●心電學英語

Lesson Sixty-six "Classical"response in a pre-excited tachycardia:What are the pathways involved?

Introduction

A 24-year-old patient presented with history of recurrent palpitation and was diagnosed as wide QRS tachycardia which was cardioverted.The sinus rhythm ECG and the tachycardia ECG are shown in Figure 1. During the electrophysiological study,2 morphologies of tachycardia were inducible,1 with right bundle branch block（RBBB）morphology（Figure 2A）and another with left bundle branch block（LBBB）morphology（Figure 2B）,which was her clinical tachycardia.The LBBB type wide QRS tachycardia was faster（Figure 2B）.DuringtheRBBBmorphologytachycardia, ventricular entrainment showed a V-A-V response and a His refractory ventricular extrastimulation1advanced the retrograde atrial activation,resetting the tachycardia.

TheLBBBmorphologytachycardiashowed variation in cycle length with a constant Ventriculo-Atrial（VA）interval.Atrial entrainment did not change the QRS morphology or VA relationship.An early premature atrial extrastimulation from the lateral right atrium showed an interesting finding（Figure 3）.Very late atrial extrastimulus from the same location did not advance the V without affecting the septal A.What are the mechanisms of the two tachycardias?

Commentary

The baseline ECG showed features typical of an accessory pathway,in the right posterior location.The clinical tachycardia was a regular wide QRS tachycardia（Figure 1B）,with LBBB morphology and left axis deviation.The 12-lead ECG of the tachycardia gives certain clues to the underlying pathways.The typical antidromic tachycardia would have resulted in a wider QRS and predominantly positive complexes in the lateral precordial leads because of ventricular activation solely through the accessory pathway.A fast conducting AVN-His bundle may,however,result in relatively narrower QRS.When the tachycardia morphology does not correspond to the pre-excitation pattern in sinus rhythm,multiple pathways should be considered.The wide QRS tachycardia shows left axis deviation and LBBB and has a sharp rapid component of the initial part and has no precordial transition.These features are moretypicalofanatriofascicular（Mahaim）tachycardia,although the sinus rhythm ECG is not typical for a Mahaim fiber.

Intracardiac recording in Figure 2shows an orthodromic tachycardia（[ORT]with RBBB aberrancy）with antegrade conduction through the His bundle,and retrograde conduction through a right-sided pathway（Figure 2A）;earliest atrial activity was noted in the distal HALO electrodes in the posterolateral tricuspid annulus.An atrial tachycardia with aberrancy was ruled out by a VAV response to ventricular entrainment.A short postpacing interval and atrial pre-excitation2by a Hisrefractoryventricularstimulusconfirmedthe diagnosis.

Figure 1Twelve-lead electrocardiograms of the patient in sinus rhythm（A）and during clinical tachycardia（B）.

The wide QRS tachycardia with LBBB morphology（Figure 2B）has a shorter cycle length but has the same eccentric retrograde activation sequence.It was initiated by catheter-induced ventricular ectopics during the ORT.The HV was negative（ventricular-His[VH] =80ms）showing that it is a truly pre-excited long VH tachycardia.At this point,it can be assumed that the H is a retrograde H（further confirmed by observations mentioned below）.Two additional points should be noted in Figure 2B∶（1）the retrograde activation sequence is same as during the ORT（tachycardia 1）and（2）the cycle length is considerably shorter during the wide QRS LBBB morphology rhythm.These essentially rule out a classic antidromic tachycardia mediated by the same AV connection.However,thepresenceofRBBBor incorporation of the slow pathway during the ORT alone may cause it to be slower than antidromic tachycardia. Orthodromic reentry with aberrancy is ruled out by the negative HV.AVNRT with bystander accessory pathway is excluded because of eccentric atrial activation and because the retrograde activation did not change between the tachycardias.Further,in AVNRT with bystander activation,the VH is usually short and the H recorded is an antegrade H.A late atrial extrastimulus during the tachycardia when the AV junction is refractory can be used to diagnose AVNRT with bystander pathway（see below）.A His refractory ventricular stimulus can also exclude AVNRT if it resets the tachycardia with the same activation sequence in atria-this was demonstrated in this case.The possibility then we have to consider is thatthesecondtachycardiaisbecauseofa pathway-to-pathway conduction-antegrade conduction through a right-sided accessory pathway（LBBB,left axis）,with a negative VH as noted in the figure and retrogradeconductionthroughthesameright posterolateral pathway mediating the ORT,with earliest atrial activation in HALO 1,2.Pathway-to-pathway tachycardia are usually possible only when the pathways are at a considerable distance anatomically.When 2 pathways are close by,like in this case,tachycardia can be sustained more easily if at least one of the pathways has decremental conduction property.In such a scenario, the AVN can conduct retrogradely and activate part of the atria.The rare possibility of ORT with bystander pathway was previously reported;however,they are associated with minimal QRS widening and a short rather than negative HV.

Figure 2Surface leadsⅠ,Ⅲ,and V1and intracardiac electrograms from right atrium（HALO 1,2 at lateral right atrium to HALO 17,18）,His bundle（His bundle distal[HBED]and His bundle middle[HBEm]）,the coronary sinus（coronary sinus distal[CSD]and coronary sinus proximal [CSP]）and right ventricular apex（RVA）.A,The orthodromic tachycardia with right bundle branch block aberrancy.B,The left bundle branch block tachycardia of shorter cycle length and long ventricular-His of 80 ms with the same retrograde eccentric atrial activation as in the initial tachycardia.

Atrialentrainmentshowedresettingofthe tachycardia without alteration of the QRS morphology or VH interval,thus confirming atria as necessary part of the circuit and also making AVNRT or ORT with bystanderpathwayunlikely.Iftheatriofascicular pathway was merely a bystander,QRS morphology and the VH relationship would change with resetting of the tachycardia.This also rules out a myocardial VT. Coupled atrial premature stimuli also showed advancing of the V.A relatively early coupled atrial stimulus produced an interesting finding as noted in Figure 3, which shows a coupled atrial extrastimuli during the pre-excited rhythm,which delayed the ventricular activation through the pathway and reset the tachycardia withoutchangingtheVHorVAinterval.This demonstrates the decremental nature of the anterograde pathway during tachycardia.It also demonstrates that the H is a retrograde H related to V.If His bundle activation contributed to activation of septal atrium,this resetting would have been expected to at least slightly alter the atrial activation pattern.Even very late atrial extrastimuli（delivered from the presumed site of antegrade pathway）advanced the septal A making it likely that atrium in the vicinity of the His is activated through the retrograde accessory pathway and there is Hto A block during the LBBB tachycardia.Further,the atrialactivationduringboththeORTandthe pre-excited tachycardia is the same showing that there is no retrograde activation of atrium through the AVN. During cycle length changes in the LBBB tachycardia the VH and VA interval remained constant.Thus,a diagnosis of pathway-to-pathway tachycardia,mediated by a Mahaim fiber and a closely located nondecremental pathway was made.

Patientsubsequentlydevelopedanatrial tachycardia with 2∶1 AV conduction through both accessory AV connection（Figure 4A）.Figure 4A shows thecharacteristicMahaimpotentialat9o′clocktricuspid location with a short M to QRS interval.This short M to QRS interval is not typical for Mahaim conduction.It shows that the QRS is also contributed by antegrade conduction through the right posterior nondecremental pathway-a case of pre-excited Mahaim conduction. Successful ablation of the Mahaim fiber resulted in change in QRS morphology.The right posterior pathway was mapped during ORT and successfully ablated at the posterior tricuspid annulus region（Figure 4B）.Post ablation of both pathways there was persistent RBBB and no VA conduction at 500 ms showing a poor retrograde conduction through the AV node.

Figure 3Surface leadsⅠ,Ⅲ,and V1and intracardiac electrograms from right atrium,His bundle,the coronary sinus and right ventricular apex.The effect of an early coupled atrial stimulus（asterisk）during tachycardia is shown.CI indicates coupling interval of atrial stimulus;TCL,tachycardia cycle length;and V-V',interval between surface QRS following the extrastimulus.

詞匯

aberrancy n.偏離正路，差異

eccentric adj.&n.古怪,古怪的,偏心;偏心輪,偏心圓

incorporation n.包含,公司,混合

anatomically adv.在解剖學上

decremental adj.減少的，遞減的

注釋

1.His refractory ventricular extrastimulation指“希氏束不應(yīng)期間的心室期外刺激”，通常在室上性心動過速時，略短于心動過速周長（＜40ms）的心室起搏即是。2.atrial pre-excitation指“心房提前激動”或“心房預(yù)激”。室上性心動過速時心室起搏，使得心房頻率加快，心動周期縮短15ms或以上，即為心房預(yù)激。希氏束不應(yīng)期間心室起搏引起心房預(yù)激，要考慮順傳型房室折返性心動過速。

Figure 4Fluoroscopic left anterior oblique projections of location and electrograms from the following catheters∶the duo-decapolar catheter along the tricuspid annulus（HALO 1,2 to 17,18）,the decapolar coronary sinus（CS）,the mapping and ablation catheter（shown with asterisk.RFd and RFp）and quadripolar catheters in the His（His bundle distal[HBED],His bundle middle[HBEm],and His bundle proximal[HBEp]）and right ventricular apex（RVA）.A.Atrial tachycardia with 2∶1 conduction and M potentials at the ablation catheter at the site of successful ablation of the Mahaim fiber.Note the short M-Local V interval and simultaneous activation of the RVA and ventricular annulus（RFd）because of antegrade conduction through both pathways.B.The recording during orthodromic tachycardia,ablation at the posterolateral tricuspid annulus results in local separation of VA and termination of tachycardia（solid down arrow）.

參考譯文

第66課預(yù)激心動過速的“經(jīng)典”反應(yīng)——涉及哪些旁道？

購買蔬菜、水果時，不買異常氣味的蔬菜和水果。有些商販為了蔬菜更好看，用化學藥劑進行浸泡，這些物質(zhì)有異味，不容易被沖洗掉。不買顏色異常的蔬菜和水果，不買形狀異常的蔬菜和水果。有的蔬菜使用了激素物質(zhì)，會長成畸形。盡量不要食用“新奇”“野味”等不常食用或從未食用過的食物。

患者女性，24歲，因反復(fù)心悸而就診，診斷為寬QRS波群心動過速并得到復(fù)律。圖1為竇性節(jié)律心電圖和心動過速心電圖。電生理檢查中，誘發(fā)出兩種形態(tài)的心動過速，一為右束支傳導阻滯（RBBB）圖形（圖2A），另一為左束支傳導阻滯（LBBB）圖形（圖2B），與她臨床發(fā)作的心動過速一樣。LBBB型寬QRS波群心動過速較快（圖2B）。RBBB圖形心動過速時，心室拖帶顯示V-A-V反應(yīng)，希氏束不應(yīng)期心室期外刺激使逆?zhèn)餍姆考犹崆?，重整心動過速。

LBBB圖形心動過速顯示周長變化而室-房（VA）間期恒定。心房拖帶不能改變QRS形態(tài)或VA關(guān)系。右心房外側(cè)壁早期房性期外刺激顯示令人感興趣的發(fā)現(xiàn)（圖3）。同一部位很晚的心房期外刺激不能提前V而不影響間隔A。這兩種心動過速的機制是什么呢?

評析

基礎(chǔ)心電圖顯示旁道特征，位于右后部位。臨床心動過速是一規(guī)則的寬QRS波群心動過速，呈LBBB圖形和心電軸左偏（圖1B）。心動過速12導聯(lián)心電圖對所涉徑路提供一定線索。典型的逆?zhèn)餍托膭舆^速因完全通過旁道激動心室理應(yīng)產(chǎn)生較寬的QRS波群，且側(cè)胸導聯(lián)以正向波為主，而快速傳導的房室結(jié)-希氏束可產(chǎn)生相對較窄的QRS波群。當心動過速圖形與竇性節(jié)律時的預(yù)激圖形不一致時，應(yīng)考慮多徑路。本例寬QRS波群心動過速呈心電軸左偏和LBBB，起始部分尖銳急速，且無胸前移行。這些是房-束（Mahaim）心動過速較為典型的特征，盡管竇性節(jié)律心電圖不典型。

圖2心內(nèi)記錄顯示順傳型心動過速[（ORT）伴RBBB差異]，經(jīng)希氏束順傳和右側(cè)旁道逆?zhèn)鳎▓D2A）；最早心房激動見于三尖瓣環(huán)后外側(cè)HALO電極的遠端。心室拖帶呈V-A-V反應(yīng)排除了房性心動過速伴差異。起搏后短間期和希氏束不應(yīng)期心室刺激時心房預(yù)激證實這一診斷。

LBBB圖形的寬QRS波群心動過速（圖2B）周長較短，但有相同的偏心性逆?zhèn)骷禹樞?，系ORT時導管刺激的心室異位激動所引發(fā)。HV是負向的[心室-希氏束（VH）=80ms]，表明這確實是預(yù)激長VH心動過速。就這一點，可以推測H是逆行H。圖2B上另外兩點值得注意∶（1）逆行激動順序與ORT（心動過速1）時相同，（2）寬QRS波群LBBB圖形節(jié)律時心動周長較短。這些基本排除了由同一AV連接介導的典型逆?zhèn)餍托膭舆^速。然而，ORT時單一RBBB或合并慢徑路傳導即可使其慢于逆?zhèn)餍托膭舆^速。負向HV排除了順傳型折返伴差異。因為心房激動呈偏心性及兩種心動過速之間逆?zhèn)骷硬o變化，可排除AVNRT合并旁觀旁道。此外，AVNRT伴旁觀旁道激動時，通常VH短且H是順傳H。心動過速房室交界不應(yīng)期時晚期房性期外刺激可用于AVNRT合并旁觀旁道的診斷。希氏束不應(yīng)期室性刺激如能重整心動過速而心房激動順序不變也可排除AVNRT，這在本例得以證實。我們必須考慮的可能情況是第二種心動過速屬于旁道-旁道傳導，即經(jīng)右側(cè)旁道順傳（LBBB,心電軸左偏），伴有圖示的負向VH，經(jīng)介導ORT相同的右后外側(cè)旁道逆?zhèn)?，最早激動位于HALO電極1-2。通常，只有當兩條旁道解剖上有相當距離時，旁道-旁道心動過速才有可能。兩條旁道靠近時，如本病例，只在至少其中一條旁道具有遞減傳導特性時，心動過速才較易維持。在此情況下，AVN能逆?zhèn)鞑⒓硬糠中姆俊Ｒ郧皥蟮肋^ORT伴旁觀旁道可能性極小，伴隨QRS波群輕微增寬、短HV而非負向HV。

心房拖帶顯示重整心動過速而不改變QRS形態(tài)或VH間期，證實心房是折返環(huán)的必需部分，不可能是AVNRT或ORT伴旁觀旁道。如果房-束旁道只是旁觀者，那么，隨著心動過速的重整，QRS形態(tài)和VH的相互關(guān)系應(yīng)發(fā)生改變。這也排除心肌VT。偶聯(lián)房性期前刺激顯示同樣提前V波。較早的偶聯(lián)房性刺激產(chǎn)生令人感興趣的發(fā)現(xiàn)，圖3所示預(yù)激心律時的偶聯(lián)心房期外刺激，通過旁路推遲了心室激動，重整心動過速而不改變VH或VA間期。這證實心動過速時前向旁道的遞減特性。也證實相對于V，H是逆行H。如果希氏束激動促進間隔心房的激動，那么，這一重整至少會輕微改變心房激動的形式。鑒于很晚的心房期外激動（來自認定的前向旁道部位）提前間隔A，使得毗鄰希氏束的心房由逆行旁道激動成為可能，而LBBB心動過速時H到A受阻。此外，ORT和預(yù)激心動過速時心房激動相同，均未見經(jīng)AVN逆?zhèn)鞯男姆考?。LBBB心動過速周長變化時，VH和VA保持恒定。這樣，可診斷為由Mahaim纖維和緊鄰其的非遞減性旁道介導的旁道-旁道心動過速。

隨后，患者發(fā)生經(jīng)兩條AV旁道2∶1 AV傳導的房性心動過速（圖4A）。圖4A顯示三尖瓣環(huán)9點處特征性Mahaim電位，M-QRS間期短。M與QRS間期短并非Mahaim傳導的特征。這表明經(jīng)右后非遞減傳導旁道的順傳也參與QRS波群的形成，是一種預(yù)激的Mahaim傳導。成功消融Mahaim纖維引起QRS形態(tài)變化。ORT期間標測到右后旁道并于三尖瓣環(huán)后區(qū)成功消融（圖4B）。兩條徑路消融后為持續(xù)性RBBB，500ms起搏無VA傳導，表明AV結(jié)逆?zhèn)鞑涣肌?/p>

圖2體表Ⅰ、Ⅱ、Ⅲ，右心房（從右房外側(cè)壁HALO1,2到HALO17,18），希氏束[遠端（HBED）和中段（EBEM）]，冠狀竇遠端[（CSD）和近端（CSP）]及右心室尖（RVA）腔內(nèi)電圖。A.順向型心動過速伴右束支傳導阻滯差異；B.周長較短和心室-希氏束間期80ms長的左束支傳導阻滯心動過速，逆行偏心性心房激動與前一心動過速相同。

圖3體表Ⅰ、Ⅲ和V1，右心房，希氏束，冠狀竇和右心室心尖腔內(nèi)電圖。心動過速時早期偶聯(lián)房性刺激（星標）的效應(yīng)。CI：房性刺激偶聯(lián)間期，TCL：心動過速周長，V-V′：期外刺激與其后體表QRS波群之間的間期。

圖4左前斜位透視定位及隨后的導管記錄電圖：沿三尖瓣環(huán)的雙十極導管（HALO 1,2 to 17,18），十極冠狀竇導管（CS），標測和消融導管（星標，RFd和RFp），希氏束四極導管（遠端：HBED,中段：HBEm和近端：HBEp），右心室心尖四極導管。A.房性心動過速2∶1傳導，Mahaim纖維成功消融部位消融導管記錄到M電位。因經(jīng)兩條徑路順傳，可見M-局部V間期短，RVA和心室環(huán)部（RFd）同時激動。B.順傳型心動過速記錄，三尖瓣環(huán)后外側(cè)消融導致局部VA分離和心動過速中止（向下實線箭頭）。

[1]Thajudeen A,Namboodiri N,Choudhary D,et al."Classical" response in a pre-excited tachycardia∶What are the pathways involved[J]?Circ Arrhythm Electrophysiol,2013,6∶e11-e16.

（童鴻）