Lesson Ninety- five A narrow complex tachycardia with atrioventricular dissociation:What is the mechanism?

Case Presentation

A 74-year-old woman underwent diagnostic electrophysiologic study because of recurrent,symptomatic supraventricular tachycardia. Baseline atrio-His1and His-ventricular intervals measured 75 ms and 50ms, respectively. Programmed atrial extrastimu-lation elicited dual atrioventricular（AV）nodal physiology and ventricular pacing showed no ventriculoatrial conduction despite isoproterenol. Figure 1 shows her clinical tachycardia. The response of tachycardia to a His-refractory ventricular premature depolarization （VPD）is shown in the top section of Figure 2, while its induction twice by rapid ventricular pacing（340 ms）is shown in the middle and bottom sections of Figure 2. Based on these observations, what is the mechanism of tachycardia?

Discussion

Figure 1 shows a narrow complex tachycardia with AV dissociation, the differential diagnosis of which includes the following: （1）junctional ectopic tachycardia（JET）with junctional-atrial block,（2）AV nodal reentrant tachycardia （AVNRT） with upper common final pathway block,（3）orthodromic reentrant tachycardia （ORT）using either a nodofascicular（NF）or nodoventricular （NV）bypass tract （BPT）with nodal-atrial block, and （4） intra-Hisian reentrant tachycardia. The absence of split His bundle potentials excludes intra-Hisian reentry. Tachycardia also shows cycle length alternans, which can be explained by JET with 3:2 exit block from an automatic focus or alternating antegrade conduction over 2 AV nodal pathways during ORT- NF/NV（eg, fast [FP] and slow[SP]） or during AVNRT. Another narrow complex tachycardia associated with cycle length alternans is dual antegrade response tachycardia resulting from simultaneous conduction over the FP and SP of the AV node after each sinus beat（"double fire"）,but the wide variability in"AH"intervals that do not reliably precede and predict His-His intervals argues against this diagnosis. Although atrial overdrive pacing and the delivery of single atrial premature depolarizations can differentiate JET from AVNRT, these maneuvers are limited in the presence of complete AV dissociation.Figure 2 （Top）shows a His-refractory VPD that resets tachycardia with delay of the subsequent His bundle（indicated by an asterisk）, proving the presence of a concealed NF/NV BPT but not necessarily its participation in tachycardia. Such a finding, however,effectively excludes pure JET, AVNRT, and dual antegrade response tachycardia. Though the delay could occur retrogradely in the BPT, it might also occur antegradely in the SP. This is then followed by 1 additional cycle of tachycardia with antegrade conduction over the FP, resulting in the shortest His-His interval on the tracing followed by tachycardia termination. （Alternatively, the second VPD[spontaneous,but also His-refractory] advances the His bundle over the BPT-FP）. Further proof of the existence of a BPT is shown with tachycardia induction（Figure 2, Middle）. During pacing, 2 consecutive His bundle electrograms occur at the pacing cycle length shortly after the second and third pacing stimuli.Although these could be retrograde His bundle potentials, the His bundle's absence after the fourth pacing stimulus would make AVNRT unlikely, as it is not possible to penetrate the AV node and initiate AVNRT without prior retrograde activation of the His bundle. Additionally, the morphology of these His bundle electrograms is identical to those during tachycardia, indicating that they are activated antegradely. A more likely explanation is that these His bundle electrograms are orthodromically activated after long stimulus-His（St-H）intervals（385 ms）.Further support for orthodromic activation of the His bundle is that initiation of tachycardia after the last paced complex is associated with a similarly long St-H interval.Orthodromic activation of the His bundle can only occur in the presence of a BPT. Tachycardia induction,however, is associated with a long postpacing interval（PPI）relative to the tachycardia cycle length（TCL）（138 ms）raising the possibility that the mechanism of tachycardia is AVNRT with upper common final pathway block in the presence of a bystander NF/NV pathway that inserts into 1 limb of the AV nodal circuit.A long PPI-TCL, however, can also result from pacing-induced retrograde delay over the nodal portion of the BPT or antegrade delay over the AV node,particularly the SP. The latter explanation supports the findings of the second tachycardia induction（Figure 2,Bottom）. The first 2 pacing stimuli orthodromically activate the His bundle over the NF/NV BPT-SP,generating a long St-H interval.The last paced complex,however,orthodromically activates the His bundle with a shorter St-H interval （346 ms）because of NF/NV BPT-FP conduction（thereby also explaining the cycle length alternans during tachycardia）, producing a shor PPI-TCL （102ms）, which excludes AVNRT and establishes a diagnosis of ORT-NF/NV. Figure 3 depicts the orthodromic activation of the His bundle（arrows）during rapid ventricular pacing by retrograde conduction over a concealed NF/NV BPT and then antegradely over the SP（longer St-H interval）or FP（shorter St-H interval）.t

Figure 1 Narrow complex tachycardia with atrioventricular dissociation.

Figure 2 Top: Response of tachycardia to a His-refractory ventricular premature depolarization. Middle,Bottom: Induction of tachycardia by rapid ventricular pacing（340 ms）

Figure 3 Induction of tachycardia by right ventricular pacing with arrows depicting orthodromic activation of the His bundle （H）over a concealed nodofascicular/nodoventricular bypass tract （BPT） and the slow pathway（SP）（longer stimulus-His interval）or fast pathway（FP）（shorter stimulus-His interval）.

The distal insertion（fascicular or ventricular）of the nodal fiber could not be identified. Para-Hisian pacing might differentiate between an NF and NV BPT by demonstrating its dependence upon His-Purkinje vs ventricular activation, respectively, but would be difficult in the absence of ventriculoatrial conduction.Entrainment with manifest fusion（particularly mild or progressive fusion）might favor an NV BPT because entrainment involving an NF BPT requires that paced antidromic wavefronts penetrate the distal Purkinje system to reach the circuit. It is theoretically possible,however, to entrain ORT-NF with manifest fusion if the collision point between antidromic and orthodromic wavefronts occurs in the proximal right bundle between the bifurcation of the His bundle and take-off of the NF BPT from the distal right bundle. In such a situation,paced antidromic wavefronts from the right ventricle would fuse with orthodromic activation of the His bundle-left bundle-left ventricle axis. Manifest fusion was not observed in this case.

In summary, the patient had ORT using a concealed NF/NV BPT with both（1）nodal-atrial block and AV dissociation and（2）dual AV nodal physiology with cycle length alternans. Although the NF/NV BPT could not be mapped, anecdotal cases have shown that its proximal insertion can be in the SP; and, therefore,the patient underwent SP ablation in the right posteroseptal region. During radiofrequency delivery,the integrity of the AV node was monitored by atrial pacing because junctional ectopy was associated with junctional-atrial block. After SP ablation, the patient had no further tachycardia and has remained symptom-free.

詞 匯

dissociation n. 脫節(jié)，分離

orthodromic adj. 順向的，順向性

nodofascicular adj. 房室結(jié)-束支的，結(jié)-束的

nodoventricular adj. 房室結(jié)-心室的，結(jié)-室的

antegrade adj. 前進(jìn)的，順傳的，順行的

retrogradely adv. 逆向地，后退地，顛倒地

antidromic adj. 逆向的，逆行的

wavefront n. 波陣面，波前

collision n. 碰撞，對(duì)立，抵觸

manifest n.&adj.&v. （船或飛機(jī)的）貨單，旅客名單；明顯的；顯而易見的；表明，顯現(xiàn)，使人注意到

anecdotal adj. 逸事的，趣聞的，傳聞的

integrity n. 誠(chéng)實(shí)正直，完整，完好

注 釋

1.His 指希氏束，又稱房室束，是心臟特殊傳導(dǎo)系統(tǒng)的重要組成部分，始于房室交接區(qū)的房室結(jié)，向下延續(xù)于室間隔內(nèi)，在室間隔膜部下緣行走，到達(dá)室間隔肌部上緣后分為

左、右束支。

參考譯文

第95 課 窄QRS 波群心動(dòng)過速伴房室分離：機(jī)制是什么？

1 例74 歲女性因反復(fù)癥狀性心動(dòng)過速行診斷性電生理檢查?；A(chǔ)狀態(tài)下心房-希氏束間期和希氏束-心室間期分別為75ms 和50ms。程序心房期外刺激誘發(fā)出房室結(jié)雙徑路，而滴注異丙腎上腺素下心室起搏未見室房傳導(dǎo)。圖1 是她臨床發(fā)作時(shí)的心動(dòng)過速。圖2 上圖顯示心動(dòng)過速對(duì)希氏束不應(yīng)期間心室期前除極（VPD）的反應(yīng)，圖2 中圖和下圖顯示快速心室起搏（340ms）二次誘發(fā)?；谶@些，心動(dòng)過速的機(jī)制是什么？

討論

圖1 顯示窄QRS 波群心動(dòng)過速伴房室分離，鑒別診斷如下：（1）交接區(qū)心動(dòng)過速（JET）伴交接區(qū)-心房傳導(dǎo)阻滯，（2）房室結(jié)折返性心動(dòng)過速（AVNRT）伴上端最后共同通路阻滯，（3）以結(jié)-束（NF）或結(jié)-室（NV）為旁道（BPT）的順傳型房室折返心動(dòng)過速（ORT）伴結(jié)-房傳導(dǎo)阻滯，（4）希氏束內(nèi)折返性心動(dòng)過速。無希氏束分裂電位排除了希氏束內(nèi)折返。心動(dòng)過速同時(shí)顯示周長(zhǎng)交替變化，這可解釋為源于自律性節(jié)點(diǎn)的JET 伴3：2 傳出阻滯，或ORT-NF/NV 或AVNRT 時(shí)經(jīng)房室結(jié)雙徑路[即快徑路（FP）和慢徑路（SP）]交替順傳。窄QRS 波群心動(dòng)過速伴周長(zhǎng)交替的另一種機(jī)制是每一竇性節(jié)律同時(shí)經(jīng)FP 和SP 傳導(dǎo)引起雙重反應(yīng)心動(dòng)過速（“雙發(fā)”），但變化不定的“AH”間期既不先于也不能預(yù)測(cè)希氏-希氏間期，因而不支持這一診斷。雖然心房超速起搏或單一的心房期前刺激能鑒別JET 和AVNRT，但因存在完全性房室分離而使這些方法受限。圖2（上圖）顯示希氏束不應(yīng)期VPD 重整心動(dòng)過速伴延遲的希氏束電位（星標(biāo)），證實(shí)存在隱匿性NF/NV BPT，但未必證實(shí)它參與心動(dòng)過速。不過，這一發(fā)現(xiàn)有效地排除了單純性JET、AVNRT 和雙重順傳的心動(dòng)過速。雖然延遲可發(fā)生于旁道的逆?zhèn)鳎部砂l(fā)生于慢徑的順傳。其后為一與心動(dòng)過速不同的波，經(jīng)快徑順傳而產(chǎn)生描記到的最短希氏-希氏間期，隨后心動(dòng)過速中止[或許，第2 個(gè)VPD（自發(fā)的，但也是處于希氏不應(yīng)期的）經(jīng)旁道-快徑而激動(dòng)希氏束]。BPT 存在的進(jìn)一步依據(jù)出現(xiàn)在心動(dòng)過速誘發(fā)中（圖2，中圖）。起搏期間，在第2 個(gè)和第3 個(gè)起搏刺激后緊隨的起搏周長(zhǎng)內(nèi)出現(xiàn)2個(gè)連續(xù)的希氏束電圖。雖然這些可以是逆?zhèn)鞯南Ｊ鲜娢?，但? 個(gè)起搏刺激后無希氏束電位，使得AVNRT 的診斷不能成立，因?yàn)闆]有先前的逆向希氏束激動(dòng)，不可能穿越房室結(jié)并引起AVNRT。另外，這些希氏束電圖與心動(dòng)過速時(shí)相一致，表明是順傳激動(dòng)的。更有可能的解釋是這些希氏束電圖是在長(zhǎng)起搏刺激-希氏束電位（St-H）間期（385ms）后順向激動(dòng)的。進(jìn)一步支持希氏束順向激動(dòng)的是最后一個(gè)起搏波后心動(dòng)過速的起始伴隨一類似的長(zhǎng)St-H 間期。只有存在旁道時(shí)才能順向激動(dòng)希氏束。然而，誘發(fā)心動(dòng)過速的起搏后間期（PPI）超出心動(dòng)過速周長(zhǎng)（TCL）138ms，這增大了下述心動(dòng)過速機(jī)制的可能性，即AVNRT 伴上端共同最后通路阻滯合并存在NF/NV BPT 插入房室結(jié)折返環(huán)的一條徑路。不過，長(zhǎng)PPI-TCL 也可由起搏逆?zhèn)髋缘澜Y(jié)部延遲或房室結(jié)順傳延遲所引起，特別是慢徑。后一種解釋支持第2 個(gè)心動(dòng)過速誘發(fā)中所見（圖2，下圖）。前兩個(gè)起搏刺激經(jīng)NF/NV BPT-SP 順向激動(dòng)希氏束，產(chǎn)生長(zhǎng)St-H 間期。最后一個(gè)起搏激動(dòng)希氏束伴隨較短的St-H 間期（346ms），這是因?yàn)榻?jīng)NF/NV BPTFP 傳導(dǎo)產(chǎn)生短PPI-TCL（102ms）（這也可解釋心動(dòng)過時(shí)的周長(zhǎng)交替），這排除了AVNRT 從而確立ORT-NF/NV 的診斷。圖3 描述快速心室起搏時(shí)經(jīng)隱匿性NF/NV BPT 逆?zhèn)黜樝蚣?dòng)希氏束（箭頭標(biāo)記），隨后經(jīng)SP（較長(zhǎng)St-H 間期）或FP（較短St-H 間期）順傳。

無法確定房室結(jié)纖維遠(yuǎn)端插入部位（束支或心室）。希氏束旁起搏通過證實(shí)其依賴希氏-浦肯氏還是心室激動(dòng)而鑒別NF 和NV BPT，但在缺乏室房傳導(dǎo)時(shí)是難以實(shí)施的。拖帶伴顯見的融合（特別是輕度或進(jìn)行性融合）傾向于NV BPT診斷，因?yàn)樯婕癗F BPT 的拖帶需要起搏的逆?zhèn)鞑娲┩钙挚鲜线h(yuǎn)端達(dá)到折返環(huán)。然而，當(dāng)逆?zhèn)骱晚槀鞑嬷g碰撞點(diǎn)位于希氏束分叉與右束支遠(yuǎn)端NF BPT 起點(diǎn)之間的右束支近端時(shí)，拖帶NF BPT 伴顯見的融合理論上是有可能的。在此情況下，來自右心室的起搏逆?zhèn)鞑鎸⑴c希氏束-左束支-左心室的順傳波融合。該病例未見明顯的融合波。

總之，該患者為利用隱匿性NV/NV BPT 的順傳型房室折返性心動(dòng)過速，同時(shí)伴（1）房室結(jié)-心房阻滯和房室分離和（2）房室結(jié)雙徑路呈周長(zhǎng)交替。雖然不能標(biāo)測(cè)NF/NV BPT，但既往的病例表明其近端插入可以位于SF，因此，在右后間隔區(qū)域?qū)颊邔?shí)施SF 消融。因?yàn)榇嬖诜渴医Y(jié)-心房傳導(dǎo)阻滯，消融放電過程中，通過心房起搏監(jiān)測(cè)房室結(jié)的傳導(dǎo)功能。SP 消融后，患者再無心動(dòng)過速發(fā)作而維持無癥狀狀態(tài)。

圖1窄QRS 波群心動(dòng)過速伴房室分離。

圖2上圖：心動(dòng)過速對(duì)希氏束不應(yīng)期室性期前除極的反應(yīng)。中、下圖：快速心室起搏（340ms）誘發(fā)心動(dòng)過速。

圖3右心室起搏誘發(fā)心動(dòng)過速，箭頭標(biāo)記顯示經(jīng)隱匿性結(jié)-束/結(jié)-室旁道（BPT）和慢徑路（SP）（較長(zhǎng)的刺激信號(hào)-希氏波間期）或快徑路（FP）（較短的刺激信號(hào)-希氏波間期）順向激動(dòng)希氏束。