Types of His capture

It is mandatory to record a 12-lead ECG at His bundle pacing（HBP）implantation because changes in QRS morphology during threshold tests may be subtle and missed if only limb leads are used.

In addition to capture of the HB, the His lead can capture ventricular and/or atrial tissue that can affect ECG findings. Type of capture depends on His lead position（Figure 1）, the anatomical variant of the HB,capture thresholds, pacing output, and pacing configuration（e.g., anodal capture in case of extended bipolar pacing）. Furthermore, in case of underlying BBB, HBP may correct the conduction disease either partially or totally, leading to additional variations in QRS morphology.It is important to correctly identify the following entities.

Selective His bundle pacing

With selective His bundle pacing（S-HBP）, an isoelectric interval is visible in all 12 leads, that corresponds to the His-ventricular（HV）interval and separates the pacing spike from QRS onset （Figures 1 and 2）. Analysis of the device electrogram also shows a delay between delivery of pacing and the local ventricular electrogram. The QRS morphology is most often identical to that in intrinsic rhythm. However,slight differences in the paced QRS morphology may be observed in case the His lead is positioned distally,such as at the right bundle branch and/or HB bifurcation. In these instances, activation through the conduction system will follow a different course compared with intrinsic conduction.The His lead may be positioned on either the atrial aspect or the ventricular aspect of the tricuspid valve. Leads implanted at sites where the HB is subendocardial and distant from the ventricular myocardium will display S-HBP as the only form of capture.

Nonselective His bundle pacing

With nonselective His bundle pacing（NS-HBP）,the lead is usually positioned in the ventricle at a site where the HB is surrounded by or at proximity to myocardial tissue. However, supravalvular lead position with either higher output and/or ventricular myocardium adjacent to the atrioventricular septum near the HB can also result in NS-HBP. The ECG shows a pseudo-delta wave corresponding to local myocardial capture,resembling pre-excitation of a para-Hisian or fasciculo-ventricular accessory pathway（Figures 1 and 2B）. The amplitude and duration of the pseudo-delta wave will depend on the surrounding myocardial fiber density and mass of the captured myocardium and the HV interval（Figures 2B, 2C）. The pseudo-delta wave may also be slightly shorter than the HV interval in case the His lead is positioned distally. QRS may show an initial isoelectric segment in some leads（especially leadⅢ） if the initial vector of depolarization is perpendicular to those leads. In addition to the pseudo-delta wave, fusion with myocardial activation results in an increase in R-wave amplitude in leads I,II, and V6（Figures 1B, 2）due to summation of the vectors of myocardial capture and activation via the His-Purkinje system.A reduction in R-wave amplitude in these leads helps identify the transition between NS-HBP and S-HBP in cases where the pseudo-delta wave may not be apparent. NS-HBP has the advantage of providing backup myocardial capture in case of loss of His capture or exit block. It is also associated with higher R-wave sensing amplitudes compared with S-HBP. No significant differences in cardiac mechanical synchrony or clinical outcome have been found between S-HBP and NS-HBP, although there was a trend in lower mortality with S-HBP.

Correction of bbb

It has been reported that approximately 60% to 90% of patients with BBB have QRS narrowing with HBP.The finding that the level of conduction block may be located proximally within the HB with longitudinal dissociation of the conduction fibers was originally described in the 1970s both for left bundle branch block（LBBB）and for right bundle branch block（RBBB）.BBB may be totally or partially corrected by HBP.Conduction blocks may exist at different levels in a given patient, and HBP may correct BBB at a proximal level,which may then unmask distal conduction disease,which results in a different QRS morphology.

Myocardial capture only

The QRS complex maysometimes be relatively narrow （and narrower than in intrinsic rhythm with BBB）. It may be difficultin some instances to distinguish myocardial capture from NS-HBP.

Transitions in QRS morphology with decrementing output

A number of different transitions in QRS morphology before loss of capture may be observed with decrementing pacing output （and starting at maximum output）（Figures 1）.

In patients with RBBB, it may be difficult to distinguish NS-HBP with and without correction of the conduction disorder （Figure 1F）. This is because myocardial capture in these instances serves to narrow the QRS （Figure 3D and section on HOT-CRT）,much as1LV fusion pacing with coronary sinus leads serves to narrow the QRS complex in patients with underlying LBBB（17）.Therefore,measuring the duration from the stimulus to the end of the QRS is not useful in this instance to determine whether RBBB has been corrected. The presence of an S- and/ or s-wave in leads I and/or aVL and a qR- and/or Qr-wave in leads V1 and/or V2 is suggestive of NS-HBP with uncorrected RBBB.

Additional transitions to those previously mentioned may be due to inhomogeneous capture of conduction tissue at different outputs （probably due to longitudinal dissociation of the HB）. Inhomogeneous capture may result in slight variations in QRS morphology, both in patients with a narrow intrinsic QRS and in those with underlying BBB.Inhomogeneous capture may also be due to slight variations in lead orientation with the cardiac or respiratory cycle and may result in alternating BBB morphology. Furthermore,transitions in morphology due to anodal capture or capture of the right atrium may be sometimes observed and should not be confounded with transitions due to loss of capture of conduction tissue.

Absence of transitions in QRS morphology before total loss of capture with decrementing output indicates either: 1） S-HBP; 2） ventricular myocardial capture only （i.e., para-Hisian pacing, which cannot be considered as being true HBP）; and 3） similar thresholds of different tissues that are simultaneously captured. To better distinguish the different capture thresholds, pulse width may be narrowed because this serves to widen the difference in capture thresholds between the HB and the adjacent myocardium.

Impossible transitions with decrementing output are: 1） S-HBP / NS-HBP; 2） S-HBP / myocardial capture only; and 3）without correction of BBB / with correction of BBB.

Thresholds of different tissues may be almost identical,and different types of capture may be observed during consecutive beats at a given output,probably due to slight variations in lead orientation and tissue contact.This is usually observed during pacing with output close to the capture threshold（s）.

Figure 1 His Lead Position and Examples of Different Types of His Capture and Transitions in QRS Morphology With Decrementing Voltage Output. （A）Proximal position over a subendocardial His bundle with obligatory selective His capture（selective His bundle pacing [S-HBP]）. Note the isoelectric interval between the pacing spike and QRS onset, visible in all 12 leads. （B）More distal position with a His bundle surrounded by a myocardial sleeve. There is close contact of the pacing lead and conduction tissue, resulting nonselective His bundle pacing （NS-HBP） with a pseudo-delta wave, which transitions to S-HBP with a reduction in output.（C）The lead is in less close contact with the conduction tissue, resulting in a transition between NS-HBP and myocardial（Myo） capture only.（D） Proximal position of the His lead with S-HBP in the setting of left bundle branch block （LBBB）. At higher output, there is recruitment of conduction tissue resulting in correction （corr+） of the conduction delay and loss of correction （corr-） at reduced output. （E）More distal position of the lead with initial NS-HBP and correction of LBBB. （F）Right bundle branch block with initial correction and NS-HBP, with loss of correction（note the presence of an s wave in lead I and a more prominent R-wave in lead V2）followed by uncorrected S-HBP.

詞 匯

configuration n.布局,配置，構(gòu)造,構(gòu)型，形狀,輪廓

spike n.&v.尖狀物，尖峰，大釘，動(dòng)作電位;用大釘釘牢，用尖物刺入（或扎破），棄置不用，阻止

bifurcation n.分歧，分叉

resemble v.看起來(lái)像，像，類(lèi)似于

summation n.總結(jié)，概括

unmask v.揭露，揭示

distinguish v.鑒別，區(qū)分，辨別

Inhomogeneous adj.不均質(zhì)的，不均一的，多相的

underlying adj.在…下面的，基本的，潛在的，優(yōu)先的

obligatory adj.強(qiáng)制的，必須的，有義務(wù)的，專(zhuān)性的，固性的，

Figure 2 Schematic Representation of Lead I and Ventricular Activation With Different Types of His Bundle Capture.（A）S-HBP with stimulus to QRS-onset interval corresponding to the His-ventricular（HV_ interval）.（B） NS-HBP in the setting of a normal HV interval, with a small pseudo-delta wave and an increase in QRS amplitude. （C）NS-HBP in the setting of uncorrected LBBB and prolonged HV interval with widening of the paced QRS due to a large pseudo-delta wave and predominant activation of the left ventricle via cell-to-cell depolarization due delayed activation of the His-Purkinje system （D）NS-HBP in the setting of uncorrected right branch bundle block （RBBB）with narrowing of the QRS complex by virtue of pre-excitation of the right ventricle（activated late in intrinsic rhythm）and fusion with ventricular activation via the His-Purkinje system. In case of intrinsic bundle branch block which is corrected by His bundle pacing, the resulting paced QRS will resemble that of （A and B）in case of S-HBP or NS-HBP, respectively. HPS =His Purkinje system; other abbreviations as in Figure 1.

anodal adj.陽(yáng)極的，正極的

decrement n.&v.遞減，減少，消耗，減縮量，消耗量；減少，減縮

注 釋

1.much as 本文中指“非常像，和…幾乎一樣”，例如：he works much as an experienced worker.他工作起來(lái)幾乎與有經(jīng)驗(yàn)的工人一樣。也可解釋為“盡管，雖然”，例如：Much as she hated cruelty,she couldn’t help watching the fight.雖然她對(duì)暴行極為憎恨，她還是不得不注視著這場(chǎng)斗毆。

參考譯文

第98 課 希氏束起搏植入時(shí)的心電圖分析（第一部分）

希氏束奪獲的類(lèi)型

希氏束起搏（His bundle pacing，HBP）植入時(shí)，如只記錄肢體導(dǎo)聯(lián)心電圖，閾值測(cè)試過(guò)程的QRS 形態(tài)變化將會(huì)細(xì)微或缺失，因此，必須記錄12 導(dǎo)聯(lián)心電圖。

希氏束電極不但奪獲希氏束，也奪獲心室和（或）心房組織，從而影響心電圖圖形。奪獲類(lèi)型決定于希氏束電極的位置（圖1）、希氏束的解剖變異、奪獲閾值、起搏輸出和起搏配置（如在擴(kuò)大雙極起搏下的陽(yáng)極奪獲）。另外，在束支傳導(dǎo)阻滯（bundle branch block，BBB）情況下，HBP 可以部分或完全糾正傳導(dǎo)異常，這會(huì)增加QRS 形態(tài)的變化。正確識(shí)別下述本質(zhì)實(shí)為重要。

選擇性希氏束起搏

選擇性希氏束起搏（selective His bundle pacing，S-HBP）時(shí)，所有12 導(dǎo)聯(lián)均可見(jiàn)等電位間期，這與希氏-心室（HV）間期相一致，將起搏刺激波與QRS 波群起始部分開(kāi)（圖1 和2）。測(cè)試儀電圖分析也顯示在起搏刺激信號(hào)與局部心室電圖之間有一延后。絕大多數(shù)情況下QRS 形態(tài)與自身節(jié)律相一致。不過(guò)，當(dāng)希氏束電極位于遠(yuǎn)端如右束支和（或）希氏束分叉處時(shí)，可觀察到起搏QRS 形態(tài)輕微不同。在此情況下，傳導(dǎo)系統(tǒng)的激動(dòng)過(guò)程會(huì)與自身傳導(dǎo)的不同。希氏束電極可位于三尖瓣環(huán)的心房面或心室面。電極植入至內(nèi)膜下希氏束而遠(yuǎn)離心室肌時(shí)，顯示S-HBP 會(huì)是唯一的奪獲。

非選擇性希氏束起搏

非選擇性希氏束起搏（nonselective His bundle pacing，NS-HBP）時(shí)，電極通常位于心室，該處的希氏束受心肌包繞或接近心肌組織。然而，當(dāng)瓣上電極輸出功率較高或心室肌毗連臨近希氏束的房室間隔時(shí)，也能引起NS-HBP。心電圖顯示局部心肌奪獲引起的假性delta 波，類(lèi)似于希氏束旁或束支-心室旁道（圖1 和圖2B）。假性delta 波的振幅與間期決定于環(huán)繞心肌纖維的密度、所奪獲心肌的量及HV 間期（圖2B、2C）。如希氏束電極位于遠(yuǎn)端，假性delta 略短于HV間期。如起始除極向量垂直于導(dǎo)聯(lián)時(shí)QRS 波群顯示起始等電位節(jié)段（特別是Ⅲ）。除了假性delta 波，心肌激動(dòng)的融入導(dǎo)致Ⅰ、Ⅱ和V6R 波振幅增大（圖1B 和圖2），這由心室?jiàn)Z獲向量與通過(guò)希浦系統(tǒng)激動(dòng)相加所致。當(dāng)假性delta 波不明顯時(shí)，這些導(dǎo)聯(lián)的R 波振幅減小有助于確定NS-HBP 和S-HBP 之間的轉(zhuǎn)換。NS-HBP 的優(yōu)點(diǎn)是在希氏束奪獲失敗或傳出阻滯時(shí)能提供后備的心室?jiàn)Z獲。與S-HBP 比較，R 波的感知振幅也較高。盡管S-HBP 的病死率趨向較低，但S-HBP 和NS-HBP之間的心臟同步性或臨床預(yù)后沒(méi)有顯著性差異。

束支傳導(dǎo)阻滯糾正

據(jù)報(bào)道，合并BBB 的患者中近60%～90%HBP 時(shí)QRS波群變窄。1970 年代有關(guān)傳導(dǎo)阻滯平面位于希氏束內(nèi)近端并存在傳導(dǎo)纖維縱向分離的最初描述是同時(shí)對(duì)于左束支傳導(dǎo)阻滯（left bundle branch block，LBBB） 和右束支傳導(dǎo)阻滯（right bundle branch block，RBBB）的。HBP 可完全或部分糾正BBB。對(duì)于特定的患者，傳導(dǎo)阻滯可發(fā)生于不同層面，HBP 糾正近端的BBB 后，遠(yuǎn)端的傳導(dǎo)病變得以顯示，這可產(chǎn)生不同的QRS 形態(tài)。

僅為心肌奪獲

QRS 波群有時(shí)較窄（較合并BBB 的自身節(jié)律窄）。這在有些情況下難以與NS-HBP 的心肌奪獲相鑒別。

隨著輸出功率降低QRS 形態(tài)的移行

隨著起搏輸出功率的降低（從最大輸出功率開(kāi)始），在失去奪獲之前可觀察到多種QRS 形態(tài)移行變化（圖1）。

對(duì)于RBBB 患者，可能難以辨別NS-HBP 是否糾正了傳導(dǎo)病變（圖1F）。這是因?yàn)檫@些情況下心肌奪獲縮短了QRS波群（圖2D），非常像LBBB 患者冠狀竇電極的左心室融合性起搏，足以縮短QRS 間期。因此，在這種情況下測(cè)定從起搏信號(hào)到QRS 波群終末間期無(wú)助于確定RBBB 是否已得到糾正。Ⅰ和（或）aVL 出現(xiàn) S 和（或）s 波以及 V1和（或）V2出現(xiàn)qR 和（或）Qr 提示 NS-HBP 未能糾正 RBBB。

除前面提到的以外，移行可由不同輸出功率下傳導(dǎo)組織的不均質(zhì)奪獲所引起（可能源于希氏束的縱向分離）。無(wú)論自身QRS 波群較窄或存在BBB 的患者，不均質(zhì)奪獲可引起QRS 形態(tài)輕微變化。不均質(zhì)奪獲也可源于電極指向心臟方向的輕微變化或呼吸周期變化，可引起交替性BBB 圖形。此外，有時(shí)可觀察到源于陽(yáng)極奪獲或右心房奪獲的形態(tài)移行，不能與傳導(dǎo)組織失去奪獲的移行相混淆。

隨著輸出功率降低，在完全失去奪獲之前缺乏QRS 形態(tài)移行提示存在以下幾種情況之一：（1）S-HBP；（2）只有心室肌奪獲（例如，希氏束旁起搏，這不能認(rèn)為是真正的HBP）；（3）不同組織閾值相似以致同步奪獲。為了更好地區(qū)分不同的奪獲閾值，可以縮短脈沖寬度，因?yàn)檫@可加大希氏束與鄰近心肌之間的奪獲閾值差異。

隨著輸出功率遞減，不可能發(fā)生以下移行：（1）從S-HBP到 NS-HBP；（2）從 S-HBP 到只有心肌奪獲；和（3）從 BBB 不能糾正到BBB 得到糾正。

不同組織的閾值幾乎是一致的，在特定的輸出功率下，連續(xù)搏動(dòng)期間可觀察到不同類(lèi)型的奪獲，可能與電極方向和組織接觸的輕微變化有關(guān)。這通常見(jiàn)于起搏輸出功率接近奪獲閾值時(shí)。

圖1希氏電極位置和隨著電壓輸出降低不同類(lèi)型希氏奪獲和QRS 形態(tài)移行示例[A：置于心內(nèi)膜下希氏束近端專(zhuān)一選擇性希氏束奪獲。注意起搏信號(hào)與QRS 波群起始之間的等電位間期，所有12 導(dǎo)聯(lián)均能見(jiàn)到；B：較遠(yuǎn)端部位希氏束包繞于心肌袖中。起搏電極與傳導(dǎo)組織接觸緊密，導(dǎo)致NS-HBP而出現(xiàn)假性delta 波，隨著輸出功率降低而移行為S-HBP；C：起搏電極與傳導(dǎo)組織接觸不緊密，導(dǎo)致從NS-HBP 移行為單純心肌奪獲；D：LBBB 時(shí)希氏電極置于近端引起S-HBP。較高輸出功率下，奪獲傳導(dǎo)組織而使傳導(dǎo)延緩得以糾正（corr+），輸出功率降低時(shí)失去糾正（corr-）；E：電極置于較遠(yuǎn)端 時(shí) 初 始 為 NS-HBP 伴 LBBB 糾 正 ；F：RBBB 時(shí) 先 后 為NS-HBP 伴糾正，NS-HBP 不伴糾正（注意Ⅰ的s 波和V2的R 波）和 S-HBP 不伴糾正]

圖2Ⅰ的模式圖和不同類(lèi)型希氏束奪獲的心室激動(dòng)[A：S-HBP 時(shí)刺激信號(hào)與QRS 波群起始之間的間期與HV 間期相一致；B：正常HV 間期下NS-HBP 伴隨一小的假性delta波和QRS 波群增幅增大；C：未糾正LBBB 下的NS-HBP 和HV 間期延長(zhǎng)伴隨因假性大delta 波致起搏QRS 波群增寬以及由于希浦系統(tǒng)延遲激動(dòng)而通過(guò)細(xì)胞-細(xì)胞除極的左心室為主激動(dòng)；D：未糾正RBBB 下的NS-HBP 通過(guò)提前激動(dòng)右心室（自身激動(dòng)較遲）并與經(jīng)希浦系統(tǒng)激動(dòng)心室的融合而縮短QRS 波。當(dāng)自身束支阻滯被希氏束起搏糾正后，S-HBP 和NS-HBP 引起的起搏QRS 波群將分別類(lèi)似于A 和B]