankel DS, Hutchinson MD, Dixit S, Cooper J, Callans D, Marchlinski FE, Gerstenfeld EP. Relationship between voltage map "channels" and the location of critical isthmus sites in patients with post-infarction cardiomyopathy and ventricular tachycardia. J Am Coll Cardiol. 2013;61:2088-2095.
14. Jaïs P, Maury P, Khairy P, Sacher F, Nault I, Komatsu Y, Hocini M,
Forclaz A, Jadidi AS, Weerasooryia R, Shah A, Derval N, Cochet H, Knecht S, Miyazaki S, Linton N, Rivard L, Wright M, Wilton SB, Scherr D, Pascale P, Roten L, Pederson M, Bordachar P, Laurent F, Kim SJ, Ritter P, Clementy J, Haïssaguerre M. Elimination of Local Abnormal Ventricular Activities : A New End Point for Substrate Modification in Patients With Scar-Related Ventricular Tachycardia. Circulation. 2012;125:2184-2196.
15. Marcus FI, Abidov A. Arrhythmogenic right ventricular cardiomyopathy 2012: diagnostic challenges and treatment. J Cardiovasc Electrophysiol. 2012;23:1149–1153.
16. Nademanee K, Veerakul G, Chandanamattha P, Chaothawee L,Ariyachaipanich A, Jirasirirojanakorn K, Likittanasombat K, Bhuripanyo K, Ngarmukos T. Prevention of ventricular fibrillation episodes in Brugada syndrome by catheter ablation over the anterior right ventricular outflow tract epicardium. Circulation. 2011;123:1270-1279.
17. Kelesidis I, Yang F, Maybaum S, Goldstein D, D'Alessandro DA, Ferrick K, Kim S, Palma E, Gross J, Fisher J, Krumerman A. Examination of explanted heart after radiofrequency ablation for intractable ventricular arrhythmia. Circ Arrhythm Electrophysiol.2012;5:e109 –110.
18. Tung R, Michowitz Y, Yu R, Mathuria N, Vaseghi M, Buch E, Bradfield J, Fujimura O, Gima J, Discepolo W, Mandapati R, Shivkumar K. Epicardial ablation of ventricular tachycardia: an institutional experience of safety and efficacy. Heart Rhythm. 2013;10:490–498.
19. Guiraudon G, Fontaine G, Frank R, Escande G, Etievent P, Cabrol C. Encircling endocardial ventriculotomy: A new surgical treatment for life-threatening ventricular tachycardias resistant to medical treatment following myocardial infarction. Ann Thorac Surg.1978; 26:438–444.
20. Josephson, M. E., Harken, A. H., Horowitz, L. N. Endocardial excision: A new surgical technique for the treatment of recurrent ventricular tachycardia. Circulation. 1979;60:1430–1439.
22. Dor V, Sabatier M, Montiglio F, Rossi P, Toso A, Di Donato M. Results of nonguided subtotal endocardiectomy associated with left ventricular reconstruction in patients with ischemic ventricular arrhythmias. J Thorac Cardiovasc Surg. 1994;107:1301–1307.
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서론
확장성심근증(dilatedcardiomyopathy,DCM)은좌
심실또는양심실의확장과심근수축기능저하를특징
으로하는심근병증으로서울혈성심부전의중요한원
인이되며,질병의경과중심실성또는심방성부정맥
이잘생기고급사의발생이증가하는것으로알려져있
다.1,2특히심실빈맥은DCM이동반된환자에서급사와
연관되는주요한원인이다.본논문에서는DCM환자에
서의심실빈맥의임상양상,발생관련인자,발생기전,
DCM의예후와관련된예측인자,치료방법등에대해
요약해서다루고자한다.
DCM환자에서의심실빈맥및급사
전체심부전환자의약50%는부정맥에의한급사
이고나머지50%정도는심부전의악화로인해사망
하는것으로알려져있으며,심부전증상이심해질수
록부정맥에의한급사보다는진행되는심부전으로사
확장성 심근증 환자에서 심실빈맥
세종병원 심장내과 김 진 석
Jin-Seok Kim, MD.Department of Cardiology, Sejong Cardiovascular Center, Sejong General Hospital, Bucheon, Gyeonggi-do, Korea
Received: May 30, 2013Accepted: September 28, 2013Correspondence: Jin-Seok Kim, MD, Department of Cardiology, Sejong Cardiovascular Center, Sejong General Hospital, Bucheon, Gyeonggi-do, Republic of KoreaTel: 82-32-340-1154, E-mail: [email protected]
Ventricular tachycardia in patients with dilated cardiomyopathy
AbSTRACTDilated cardiomyopathy (DCM) is the most common cardiomyopathy characterized by left or
biventricular dilatation and systolic dysfunction. Ventricular tachycardia (VT) may be an important
cause of sudden death and morbidity in patients with DCM. Although advances in both drug and
device therapy have led to an improvement in overall survival of patients with DCM, symptomatic
VT and the risk of sudden death are still issues that must be considered. Recent advances in
catheter ablation technology have led to an improved success rate, and they have facilitated the
24 The Official Journal of Korean Heart Rhythm Society
명확하지않다.또한NSVT를가진환자들에서급사의
고위험군을평가하기위한방법으로신호평균화심전
도(signalaverageelectrocardiogram),전기생리학검
사등이이용되어왔으나,DCM환자에서의그유용성
은아직확실하지않다.15
약물치료및device치료
DCM환자에서의안지오텐신전환효소억제제,안지
오텐신수용체차단제,베타차단제등을이용한약물치
료는좌심실기능저하를개선하여생존율을향상시키는
것으로알려져있다.하지만장기간의약물치료에도호
전이없는경우이식형제세동기(implantablecardio-
verterdefibrillator,ICD)나심장재동기화치료(cardiac
resynchronizationtherapy,CRT)등이도움이될수
있다.ICD는허혈성혹은비허혈성심근병증또는심
실기능이낮고증상을동반하는지속성심실빈맥을가
진환자의이차예방효과에서amiodarone보다우월
하다는것이입증되었다.16고위험군에서ICD의일차적
예방역할또한DEFINITE(DefibrillatorinNon-Is-
chemicCardiomyopathyTreatmentEvaluation)연구
와SCD-HeFT(SuddenCardiacDeathHeartFailure
Trial)연구등을통해긍정적으로보고되었다.DEFI-
NITE연구에서ICD는DCM환자에서부정맥에의한
사망률을80%낮추고,이러한사망률의감소는NYHA
classII보다는III의환자에서보다큰것으로보고되었
다.17SCD-HeFT연구에서는NYHAclassII혹은III의
심부전을가지고좌심실구혈률이35%미만인관상동
맥질환혹은비허혈성DCM환자에서표준약물치료와
amiodarone을사용한경우전체사망률개선효과는없
었으나,ICD를시술한군에서는5년후에7.2%의의미
있는사망률감소를보였다.18
DCM환자의30~50%에서심전도상심실내전도
장애 및 좌각차단이 동반되는 것으로 알려져 있다.
CRT의경우NYHAclassIII또는IV,좌심실구혈률
35%미만,QRS파의간격이120ms이상이면서좌심
실의dyssynchrony를가진심부전환자를대상으로
한 CARE-HF (CArdiac REsynchronisation in
HeartFailure)와COMPANION(Comparisonof
MedicalTherapy,Pacing,andDefibrillationin
HeartFailure)연구등에서사망률및유병률을낮추
는데효과가있음을보여주었다.19,20
전극도자절제술
ICD가DCM환자의사망률은감소시키지만,증상을
동반하는심실빈맥의재발을예방하지는못한다.또한
고위험도환자에서일차적예방목적으로ICD를삽입
한환자중2.5~12%가부정맥을경험하는것으로알려
져있다.21따라서전극도자절제술의역할이중요시되고
있으며,심실빈맥에대한전극도자절제술은3차원영상
의전기해부학적mapping시스템의도입등기술적발
전과더불어서그치료성공률또한향상되고있다.특
히전극도자절제술은DCM환자에서자주관찰되는각
회귀심실빈맥에효과적일수있다.
결론
DCM환자에서심실빈맥의치료목적은첫째,급사의
위험을줄이는것이고,둘째,증상을동반하는심실빈맥
발현을최소화하는것이다.DCM환자는좌심실의기능
저하가악화됨에따라급사및심부전과관련된사망이
증가하는것으로보고되었다.그러나베타차단제,안지
오텐신전환효소억제제및안지오텐신수용체차단제등
의약물치료및의료기치료가발전됨에따라전반적인
생존율이높아지고있다.이와함께DCM의유병률또
한높아지고,심실성부정맥의빈도가높아짐에따라이
에대한적절한치료가요구된다.최근전극도자절제술
의발전으로DCM에동반된심실빈맥에서이를이용한
치료성공률이점차높아지고있다.
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References
1. Komajda M, Jais JP, Reeves F, Goldfarb B, Bouhour JB, Juillieres Y,Lanfranchi J, Peycelon P, Geslin P, Carrie D, Grosgogeat Y. Factorspredicting mortality in idiopathic dilated cardiomyopathy. Eur Heart J. 1990;11:824-831.
2. Sugrue DD, Rodeheffer RJ, Codd MB, Ballard DJ, Fuster V, Gersh BJ. The clinical course of idiopathic dilated cardiomyopathy. A population-based study. Ann Intern Med. 1992;117:117-123.
3. Effect of metoprolol cr/xl in chronic heart failure: Metoprolol cr/xl randomised intervention trial in congestive heart failure (merit-hf).Lancet. 1999;353:2001-2007.
4. Larsen L, Markham J, Haffajee CI. Sudden death in idiopathic dilated cardiomyopathy: Role of ventricular arrhythmias. Pacing Clin Electrophysiol. 1993;16:1051-1059.
5. Luu M, Stevenson WG, Stevenson LW, Baron K, Walden J. Diversemechanisms of unexpected cardiac arrest in advanced heart failure. Circulation. 1989;80:1675-1680.
6. Pogwizd SM, McKenzie JP, Cain ME. Mechanisms underlying spontaneous and induced ventricular arrhythmias in patients with idiopathic dilated cardiomyopathy. Circulation. 1998;98:2404-2414.
7. Hsia HH, Marchlinski FE. Characterization of the electroanatomic substrate for monomorphic ventricular tachycardia in patients with nonischemic cardiomyopathy. Pacing Clin Electrophysiol.2002;25:1114-1127.
8. Soejima K, Stevenson WG, Sapp JL, Selwyn AP, Couper G, Epstein LM. Endocardial and epicardial radiofrequency ablation of ventricular tachycardia associated with dilated cardiomyopathy: The importance of low-voltage scars. J Am Coll Cardiol. 2004;43:1834-1842.
9. Felker GM, Thompson RE, Hare JM, Hruban RH, Clemetson DE,Howard DL, Baughman KL, Kasper EK. Underlying causes and long-term survival in patients with initially unexplained cardiomyopathy. N Engl J Med. 2000;342:1077-1084.
10. Dec GW, Fuster V. Idiopathic dilated cardiomyopathy. N Engl J Med. 1994;331:1564-1575.
11. Keogh AM, Baron DW, Hickie JB. Prognostic guides in patients with idiopathic or ischemic dilated cardiomyopathy assessed for cardiac transplantation. Am J Cardiol. 1990;65:903-908.
12. Lee WH, Packer M. Prognostic importance of serum sodium concentration and its modification by converting-enzyme inhibition in patients with severe chronic heart failure. Circulation. 1986;
JK, Leier CV. Factors influencing the one-year mortality of dilated cardiomyopathy. Am J Cardiol. 1984;54:147-152.
14. Schoeller R, Andresen D, Buttner P, Oezcelik K, Vey G, Schroder R.First- or second-degree atrioventricular block as a risk factor in idiopathic dilated cardiomyopathy. Am J Cardiol. 1993;71:720-726.
15. Grimm W, Christ M, Bach J, Muller HH, Maisch B. Noninvasive arrhythmia risk stratification in idiopathic dilated cardiomyopathy: Results of the marburg cardiomyopathy study. Circulation. 2003;108:2883-2891.
16. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. The antiarrhythmics versus implantable defibrillators (avid) investigators. N Engl J Med. 1997;337:1576-1583.
17. Kadish A, Dyer A, Daubert JP, Quigg R, Estes NA, Anderson KP, Calkins H, Hoch D, Goldberger J, Shalaby A, Sanders WE, Schaechter A, Levine JH, Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation I. Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy. N Engl J Med. 2004;350:2151-2158.
18. Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, Domanski M, Troutman C, Anderson J, Johnson G, McNulty SE, Clapp-Channing N, Davidson-Ray LD, Fraulo ES, Fishbein DP, Luceri RM, Ip JH, Sudden Cardiac Death in Heart Failure Trial I. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005;352:225-237.
19. Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, Tavazzi L, Cardiac Resynchronization-Heart Failure Study I. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med. 2005;352:1539-1549.
20. Saxon LA, Bristow MR, Boehmer J, Krueger S, Kass DA, De Marco T, Carson P, DiCarlo L, Feldman AM, Galle E, Ecklund F. Predictors of sudden cardiac death and appropriate shock in the comparison of medical therapy, pacing, and defibrillation in heart failure (companion) trial. Circulation. 2006;114:2766-2772.
21. Moss AJ, Greenberg H, Case RB, Zareba W, Hall WJ, Brown MW,Daubert JP, McNitt S, Andrews ML, Elkin AD, Multicenter Automatic Defibrillator Implantation Trial IIRG. Long-term clinical course of patients after termination of ventricular tachyarrhythmia by an implanted defibrillator. Circulation. 2004;110:3760-3765.
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배경
브루가다증후군은젊은남성에서주로발생하고심
실빈맥에의해서심장돌연사가일어나는유전질환이다.
Milrinone과cilostazol등의phosphodiesterase
(PDE)3억제제는Ltypecalciumcurrent(ICaL)를증
가시키고세포내cAMP농도를상승시킨다.Cilostazol
은혈소판응집을억제하며혈관을확장시키고특히다
리쪽혈관을확장시킨다.그렇기때문에cilostazol은간
헐적파행(intermittentclaudication)그리고뇌혈관동
맥경화증과뇌졸증의2차예방에사용된다.
Milrinone은심부전증에사용하며,cAMP를증가시
켜서심부전증심장의수축력을증가시키고혈관확장
기능이있다.이연구는브루가다증후군에서milrinone
을cilostazol대신사용할수있을것으로생각되어mil-
rinone의사용가능성에대해알아보았다.
방법
관상동맥관류를하는우심실wedgepreparation을
이용하여 epicardial 그리고 endocardial site에서활
동전위(action potential, AP) 그리고 electrocardio-
graphic기록을시행하였다.Transientoutwardcur-
rent(Ito)활성제NS5806(5μM)그리고칼슘차단제
verapamil(2μM)을사용하여인위적으로브루가다표
현형을유발하였다.
결과
NS5806+verapamil을 투여하니 all-or-none re-
polarization이epicardium어떤곳에서는발생하고또
브루가다 증후군에서 milrinone 그리고 cilostazol이 부정맥 발생을 억제하는 세포 기전
고신대학교 의과대학 내과학교실 차 태 준
Tae-Joon Cha, MD, PhDDivision of Cardiology, Department of Internal Medicine, Kosin University College of Medicine, Busan, South Korea.
Received: September 10, 2013Accepted: September 28, 2013Correspondence: Tae-Joon Cha, MD, PhD, Division of Cardiology, Department of Internal Medicine, Kosin University College of Medicine, 34 Amnam-Dong, Seo-Gu, Busan, 602-702, South Korea.Tel: 051-990-6105, Fax: 051-990-3047, E-mail: [email protected]
Cellular mechanism underlying the effects of milrinone and cilostazol to suppress arrhythmogenesis associated with brugada syndrome
Szél T, Koncz I, Antzelevitch C.
Heart Rhythm. 2013 Aug 1. pii: S1547-5271(13)00795-9. doi: 10.1016/j.hrthm.2013.07.047.
[Epub ahead of print]
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Vol.14 No.3
다른곳에서는발생하지않아서epicardium의ST분절
상승,epicardialdispersionofrepolarization(EDR),
transmuraldispersionofrepolarization(TDR)등의발
생증가가일어나게되었다.이런상태에서는epicardial
APdome이유지되는곳에서APdome이유지되지않
는곳으로phase2reentry가발생하여선행하는박동
과매우근접한시점에심실기외수축,심실빈맥등이발
생하였다.Epicardium의APdome의소실은endocar-
diumAPdome사이에서TDR이발생하게된다.이런
EDRTDR등이부정맥이잘발생하게되는위험한시
점(vulnerablewindow)을만들게된다.이런것을치유
하기위해서는활동전위2기에inwardcalciumcurrent
를활성화하게하면APdome이복원화되며부정맥발
생을억제하게된다.PDEinhibitor인milrinone(2.5
μM)혹은cilostazol(5~10μM)을관상동맥으로관류시
키니epicardialAPdome을회복시키고,dispersion을
감소시키며,기외수축과심실빈맥을유발시키는phase
2reentry를소멸시켰다.Milrinone과cilostazol은in-
wardcalciumcurrent를증가시키는효과가있어서심
근의수축력을증가시키고심장박동을빠르게한다.심
장박동수가빨라지면간접적으로Ito의감소를유발시
키며,특히cilostazol은고농도에서직접적으로Ito를억
제시키는효과가있다.
결론
이연구는브루가다증후군의심전도적그리고부
정맥적인 표현인 재분극의 결함을 반전시키기 위해
cilostazol과milrinone을사용할수있음을보여주었
다.이약들은우심실epicardium에서ICa를증가시켜
서APdome을복원시키며우심실심근의전기적이질
성(heterogeneity)의발생을억제시켰다.그래서PDE3
inhibitor특히cilostazol그리고milrinone이브루가다
증후군의치료약제로사용할수있음을실험적으로증
명하였다.
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Ventricular Tachycardia Originating from the Right Ventricular Outflow Tract Terminated by Steam Pop
Introduction
Steampopsare infrequent inradiofrequency
(RF) ablation for ventricular tachycardia (VT);
although they have been reported to occur in
only1~1.5%ofallRFablations,theycancause
cardiactamponade,especiallyintherightven-
tricularoutflowtract(RVOT).1-3
CaseReport
A57-year-oldwomanpresentedtoouremer-
gencydepartmentwitha1-weekhistoryofwax-
ingandwaningpalpitationsthatworsenedand
persistedonthedayofadmission,withassociat-
eddizzinessandchestdiscomfort.Hypertension
hadbeendiagnosed2yearsearlierandwascon-
trolledbyanangiotensinreceptorblocker.Her
familyandsocialhistorywereunremarkable.Her
initial blood pressure (BP)was 130/98mmHg,
withapulserateof170beats/minandarespi-
rationrateof22breaths/min.Herelectrocardio-
gramshowedawideQRStachycardiawithleft
bundlebranchblockmorphology,inferioraxis,
QRSwidth›140ms,aVLsizeslightlygreater
thanaVR,andasmallrwaveof›0.2mVinthe
V2 lead,whichsuggestedthatthetachycardia
originatedfromtheleftsuperiorfreewallofthe
RVOT(Figure1).Rapidadministrationofintra-
venousadenosineandslowlyrepeatedinfusions
ofdiltiazemandverapamilhadnoeffect.After
Ki-Hun Kim, MDCardiology Division, Department of Internal Medicine, Haeundae Paik Hospital, Inje University College of Medicine, Busan, Korea
Received: July 19, 2013Accepted: September 28, 2013Correspondence: Ki-Hun Kim, MD, Division of Cardiology, Department of Internal Medicine, Inje University College of Medicine, Busan, KoreaTel: 82-51-797-3010, Fax: 82-51-797-3009E-mail: [email protected]
AbSTRACTSteam pops occur when tissue temperature exceeds 100°C. This can lead to tissue disruption and
sometimes subsequent cardiac tamponade, especially in thin-walled structures such as the right
ventricular outflow tract (RVOT). This event is potentially disastrous; however, in our case,
ventricular tachycardia originating from the RVOT was successfully terminated by a steam pop,
although it required pericardiocentesis and drainage.
Figure 1. Initial electrocardiogram of the ventricular tachycardia originating from the right ventricular outflow tract
A b
Figure 2. A, Catheter tip position on the ablation success point, targeting the ventricular tachycardia originating from the right ven-tricular outflow tract. Right anterior oblique view (30°). B, 3D electroanatomic mapping shows that the focus of ventricular tachycardia originated from the right ventricular outflow tract.
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Figure 4. Electrogram when the steam pop developed
Figure 3. Electrogram when the ventricular tachycardia originating from the right ventricular outflow tract was terminated. Presystolic potential at the ablation catheter (ABLd) was earlier than the surface QRS onset at lead V2 by approximately 22 ms.
Figure 5. Final electrogram after the steam pop showing sinus rhythm
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portable transthoracic echocardiography, peri-
cardiocentesiswithdrainagewasperformed.Af-
terdrainage,thepatient’sBPimprovedto100/70
mmHg.Fortunately,afterthisevent,nomore
VPCsorVTswereobservedfor›30min(Figure
5).Wefinishedtheprocedure,keepingtheperi-
cardialdrainageinplace.After3daysofsup-
portivecare,shewasdischarged.Therewereno
furthereventsoverthe2-yearfollow-upperiod.
Discussion
RFablationcauseslesiondevelopmentbyin-
ducingcelldeathwhentissuetemperatureex-
ceeds 50°C; however, it can also cause steam
pops when the tissue temperature is ›100°C,
sometimesfarexceedingthecathetertiptem-
perature.1,3Whensteamexplosionsoccur,which
maybeaudible as steampops, they can cause
cardiac perforation. This dangerous situation
occursmore commonly in theRV than in the
leftventriclebecauseofthethin-walledstruc-
tureoftheRV.2,4ExternallyirrigatedRFablation
cancool thecatheter-tissue interface,making
itpossibletoincreasepowerdeliveryandreduce
coagulumformation.However,irrigatedRFalso
causesanimbalancebetweentissueandcatheter
tip temperaturesduringablation, causingdif-
ficultyinpredictingsteampops.3Cooperetal.
foundarelationshipbetweenpopsandelectrode
temperatureduringatrialablationandrecom-
mendedmaintainingacathetertiptemperature
‹40°Ctopreventsteampops.5However,steam
popswereobservedwhenthemeancathetertip
temperaturewas39°Cwithopenirrigationand
evenoccurredwithcathetertiptemperaturesas
lowas34°C.1Yokoyamaetal.demonstratedthat
steampopsoccurredmorefrequentlyaspower
wasincreasedfrom30to50W.6Hsuetal.sug-
gestedthatpopsoccurredwhenpowerexceeded
48W,andpopformationwaslimitedwhenpow-
erremainedunder42W.7However,Seileretal.
showednosignificantdifferencebetweenpower
settingsforlesionswithandwithoutpops,and
foundthatlimitingRFpowertoachieveanim-
pedancedecreaseof‹18Ωisafeasiblemethod
of reducing steam pops.1 Nonetheless, higher
maximum energies and larger impedance falls
areassociatedwithsteampops.4Koruthetal.
demonstratedthatsteampopscanbepredicted
bytherateoftemperatureriseandthemaximum
volumetrictemperaturemeasuredbymicrowave
radiometry during irrigated RF ablation.3 In-
creasing contact force also was proportionally
associatedwithmoresteampops.8Inourcase,
therelativelyhighpower(45W)andtechnically
increasingcontactforcemayhavebeenrelated
causesofthesteampops,butwecouldnotcheck
thespikeinimpedancebecauseoftheunstable
situation.WhethertheVTfocuswasabolished
byelevatedRFpowerdeliveryorthesteampop,
theinterpretationwastangled.Anywaycareful
handlingoftheablationcatheterandmonitor-
ingofimpedanceandcathetertiptemperature,
andpossiblyalowpowersetting,isrequiredto
preventsteampops.
References
1. Seiler J, Roberts-Thomson KC, Raymond JM, Vest J, Delacretaz E, Stevenson WG. Steam pops during irrigated radiofrequency ablation: feasibility of impedance monitoring for prevention. Heart Rhythm. 2008;5:1411-1416.
2. Tokuda M, Kojodjojo P, Epstein LM, Koplan BA, Michaud GF, Tedrow UB, Stevenson WG, John RM. Outcomes of cardiac perforation complicating catheter ablation of ventricular arrhythmias. Circ Arrhythm Electrophysiol. 2011;4:660-666.
3. Koruth JS, Dukkipati S, Gangireddy S, McCarthy J, Spencer D, Weinberg AD, Miller MA, D'Avila A, Reddy VY. Occurrence of
33
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Steam Pops During Irrigated RF Ablation: Novel Insights from Microwave Radiometry. J Cardiovasc Electrophysiol. 2013 [Epub ahead of print].
4. Tokuda M, Tedrow UB, Stevenson WG. Silent steam pop detected by intracardiac echocardiography. Heart Rhythm. 2012 [Epub ahead of print].
5. Cooper JM, Sapp JL, Tedrow U, Pellegrini CP, Robinson D, Epstein LM, Stevenson WG. Ablation with an internally irrigated radiofrequency catheter: learning how to avoid steam pops. Heart Rhythm. 2004;1:329-333.
6. Yokoyama K, Nakagawa H, Wittkampf FH, Pitha JV, Lazzara R, Jackman WM. Comparison of electrode cooling between internal
and open irrigation in radiofrequency ablation lesion depth and incidence of thrombus and steam pop. Circulation. 2006;113:11-19.
7. Hsu LF, Jais P, Hocini M, Sanders P, Scavee C, Sacher F, Takahashi Y, Rotter M, Pasquie JL, Clementy J, Haissaguerre M. Incidence and prevention of cardiac tamponade complicating ablation for atrial fibrillation. Pacing Clin Electrophysiol. 2005;28 Suppl 1:S106-109.
8. Yokoyama K, Nakagawa H, Shah DC, Lambert H, Leo G, Aeby N, Ikeda A, Pitha JV, Sharma T, Lazzara R, Jackman WM. Novel contact force sensor incorporated in irrigated radiofrequency ablation catheter predicts lesion size and incidence of steam pop andthrombus. Circ Arrhythm Electrophysiol. 2008;1:354-362.
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A Case of Left Bundle Branch Block-shaped wide QRS Complex Tachycardia with diagnostic Ambiguity on a Surface Electrocardiogram
Introduction
In cases of tachycardia with a broad QRS
complex, it is important to differentiate be-
tween supraventricular tachycardia (SVT) and
ventriculartachycardia(VT).Electrocardiogram
(ECG)-based differential diagnoses include VT
vs. SVTwith aberrant conduction, pre-exist-
ingbundlebranchblock(BBB),intraventricular
conduction disturbances, and pre-excitation.
Severalcriteriahavebeendescribedfordiffer-
entiationbetweenVTandSVTinthepresence
ofawideQRScomplex.Wereportacaseofwide
QRScomplextachycardiawithleftBBB(LBBB)
morphologyandaretrogradePwaveonthesur-
faceECG.
Casereport
A78-year-oldwomanpresentedtoourhos-
pitalwithpalpitationsandchestdiscomfort.She
hada6-yearhistoryofnon-STsegmenteleva-
tion myocardial infarction (MI); however, she
hadnotreceivedtreatment.Onphysicalexami-
nation,bloodpressure,pulserate,andrespira-
toryratewere94/63mmHg,171bpm,and18/
min,respectively.Echocardiographyrevealedan
enlargedleftventricle(5.7cm)andleftatrium
(5.0cm)withpreservedleftventricularsystol-
ic function (ejection fraction, 53%).Therewas
moderatehypokinesiaontheinferiorwallfrom
thebasetotheapexandfromthemid-postero-
lateralwalltotheapexoftheposterolateralwall.
Min-Soo Ahn, MD Cardiology Division, Department of Internal Medicine, Wonju College of Medicine, Yonsei University, Wonju, Korea
Received: July 7, 2013Revision Received: August 28, 2013Accepted: September 28, 2013Correspondence: Min-Soo Ahn, MD, Department of Internal Medicine, Wonju College of Medicine, Yonsei University, 162 Ilsan-dong, Wonju, 220-701. Korea. Tel: +82-33-741-0909 Fax: +82-33-741-1219E-mail: [email protected]
AbSTRACTA 78-year-old woman presented with palpitations and wide QRS complex tachycardia with left
bundle branch block morphology on an electrocardiogram (ECG). The Brugada algorithm
suggested that the tachycardia was supraventricular in origin. However, electrophysiological study
showed that the tachycardia was ventricular in origin with 1:1 ventriculoatrial conduction. Here,
we report a case of broad complex tachycardia with diagnostic ambiguity on a surface ECG.
Figure 1. Initial surface 12-lead ECG (A) and the ECG after administration of diltiazem (B).
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Figure 3. Atrial pacing during tachycardia revealed atrioventricular dissociation. The response immediately after cessation of atrial pacing was a ventricular-ventricular-atrial response.
Figure 2. Surface electrodcardiogram with intracardiac electrograms was displayed from top to bottom. Wide tachycardia that was identical with clinical tachycardia was induced with ventricular pacing. Immediately after cessation of ventricular pacing, another mor-phology of PVC was observed and tachycardia was sustained. That was fusion beat. The arrow indicates a fusion beat.
⬅
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withnoQwave.Thetachycardiawasterminated
bya10mgintravenousdoseofdiltiazem(Fig-
ure 1B).Basedon theBrugadaalgorithm, the
ECGfindingsofthispatientstronglysuggesteda
tachycardiaofsupraventricularorigin.1
Afterinformedconsentwasobtained,thepa-
tient underwent a cardiac electrophysiological
study.Multipolarelectrodecathetersweread-
vancedintothefemoralveinandpositionedin
the right atrium, His-recording region, right
ventricularapex,andcoronarysinus.Retrograde
conductionwasexistedviatheatrioventricular
(AV)node.Afusionbeatwasobservedimmedi-
atelyaftercessationofventricularpacing,anda
sustainedtachycardia,whichwasmorphologi-
callyidenticaltothepatient’sclinicaltachycar-
dia,wasinduced.Duringtachycardia,theven-
tricularelectrogramprecededeachHispotential,
and1:1ventriculoatrialconductionwasobserved
(Figure2).Thistachycardiawasentrainedwith
ventricularpacingattherightventricularapex,
andthedifferencebetweenthepost-pacingin-
tervalandthetachycardiacyclelengthwas103
ms. Atrial pacing during tachycardia revealed
AVdissociationandaventricular–ventricular–
atrialresponse,whichwasobservedimmediately
afterthelastatrialpacedcomplex(Figure3).The
morphologyofthetachycardiawaschanged,and
thetachycardiawasterminated(Figure4).Be-
causethetachycardiahadbeenconsideredsu-
praventricularinoriginbeforeelectrophysiologic
study,a3Dmappingsystemwasnotprepared,
andtheprocedurewasfinished.
Discussion
WideQRScomplextachycardiastillpresentsa
diagnosticchallengewitha12-leadECG.ECG-
baseddifferentialdiagnosesincludeVTvs.SVT
withaberrantconduction,pre-existingBBB,in-
Figure 4. Change in tachycardia morphology
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traventricularconductiondisturbances,andpre-
excitation.VTisthemostimportantdifferential
diagnosisbecauseofitsunfavorableprognosis.
An accurate diagnosis with immediate treat-
mentisusuallyrequired.Adelayeddiagnosisof
VToramisdiagnosisfollowedbyinappropriate
intravenousadministrationofdrugsusedforthe
treatmentofSVT,suchasverapamilandadeno-
sine,cancauseseverehemodynamicdeteriora-
tionandmayprovokeventricularfibrillationand
cardiacarrest.
SurfaceECGmayprovideimportantcluesfor
theclassificationofatachycardiaaseitherSVT
orVT.In1978,Wellensetal.notedthatamong
LBBBtachycardias,QRorQScomplexesinlead
V6favoredadiagnosisofVT,althoughallother
QRSmorphologiesinthisleadwerenonspecific,
andsignificantQwavesinV6occurredinfre-
quentlyinpatientswithVT.2However,Kindwall
etal.determined thatSVTwithLBBBexhib-
itedfeaturesofintactrightbundlebranchcon-
duction, reflected in a frequent occurrence of
small,narrow(‹30ms)Rwavesintheanterior
precordial leads (V1andV2) followedbyrapid
andabruptnegativeSwaveswithcorrespond-
ingRtonadirofSintervalsof‹60ms.Incon-
trast,anRwaveduration›30ms,notchedand
slurreddownstrokestotheSwaves,and/orRto
nadirofSintervalsof›60msinleadsV1orV2
favoredthediagnosisofVT,asdidQwavesin
leadV6.3Basedonamodificationoftheseobser-
vations,Brugadaetal.developedanalgorithm
fordifferentiationofwidecomplextachycardia.
TheabsenceofanRScomplexoranRtonadir
ofSintervalof›100msinanyprecordiallead
strongly favorsVT. Ifneitherof thesecriteria
aresatisfied,thepresenceofAVdissociationor,
inthecaseofLBBBmorphologies,anotchedS
waveinV1orQwaveinV6alsosuggestVT.
Taken in sequence, the algorithm provides a
sensitivityandspecificityof98.7%and96.5%,
respectively,forthediagnosisofVT.However,in
additiontotheambiguityofdiagnosis,itisdif-
ficulttomeasureprecisefiguresatapaperspeed
of25mm/s,asthedifferencebetween30and
40msis0.25mm.Thesefactors,incombina-
tionwiththedifficultyindeterminingtheonset
oftheinitialdeflectionoftheQRScomplex,led
toadegreeof inter-observervariation inthis
study,therebyreducingtheobjectivediagnostic
potentialofthetechnique.In1991,Griffithetal.
performedamultivariateanalysisin102patients
toidentifywhichof15clinicalor11ECGvariables
are independent predictors ofVT. They found
thatthefollowingfactorsassisteddiagnosisof
VT:(i)PreviousMIisanindependentpredictor
ofVT.(ii)Apredominantnegativedeflectionin
leadaVFissuggestiveofVT,especiallywhena
QwaveispresentinrightBBB(RBBB)pattern
tachycardia.InLBBBpatterntachycardia,aQS
orqRwaveforminleadaVFishighlysuggestive
ofVT,whereasanRscomplexisspecificforSVT.
(iii)InRBBBpatterntachycardia,amonophasic
orbiphasicwaveforminleadV1suggestsVTand
atriphasicRSR,rSRconfigurationsuggestsSVT.
(iv)A≥40°changeinaxisbetweensinusrhythm
andtachycardiaisanindependentpredictorof
VT.Ifnoneoftheabovevariablesareobserved,
thediagnosisisalmostcertainlySVT.Ifonecri-
terionisnoted,thediagnosisisprobablySVT.If
2criteriawerenoted,thediagnosisisprobably
VT.If3or4criteriaareobserved,thediagnosis
isalmostcertainlyVT.Thepredictiveaccuracy
ofthismethodwas93%,whichincreasedto95%
withtheinclusionof2othercriteria:independ-
entPwaveactivityandventricularectopicbeats
duringsinusrhythmwiththesameQRSmor-
phology as that in tachycardia.4 According to
Griffith'scriteria,thehistoryofMIandpresence
ofaQSwaveinleadaVFinourcasefavorsadi-
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agnosisofVT.In2008,Vereckeietal.presented
asimplifiedalgorithmusingonlyleadaVR;this
algorithmshowedhighaccuracyintheanaly-
sisof313patients.ThecriteriaforVTinlead
aVRwereasfollows:(i)thepresenceofaninitial
Rwave,(ii)›40mswidthofaninitialRorQ
wave,(iii)notchingontheinitialdownstrokeof
apredominantlynegativeQRScomplex,and(iv)
Vi/Vt≤1.5Inthepresentcase,ViandVtwere
239and400μV,respectively,resultinginVi/Vt
≤1andthereforefavoringadiagnosisofVTby
Vereckei'scriteria.
Inconclusion,widecomplextachycardiaoften
exhibitsanindistinctmorphology,especiallyat
higher frequencies,making diagnosis difficult.
Despiteallavailablemorphologicalcriteria,wide
complex tachycardiasare stillmisdiagnosedor
canremainundiagnosed.Toachieveahighpos-
itivepredictivevalueof›95%intheidentifica-
tionofVT,asystemicapproachthatemploysa
combinationofvariousECGandclinicalcriteria
isneeded.
References
1. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with
a wide QRS complex. Circulation. 1991;83:1649-1659.2. Wellens HJ, Bar FW, Lie KI. The value of the electrocardiogram in
the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med. 1978;64:27-33.
3. Kindwall KE, Brown J, Josephson ME. Electrocardiographic criteria for ventricular tachycardia in wide complex left bundle branch block morphology tachycardias. Am J Cardiol. 1988;61:1279-1283.
4. Griffith MJ, de Belder MA, Linker NJ, Ward DE, Camm AJ. Multivariate analysis to simplify the differential diagnosis of broad complex tachycardia. Br Heart J. 1991;66:166-174.
5. Vereckei A, Duray G, Szenasi G, Altemose GT, Miller JM. Newalgorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm. 2008;5:89-98.
자율 학습 문제
부정맥연구회지에서는매호자율학습문제를수록합니다.해당호에실린원고를바탕으로출제된문제로선
생님들의자기계발에도움이되시길바랍니다.많은참여부탁드립니다.모범답안은다음호에게재합니다.
1. 심실조기수축에 대한 설명으로 적당하지 않은 것은?
① 건강한성인에서흔히볼수있는부정맥이다.
②최근보고에서증상이없어도하루동안24%이상발생할경우심근기능저하를일으킬수있으나그간격은
의미가없다고보고되고있다.
③3회이상심실조기수축이생기는경우심실빈맥으로분류한다.
④이뇨제를투여중저칼륨혈증이생기면잘발생할수있다.
2. 특발성 심실빈맥에 대한 설명으로 적절한 것은?
① Catecholamine에의한earlyafterdepolarization에의해이루어진다
②Aorticcusp심실빈맥의경우non-coronarycusp에서가장빈도가높다.
③유출로심실빈맥의경우베타차단제는거의도움이되지않는다.
④Fascicular심실빈맥은verapamil이효과적이다.
3. 허혈성 심실빈맥의 전극도자절제술 시 reentrant circuit에서 entrainment with concealed fusion이 있고,
post-pacing interval과 tachycardia cycle length가 동일하며, mid-diastolic potential이 보이는 경우는 어느