IdenticalAtrio-Hisintervaland A-AintervalsduringlongRP tachycardia What is the mechanism?

●心電學英語

IdenticalAtrio-Hisintervaland A-AintervalsduringlongRP tachycardia What is the mechanism?

Case Presentation

A 46-year-old woman with frequent palpitations underwent electrophysiological study.The findings of transthoracic echocardiography were normal,and a 12-lead ECG showed no ventricular pre-excitation. Four catheters were placed in standard locations:high right atrium,His bundle,coronary sinus(CS),and right ventricular apex.All the recorded baseline intervals were within normal limits.Retrograde ventriculoatrial (VA)conduction showed decremental and dual pathways during ventricular pacing and single extrastimulus testing.Antegrade atrioventricular(AV)nodal conduction showed decremental and triple pathways during atrial single extrastimulus testing.Narrow-complex supraventricular tachycardia(SVT)was reliably induced with a V-A-V sequence by a single ventricular extrastimulus (Figure 1).Ventricular premature depolarization(VPD) during tachycardia,when the His bundle was refractory, did not reset the atrial cycle.Retrograde Wenckebach periodicity occurred during right ventricular overdrive pacing at a cycle length(CL)of 500 ms.The tachycardia was terminated with atrio-His(A-H)and VA block during atrial and ventricular entrainment pacing.Figure 2 shows progressive prolongation and abrupt shortening of the A-A interval with block during SVT.In addition, the A-H interval was identical to the A-A interval during SVT.On the basis of these findings,what is the mechanism of the tachycardia?

Commentary

The differential diagnoses of long RP interval tachycardia,with the earliest atrial activation near the ostium of the CS,are atypical AV nodal reentrant tachycardia(AVNRT),orthodromic reciprocating tachycardia with a slowly conducting and decremental accessory pathway and posteroseptal atrial tachycardia(AT).Because of the presence of the His-refractory VPD without the reset phenomenon as well as sustained SVT during A-H block,the possibility of orthodromic reciprocating tachycardia was excluded.Moreover,automatic AT with initiating AV nodal echo was not completely excluded by the V-A-V sequence1on tachycardia initiation. However,AT was less likely because of the termination of tachycardia with A-H/V-A block during atrial/ventricular entrainment pacing and the direct correlation between the A-A interval and the A-H interval during SVT.Therefore,on the basis of these findings,atypical AVNRT was the most likely diagnosis.

In Figure 2,the first 3 A-A intervals were 450 ms, whereas the A-H intervals were gradually prolonged.

This observation could be explained by the presence of a lower common pathway(LCP,which is defined as the conduction pathway between the tachycardia circuit and the His bundle)with decremental conduction. The presence of an LCP was proven by the fact that the retrograde Wenckebach CL(500 ms)during ventricular pacing was longer than the tachycardia CL(450 ms). Subsequently,the next A-A intervals were progressivelyprolonged to 455-480 ms and further to 540 ms and abruptly shortened to 440 ms with an A-H block.Interestingly,the fifth and sixth A-H intervals were identical to the A-A interval.There are several potential mechanisms that can explain these findings.First,a simple hypothesis was that the A-H intervals became progressively longer because of the decremental conduction of an LCP,which was much stronger than that of the antegrade AV nodal pathway,thereby causing a block of the LCP that was reflected as an A-H block.However,this hypothesis does not explain the abrupt shortening of the A-A intervals with an A-H block.The second hypothesis was that the fifth and sixth As switched to a slow pathway,with a slow LCP resulting in the retrograde A preceding the His bundle.Subsequently,the seventh and eighth As are the result of a double fire from the upper turn around point above the LCP and a lower turn around point(LTP)below the LCP.However,during the first 4 A-A intervals,the conduction of the LCP was progressively prolonged,whereas the conduction of the antegrade AV nodal pathway was only 5 ms.Therefore, in the subsequent As,the hypothesis of an LCP block was more likely.Finally,the most likely mechanism may be the dual ventricular response with an LCP block,that is,the antegrade impulse of the tachycardia circuit traveled down a fast pathway,which was followed by a turn to a retrograde slow pathway via the LTP1 with LCP block before the His bundle(Figure 3).Although,at the same time,the antegrade impulse showed a double ventricular response(Figure 3,asterisk),an antegrade slow pathway was conducted to LTP2 but did not turn to a retrograde slow pathway because of the effective refractory period.The next beat also showed a double ventricular response.First,the antegrade fast pathway was conducted to LTP1 and turned to the retrograde slow pathway,while at the same time,an antegrade slow pathway was conducted to LTP2 with decremental conduction and turned to the retrograde slow pathway, which was characterized by recovered excitability and resumed conduction because of the greater prolongationof the A-A interval.However,the impulse from the retrograde slow pathway,which was turned from the antegrade fast pathway,did not travel down the both antegrade fast and slow pathways because of the effective refractory period.As a result of these conduction pathways,the A-A interval was shortened to 440 ms with an A-H block.

Figure 1Intracardiac electrogram showing that narrow-complex supraventricular tachycardia was induced with a V-A-V sequence by a single ventricular extrastimulus(600/370 ms).CS indicates coronary sinus;HBE,His bundle electrogram;HRA,high right atrium;and RVA,right ventricular apex.

Figure 2Intracardiac electrogram showing progressive prolongation and abrupt shortening of the A-A interval during supraventricular tachycardia.*The atrial and His bundle potentials were fused.

Figure 3Ladder diagram demonstrating the mechanism of supraventricular tachycardia with alternate cycles.*The impulse antegrade of the tachycardia circuit showed dual ventricular response;the fast pathway(solid arrow)turned to the retrograde slow pathway via lower turnaround point(LTP, termed LTP1)with lower common pathway(LCP)block,while at the same time,the antegrade slow pathway(dashed arrow)was conducted to LTP2 and turned to the retrograde slow pathway.AVN indicates atrioventricular node;and LCP,lower common pathway.

Long RP tachycardia with variable A-H intervals is usually diagnosed as AT.However,atypical AVNRT with variable A-H intervals has been reported previously.These reports demonstrated that the A-H intervals during atypical AVNRT were progressively prolonged compared with the prolongation of A-A intervals. This observation was evidenced by the presence of an LCP,as an out-of-tachycardia circuit.In addition,adual ventricular response can be sustained,producing a 1:2 tachycardia,which is otherwise known as a nonreentrant SVT.Nonreentrant SVT typically showed that a single atrial impulse conducts both dual AV nodal pathways,and this is followed by excitation of both the His bundle and the ventricles.The main point of interest of the present case is that the A-A interval were identical to the A-H interval during AVNRT.These observations could be explained by a dual ventricular response with an LCP block.To our knowledge,this is the first case in which atypical AVNRT was sustained via a dual ventricular response.Radiofrequency catheter ablation was applied at the earliest retrograde slow pathway lesion at the posteroseptum,with successful elimination and the absence of inducible tachycardia.

詞匯

retrograde adj.&adv.&v.向后的,倒轉(zhuǎn)的,逆向的；向后地；衰退,重述，使倒退

decremental adj.減少的

antegrade adj.順行的，前進的

abrupt adj.突然的,粗魯?shù)?陡峭的,唐突的

orthodromic adj.順行的，順向傳導的

reciprocate v.回報,回報,互換,互給，往復運動

switch n.&v.開關(guān),鞭子,長假發(fā),一擊；交換,鞭打,甩動,擺動,揮動,轉(zhuǎn)轍

注釋

1.V-A-V sequence也有以V-A-V response表達的，指V-A-V順序或反應，是心內(nèi)電生理檢查中心室拖帶起搏時出現(xiàn)的一種心室-心房-心室序貫波形，提示房室之間至少存在兩條傳導徑路，一條保證心室-心房逆?zhèn)?，而另一條保證心房-心室順傳。通?？梢該?jù)此來排除自律性增高引起的房性心動過速。有學者認為，當房性心動過速合并存在房室結(jié)以外多條房室徑路，且其中至少有一條能順傳時，也可出現(xiàn)V-A-V反應，即逆?zhèn)鲝铰樊a(chǎn)生V-A而順傳徑路產(chǎn)生A-V波，只不過都是旁觀者而已。

參考譯文

第64課長R-P間期心動過速時心房-希氏束間期與心房-心房間期一致——機制如何？

病例資料

患者女性，46歲。因經(jīng)常發(fā)作心悸而行電生理檢查。經(jīng)胸心臟超聲檢查結(jié)果正常，12導聯(lián)心電圖無心室預激。常規(guī)放置4根導管：高位右心房，希氏束，冠狀竇（CS）和右心室心尖。所有記錄的基礎(chǔ)間期在正常范圍。在心室起搏和單個期外刺激測試中，逆向室房（VA）傳導顯示遞減性和雙徑路。在心房單個期外刺激測試中，順向房室（AV）結(jié)傳導顯示遞減性及三徑路。單一心室期外刺激伴隨V-A-V順序即能誘發(fā)出窄綜合波室上性心動過速（SVT）（圖1）。希氏束處于不應期時，心動過速期間的室性期前除極（VPD）不能重整心房周期。于周長（CL）500ms的右心室超速起搏時發(fā)生逆?zhèn)魑氖现芷?。在心房和心室拖帶起搏時心動過速中止伴隨心房-希氏束（A-H）和VA阻滯。圖2顯示SVT期間A-A間期進行性延長及突發(fā)縮短伴隨阻滯。另外，SVT期間A-H間期與A-A間期一致?；谶@些結(jié)果，心動過速的機制是什么？

討論

伴CS口附近最早心房激動的長R-P間期心動過速的鑒別診斷有不典型AV結(jié)折返性心動過速（AVNRT），伴隨緩慢且遞減傳導旁道的順傳型折返性心動過速和后間隔房性心動過速（AT）。鑒于希氏束-不應期時VPD不伴重整現(xiàn)象以及A-H阻滯時SVT持續(xù)，可排除順傳型折返性心動過速。此外，心動過速開始時的V-A-V順序不能完全排除發(fā)作開始于AV結(jié)回波的自主AT。然而，由于心房/心室拖帶起搏時心動過速的中止伴隨著A-H/V-A的阻滯，而且SVT時A-A間期與A-H間期直接相關(guān)，AT可能性小。因此，基于這些結(jié)果，不典型AVNRT是最可能的診斷。

圖2中，最初3個A-A間期450ms,而A-H間期逐漸延長。這可由存在一遞減傳導的下部共同徑路（LCP,指位于心動過速環(huán)路與希氏束之間的傳導徑路）來解釋。心室起搏下逆?zhèn)魑氖螩L（500ms）大于心動過速CL（450ms）證實存在LCP。隨后，緊鄰的A-A間期進行性延長至455～480ms，進一步達540ms，及突發(fā)縮短至440ms伴隨A-H阻滯。令人感興趣的是第5和第6個A-H間期與A-A間期一致。有幾種機制可解釋這些現(xiàn)象。簡單的假設(shè)是由于LCP的遞減性傳導導致A-H間期進行性延長，LCP的遞減性傳導明顯超過順傳AV結(jié)徑路的遞減性傳導，從而引起LCP阻滯，表現(xiàn)為A-H阻滯。然而，這不能解釋突發(fā)A-A間期縮短伴A-H阻滯。第二個假設(shè)是第5和第6個As轉(zhuǎn)向慢徑路，緩慢的LCP導致逆向A波提前于希氏束。隨后，第7和第8個As是來自LCP上方高位折返點和LCP下方（LTP）低位折返點的二重激動所致。然而，在最初4個A-A間期，LCP的傳導是進行性延長的，而順向AV結(jié)徑路傳導只有5ms。因此，在隨后的As，LCP阻滯的假設(shè)更有可能。最后，最有可能的機制是雙心室反應伴LCP阻滯，即心動過速環(huán)路的前向沖動沿著快徑路順傳，接著經(jīng)LTP1折向逆向慢徑路，伴隨希氏束前LCP的阻滯（圖3）。雖然在同一時間，順傳沖動顯示雙心室反應（圖3，星標），順向慢徑路傳導至LTP2，但因有效不應期而不能折向逆向慢徑路。下一搏動也顯示雙心室反應。首先，順向快徑路傳導至LTP1并折向逆向慢徑路，與此同時，順向慢徑路遞減傳導至LTP2并折向逆向慢徑路，此時逆向慢徑路因A-A間期的較明顯延長而恢復興奮性并保持傳導。然而，從順向快徑路折向逆向慢徑路的沖動，因有效不應期而未能順傳至前向快徑路和慢徑路。由于這些傳導徑路，A-A間期縮短至440ms伴A-H阻滯。

長R-P間期心動過速伴不同A-H間期通常診斷為AT。然而，已有不典型AVNRT伴不同A-H間期的報道。這些報道證實不典型AVNRT時，與A-A間期延長相比A-H間期呈進行性延長。這一觀察由心動過速環(huán)路以外的LCP加以證實。此外，雙心室反應可以維持，從而產(chǎn)生1∶2的心動過速，這卻被認為是非折返性SVT。非折返性SVT典型的表現(xiàn)為一個房性沖動同時經(jīng)房室結(jié)雙徑路傳導，其后希氏束和心室均被激動。本病例令人興趣的要點是AVNRT期間A-A間期與A-H間期一致。這一觀察可用心室雙重反應伴LCP阻滯加以解釋。據(jù)我們所知，這是通過雙重心室反應來維持不典型AVNRT的首例病例。于后間隔慢徑路逆?zhèn)髯钤琰c行射頻消融，成功消除心動過速且不能被誘發(fā)。

圖1心內(nèi)電圖顯示單一室性期前刺激（600/370 ms）伴V-A-V順序誘發(fā)出窄綜合波室上性心動過速。CS.冠狀竇；HBE.希氏束電圖；HRA.高位右房；RVA.右心室心尖。

圖2心內(nèi)電圖顯示室上性心動過速時A-A間期進行性延長和突發(fā)縮短。*心房和希氏束電位融合。

圖3梯形圖證實伴周長交替變化的室上性心動過速的機制。*心動過速環(huán)路前傳沖動顯示心室雙重反應；快徑（實線箭頭）經(jīng)低位折返點（LTP,稱作LTP1）轉(zhuǎn)向逆向慢徑，伴低位共同徑路（LCP）阻滯，而在同一時間，前傳慢徑路（虛線箭頭）傳至LTP2并轉(zhuǎn)向逆向慢徑路。AVN.房室結(jié)；LCP.低位共同徑路。

[1]Hayashi T,Fukamizu S,Hojo R,etal.Identical Atrio-His Interval and A-A Intervals During Long RP Tachycardia:What Is the Mechanism?Circ Arrhythm Electrophysiol.2014;7∶352-354.

（童鴻）