A 49-year-old woman presented with a 2-year history ofrecurrentpalpitationsand documented episodes of paroxysmal supraventricular tachycardia(SVT)terminated with adenosine.Resting 12-lead electrocardiogram (ECG)revealed normal sinus rhythm without preexcitation.She had a structurally normal heart on echocardiogram.After having obtained an informed consent,an electrophysiology study was performed using standard technique and a decapolar coronary sinus(CS)catheter was inserted with the distal pole positioned at the lateral mitral annulus(Figure 1A).Baseline measurements revealed a sinus cycle length of 804 milliseconds and an atrial-His(AH)interval and His-ventricular (HV)of 72 and 36 milliseconds,respectively.Incremental ventricular pacing showed eccentric retrograde atrialactivation with earliest activation noted at CS bipolar pair 3-4.Although atrial activation was earlier on the more distal CS electrodes versus the His bundle electrode,the difference in activation between CS 3-4 and CS 4-5 was minimal(Figure 1B).The ventricular-atrial(VA)conduction was decremental. Programmed atrial extrastimulation established the presence of anterograde dual AV nodal physiology with an AH jump of 78 milliseconds.A narrow QRS complex tachycardia with a cycle length varying between 440 and 460 millisecondswas reproducibly induced with programmed atrial stimulation.The retrograde atrial activation sequence was eccentric and identical to that observed during ventricular pacing.Overdrive ventricular pacing during the tachycardia resulted in a VAV response(Figure 1B).Premature ventricular complexes (PVCs)introduced during SVT to scan diastole preexcited the atrium with a preexcitation index of 125 milliseconds.What is the mechanism of the tachycardia?

Commentary

An eccentric retrograde atrial activation sequence with earliest atrial activation at or near the lateral mitral annulus suggests retrograde conduction over a concealed left free wall accessory pathway (AP) during atrioventricular reentrant tachycardia(AVRT).The atrial activation during ventricular pacing was also eccentric and identicalto thatduring the SVT.Although extremely uncommon,the possibility of an atypical atrioventricular nodal reentrant tachycardia(AVNRT)with eccentric retrograde atrial activation remains in the differential diagnosis.A left atrial focal tachycardia was eliminated by the V-A-V response during ventricular overdrive pacing.

Because the pattern of atrial activation alone,even when it is eccentric as in this case,does not definitively rule out AVNRT,other maneuvers are required to establish a diagnosis. Postpacing interval(PPI)-tachycardia cycle length(TCL)was 138 milliseconds,and stimulus to atrial interval-VA tachycardia(SA-VA)was 122 milliseconds with a basal right ventricular(RV)pacing site(Figure 1B),findings that are more consistent with AVNRT than AVRT.However,these observations do not exclude AVRT with a slowly conducting decremental AP.These ventricular entrainment criteria depend on nondecrementalretrograde conduction through an AP and are limited in differentiating atypical AVNRT from AVRT using decrementally conducting AP.Furthermore,in the setting of AVRT employing a left lateral AP,the PPI-TCL,and SA-VA interval differences may be longer simply by virtue of the distance of the RV pacing site from the circuit.The preexcitation index in this case was 125 milliseconds,a number usually suggesting AVNRT.However,studies utilizing the concept ofpreexcitation index to differentiate AVNRT from AVRT did not include patients with decremental pathways or atypical AVNRT and hence cannotbe used to differentiate the tachycardia mechanism in this case.Intravenous adenosine to differentiate nodal versus AP retrograde conduction was not used,as retrograde decremental pathways can be adenosine sensitive and the response would not have helped in elucidating the tachycardia mechanism.

Figure1 A：The catheter positions during diagnostic electrophysiology study with the most distal pole of the CS catheter positioned at the lateral mitral annulus.B：Response to ventricular overdrive pacing during SVT with recordings from surface leads I,II,III,and V1 and intracardiac electrogramsfrom the proximalHis bundle,distal His bundle,proximal to distal coronary sinus (CS 9-10 to CS 1-2,respectively),and right ventricular(RV)apex are displayed.

How do we definitively establish the route of retrograde conduction?Lack of positive proofs of AP conduction including response to PVC timed to His,HV change predicting HA change and bundle branch block resulting in VA change do not rule out its presence.In the case of left free wall APs,the PVCs often need to be delivered early again,since the RV pacing site is often distant from the tachycardia circuit.As the retrograde conduction was eccentric and identical during SVT and ventricular pacing,we used maneuvers to establish whetherthe retrograde conduction was occurring through AV node or AP during ventricular pacing.Programmed ventricular stimulation at 600 milliseconds CL with a S2 of 330 milliseconds showed the sudden appearance of a retrograde His with the similar eccentric atrial activation.With progressively earlier ventricular extrastimuli the increase in VA interval paralleled the increase of retrograde ventricular to His(VH)interval with no change in HA interval(Figure 2).This pattern of VA conduction with the same eccentric atrial activation confirmed retrograde conduction over the AV node and not an AP.One would not expect a constant HA relationship during retrograde conduction over an AP unless there happened to be equal decrement in VH conduction and retrograde AP conduction,a highly unlikely possibility.Parahisian pacing resulted in an SA interval of 172 milliseconds with His bundle and local myocardium capture while SA intervalwas204 milliseconds with ventricular myocardium capture only without change in retrograde atrial activation sequence(Figure 3).This was highly suggestive of retrograde AV nodal conduction,but did not exclude the possibility of a left free wall AP.

Radiofrequency ablation(RFA)of AVNRT was attempted in the right posteroinferior septum near the CS ostium.Difficulty in tracking VA conduction during RFA resulted in switching to cryoablation.The successful site was slightly anterior to the CS ostium and was anatomically far off from earliest atrial activation.Postablation,the tachycardia could not be reinduced and there was no evidence of anterograde slow pathway conduction with absent VA conduction at all pacing cycle lengths.This case illustrates the importance of relying on electrophysiological evidence rather than patterns in establishing mechanisms of tachycardia.

Figure 2 Programmed ventricular stimulation.In the lefthand panel with S1S2of 330 milliseconds,the H2A2interval is 230 milliseconds.In the right panel,a S1S2of 270 milliseconds prolongs the V2H2interval with H2A2 interval of 230 milliseconds.The abbreviations are as in Figure 1.

Figure 3 Parahisian pacing.In the lefthand panel with His and ventricular capture (narrow QRS complex),the SA interval is 172 milliseconds.In the righthand panel with ventricular capture only the SA interval is 204 milliseconds(see text for details).Abbreviations as in Figure 1.

詞 匯

palpitation n.心悸，心慌，跳動(dòng)

incremental adj.增加的，增值的，遞增的

eccentric adj.偏心的，離心的，反常的，古怪的，n.古怪的人，偏心圓

decremental adj.減少的，遞減的

conceal vt.隱藏；隱瞞

entrainment n.夾帶，拖帶，帶走，生物的周期轉(zhuǎn)換

elucidate vt.闡明，說(shuō)明

proof n.&adj.&vt.證明，證據(jù)，校樣，考驗(yàn)，驗(yàn)證，試驗(yàn)；防…的，不能透入的，證明用的，耐…的；試驗(yàn)，校對(duì)，使不被穿透

maneuver n.&vi.&機(jī)動(dòng)，演習(xí)，策略，調(diào)遣；演習(xí)，調(diào)遣，用計(jì)謀；機(jī)動(dòng)，演習(xí)，用計(jì)，調(diào)遣

track n.&vt.軌道，足跡，蹤跡，小道；追蹤，通過(guò)，循路而行，留下足跡

cryoablation n.冷凍消融術(shù)，冷凍剝脫術(shù)

anterograde adj.順行的，前進(jìn)的

注 釋

1.preexcitation index預(yù)激指數(shù)，反映心動(dòng)過(guò)速時(shí)剛能引起心房預(yù)激的期前心室刺激的提前程度，由心動(dòng)過(guò)速周長(zhǎng)減期前心室刺激的聯(lián)律間期計(jì)算而得，單位ms。假設(shè)心動(dòng)過(guò)速頻率為150次/min,那么心動(dòng)過(guò)速的周長(zhǎng)為400ms。如剛能進(jìn)入折返環(huán)并引起心房預(yù)激的期前心室刺激的聯(lián)律間期為300ms，那么預(yù)激指數(shù)為400-300=100ms，即提前100ms的期前心室刺激能進(jìn)入折返環(huán)，提前＜100ms的心室刺激不能進(jìn)入折返環(huán)。因此，預(yù)激指數(shù)常用來(lái)判斷心室刺激部位與折返環(huán)的距離，距離越遠(yuǎn)，所需提前程度越大，有助于分析折返型心動(dòng)過(guò)速的類(lèi)型或旁道位置。通常房室結(jié)折返型心動(dòng)過(guò)速的預(yù)激指數(shù)最大，左心室游離壁旁道折返型心動(dòng)過(guò)速的預(yù)激指數(shù)略小，而間隔部旁道的折返型心動(dòng)過(guò)速的預(yù)激指數(shù)最小。2.PPI-TCL interval指起搏后間期與心動(dòng)過(guò)速周長(zhǎng)之間的差值，其中PPI指最后1個(gè)起搏奪獲至下一次起搏部位激動(dòng)之間的時(shí)間，反映的是從起搏部位到折返環(huán)，通過(guò)折返環(huán)并返回起搏部位的傳導(dǎo)時(shí)間，因此，如起搏點(diǎn)距離折返環(huán)越近，PPI越短，反之越長(zhǎng)。TCL是指折返型心動(dòng)過(guò)速的周長(zhǎng)，反映的是通過(guò)折返環(huán)1周的傳導(dǎo)時(shí)間。房室折返型心動(dòng)過(guò)速為大折返環(huán)，心室肌參與其中，因此，右心室期起搏部位通常距離折返環(huán)較近，PPI與TCL間期的差值較小，常＜115ms；而房室結(jié)折返型心動(dòng)過(guò)速折返環(huán)較小，局限在房室結(jié)附近，右心室起搏部位通常距離折返環(huán)較遠(yuǎn)，PPI與TCL間期的差值較大，常＞125ms。

參考譯文

第82課 窄QRS波群心動(dòng)過(guò)速時(shí)偏心性心房激動(dòng)是什么機(jī)制？

患者女性，49歲，反復(fù)心悸2年，記錄到陣發(fā)性室上性心動(dòng)過(guò)速（SVT），腺苷中止。靜息12導(dǎo)聯(lián)心電圖顯示正常竇性心律，無(wú)預(yù)激。超聲心動(dòng)圖檢查提示心臟結(jié)構(gòu)正常。簽署知情同意書(shū)后，采用標(biāo)準(zhǔn)技術(shù)行電生理檢查，十極冠狀竇（CS）電極遠(yuǎn)端電極位于二尖瓣環(huán)外側(cè)（圖1A）?；A(chǔ)測(cè)試顯示竇性心律周長(zhǎng)804ms、心房-希氏束間期（AH）和希氏束-心室間期（HV）分別為72ms和36ms。遞增心室起搏顯示偏心性逆行心房激動(dòng)，最早激動(dòng)位于CS電極3-4電極對(duì)。雖然CS較遠(yuǎn)端電極心房激動(dòng)早于希氏束電極，但CS電極3-4與4-5之間的激動(dòng)差異最?。▓D1B）。室房（VA）傳導(dǎo)呈遞減性。程序心房期外刺激顯示AH跳躍78ms，證實(shí)存在房室結(jié)前向雙徑路。程序心房刺激能重復(fù)誘發(fā)周長(zhǎng)為440～460ms的窄QRS波群心動(dòng)過(guò)速。逆行心房激動(dòng)順序呈偏心性，與心室起搏時(shí)見(jiàn)到的相一致。心動(dòng)過(guò)速期間超速心室起搏引發(fā)VAV反應(yīng)（圖1B）。SVT期間掃描舒張期的期前室性刺激（PVCs）預(yù)激心房，預(yù)激指數(shù)為125ms。心動(dòng)過(guò)速的機(jī)制是什么？

分析討論

偏心性逆行心房激動(dòng)順序、最早心房激動(dòng)位于或接近二尖瓣環(huán)外側(cè)，提示房室折返型心動(dòng)過(guò)速（AVRT）經(jīng)左側(cè)游離壁隱性旁道（AP）逆?zhèn)鳌Ｐ氖移鸩珪r(shí)心房的激動(dòng)也是偏心性的，與SVT時(shí)相一致。雖然極不常見(jiàn)，鑒別診斷中仍然要考慮不典型房室結(jié)折返型心動(dòng)過(guò)速（AVNRT）的可能性。心室超速起搏時(shí)的VAV反應(yīng)排除了灶性房性心動(dòng)過(guò)速。

鑒于單一的心房激動(dòng)圖形，即使像本例一樣呈偏心性順序，不能確切排除AVNRT,因此，需要其他方法去確定診斷。右心室基底部起搏，起搏后間期（PPI）-心動(dòng)過(guò)速周長(zhǎng)（TCL）為138 ms，起搏刺激心房間期-VA心動(dòng)過(guò)速（SA-VA）為122ms（圖1B）,這些數(shù)值與AVNRT的一致性高于AVRT。然而，這些觀察不能排除經(jīng)遞減性AP緩慢傳導(dǎo)的AVRT。這些心室拖帶標(biāo)準(zhǔn)依賴(lài)經(jīng)AP的非遞減性逆行傳導(dǎo)，對(duì)非典型AVNRT與經(jīng)AP遞減性傳導(dǎo)AVRT的鑒別作用有限。此外，對(duì)于經(jīng)左外側(cè)AP的AVRT，PPI-TCL以及SA-VA間期可因右心室起搏部位與折返環(huán)的距離而較長(zhǎng)。本例的預(yù)激指數(shù)為125ms，這一數(shù)值通常提示為AVNRT。然而，利用預(yù)激指數(shù)概念去鑒別AVNRT與AVRT的研究并非包含遞減旁道或非典型AVNRT患者，因此，不能用于鑒別本例的心動(dòng)過(guò)速機(jī)制。沒(méi)有靜注腺苷去鑒別房室結(jié)與旁道逆?zhèn)?，因?yàn)槟鎮(zhèn)鬟f減旁道對(duì)腺苷敏感，其反應(yīng)無(wú)助于闡明心動(dòng)過(guò)速機(jī)制。

我們?cè)撊绾未_定逆?zhèn)魍緩?？缺乏AP傳導(dǎo)的陽(yáng)性證據(jù)包括對(duì)適配希氏束的PVC反應(yīng)、預(yù)示HA變化的HV變化以及引起VA變化的束支阻滯，不能排除它的存在。存在左側(cè)游離壁AP的情況下，常需要更早的PVC，因右心室起搏部位經(jīng)常遠(yuǎn)離心動(dòng)過(guò)速折返環(huán)。鑒于SVT與心室起搏時(shí)，逆行傳導(dǎo)呈偏心性而且一致，我們?cè)O(shè)法確定心室起搏時(shí)是否通過(guò)AV結(jié)或AP逆行傳導(dǎo)。采用600ms周長(zhǎng)加330msS2程控心室起搏顯示意外出現(xiàn)逆?zhèn)飨Ｊ鲜皖?lèi)似的偏心性心房激動(dòng)。隨著心室期外刺激的進(jìn)行性提前，VA間期的增加與逆?zhèn)鞯男氖?希氏束間期（VH）增加相平行，而HA無(wú)變化（圖2）。這一VA傳導(dǎo)結(jié)合相同的偏心性心房激動(dòng)圖形證實(shí)經(jīng)AV結(jié)逆?zhèn)鞫墙?jīng)AP逆?zhèn)?。人們無(wú)法期待經(jīng)AP逆?zhèn)鲿r(shí)有恒定的HA關(guān)系，除非碰巧VH傳導(dǎo)與逆行AP傳導(dǎo)的遞減相等，這是極不可能的。希氏束旁起搏引起SA間期172ms伴希氏束和局部心室?jiàn)Z獲，而當(dāng)SA間期204ms時(shí)只有心室?jiàn)Z獲而無(wú)逆?zhèn)餍姆考?dòng)順序改變（圖3）。這高度提示經(jīng)AV結(jié)逆?zhèn)?，但不能排除左?cè)游離壁AP的可能性。

于右后下間隔近CS口處行AVNRT射頻消融。射頻消融期間難以跟蹤VA傳導(dǎo)，改用冷凍消融。成功消融部位位于CS口略前方，解剖上遠(yuǎn)離最早心房激動(dòng)部位。消融后，于所有周長(zhǎng)起搏下，不能再次誘發(fā)心動(dòng)過(guò)速，無(wú)前向慢徑傳導(dǎo)和VA傳導(dǎo)。本例闡明了依靠電生理依據(jù)而非圖形確定心動(dòng)過(guò)速機(jī)制的重要性。

圖1 A：診斷性電生理檢查中導(dǎo)管位置，冠狀竇最遠(yuǎn)端電極位于二尖瓣環(huán)外側(cè)。BSVT時(shí)對(duì)心室超速起搏的反應(yīng)，記錄順序?yàn)轶w表Ⅰ、Ⅱ、Ⅲ和V1，心內(nèi)電圖為希氏束近端，希氏束遠(yuǎn)端，冠狀竇由近及遠(yuǎn)（分別為 CS9-10到CS1-2），右心室（RV）尖。

圖2 程控心室刺激。上圖：S12300ms，H2A2間期為230ms，下圖：S1S2270ms，延長(zhǎng) V2H2而 H2A2為 230ms。

圖3 希氏束旁起搏。左圖為希氏束和心室?jiàn)Z獲（窄QRS波群），SA間期172ms，右圖為只有心室?jiàn)Z獲，SA間期204ms。

[1]Bagga S,Padanilam BJ,Prystowsky EN.Eccentric Atrial Activation During a Narrow QRS Tachycardia：What Is the Mechanism?[J].J Cardiovasc Electrophysiol,2016,27∶1353-1355.