In contrast to ventricular tachycardia（VT） that occurs in the setting of a structurally normal heart,VT that occurs in patients with myocardial infarction carries anelevatedriskforsuddencardiacdeath（SCD）,andimplantablecardioverter-defibrillators（ICDs）arethemainstay of therapy.In these individuals,catheter ablation may be used as adjunctive therapy to treat or prevent repetitive ICD therapies when antiarrhythmic drugs are ineffective or not desired.However,certain patients with frequent premature ventricular contrac-tions（PVCs）or VT and tachycardiomyopathy should be considered for ablation before ICD implantation because left ventricular function may improve,consequently decreasing the risk of SCD and obviating the need for an ICD.

Mechanism and S ubstrate forVT in Postmyocardial Infarction

The prototypical,and best understood,substrate for scar-related reentrant VT is post-myocardial infarction（MI）VT.1Following MI,ventricular myocardium can broadly be classified as normal,dense scar,or border zone tissue-the latter consisting of interconnected surviving myocardial fibrils interspersed among a bed of electrically inert fibrotic tissue.Together with decreased cell-to-cell coupling,partly related to altered connexin 43 expression,slow and circuitous electrical conduction through the border zone predisposes to re-entrant VT.Additionally,there are adaptive and maladaptive changes in cardiac autonomic innervation that also predispose to VT.Sympathetic and parasympathetic efferent inputs to the convergent local circuit neurons are increased,whereas afferent inputs from infarcted tissue are decreased relative to those from the border zone and normal tissue;this results in a heterogeneity of autonomic innervation,contributing to the arrhythmogenic substrate.

As multiple pathways often exist,numerous circuits are commonly present and manifest as multiple inducible VTs during electrophysiological testing.The 12-lead electrocardiogram（ECG）morphologyofeachVTdepends on the exit of the re-entrant circuit into the normal myocardium.Although most VT exit sites are subendocardial,midmyocardial or epicardial exit sites also exist.Survivingtissueintheborderzonecanbeidentifiedbased on its abnormal conduction properties and characteristic electrograms（i.e.,lateandfraction-atedpotentials）（Figure 1）andisoftenthetargetforablation.

Although this fundamental understanding of the pathophysiology of post-MI VT has not changed since the mid-1990s,recent post-MI mapping studies using ultra high-resolution mapping technologies have suggested that patients may have few arrhythmogenic border zone areas of relatively constrained size.These small,anatomically fixed areas display direction-and ratedependent slowing of conduction velocity related to highly curved activation patterns in areas of voltage＜0.1 mV,and ablation of these relatively small areas resulted in VTtermination and noninducibility.However,the generalizability of this observation is unknown and requires additional study.

In addition to scar-related re-entry,certain post-MI patients may present with ventricular arr-hythmias related to the Purkinje system.First described in patients with idiopathic polymorphic VT or VF,focal premature PVCs originating from Purkinje fibers may serve as triggers for these arrhythmias.Similarly,followingMI,triggeredactivity（duetodelayedafterdepolarizations）from surviving Purkinje fibers situated along the scarbordermay cause focalPVCsthattrigger polymorphic VT/VF.Additionally,focal VT originating from the Purkinje system in the setting of acute ischemia has been attributed to triggered activity and delayed a fter depolarizations,in contrast to a re-entrant mechanism that is responsible for monomorphic VT following remote MI.Catheter ablation is possible for the treatment of these various Purkinje-related ventricular arrhythmias.

Catheter Ablation Techniques

The general approach to catheter ablation of VT involves the characterization of target VTs,delineation of the arrhythmic substrate,and radiofrequency ablation of the arrhythmic tissue.Target VTs include all clinically occurring VTs and those induced with programmed stimulation.Typically,programmed ventricular stimulation is performed at 2 drive cycle lengths with up to 3 extrastimuli delivered at progressively shorter coupling intervals at 2 ventricular locations.When VT is induced,pace termination or electrical cardioversion is performed,and programmed stimulation is continued until the same VT is repeatedly induced or multiple electrical cardioversions are required.For each VT,the 12-lead ECG morphology,the rate（or cycle length）,bundle branch block morphology,axis,precordial transition,and the hemodynamic effect are all recorded.This not only helps localize the VT exit site,but also helps determine the ablation strategy as described in the following text.

The myocardial scar is identified using a 3-dimensional（3D）electroanatomic mapping system that allows:1）spatial localization of a mapping catheter;2）generation of a 3D anatomic representation of the ventricle that is color-coded based on electrogram voltage amplitude recorded from the mapping catheter to differentiate normal myocardium from scar or border zone tissue;and 3）cataloging of myocardial channels and potential VT circuit isthmus sites identified on the basis of abnormal electrogram characteristics,entrainment,or pace mapping.Normal myocardium is typically characterized by bipolar voltage＞1.5 mV,dense scar by bipolar voltage＜0.5 mV,and border zone tissue by bipolar voltage of 0.5 to 1.5 mV.As previously described,myocardial channels responsible for re-entrant VT reside in the border zone.These channels have characteristic bipolar electrograms and can be classified as fractionated electrograms or as late （or isolated）potentials.Fractionated electrograms have multiple components without an isoelectric segment and an amplitude≤0.5 mV,a duration≥133 ms,and/or an amplitude/duration ratio≤0.005.A late or isolated potential occurs after the QRS complex and is separated from the ventricular electrogram by an isoelectric interval of＞20 ms （Figure 1）.Limitations of voltage mapping include variation of bipolar and unipolar amplitudes due to wave front direction,electrode size and spacing,as well as annotation of multiple component signals to the largest peak.

Sites demonstrating late or isolated potentials correlate with critical portions of the VT circuit isthmus and are desirable targets for ablation.Fractionated and late/isolated potentials may be underappreciated during sinus rhythm and may manifest only with ventricular pacing.In sinus rhythm,these electrograms may demonstrate superimposed local electrical activity and far-field ventricular activity inscribed during the QRS complex.Ventricular pacing may cause a delay of the local electrogram and cause separation from the far-field component.These abnormal electrograms,together with fractionated and late/isolated potentials,are broadly classified as local abnormal ventricular activity（LAVA）and have also been shown to be desirable ablation targets for VT.However,it should be noted that zones of slow conduction or deceleration may be more functionally relevant than the latest activated regions.

After VT induction and delineation of the arrhythmic substrate,ablation strategies typically include a combination of entrainment mapping, activation mapping,pace mapping,and substrate modification for VT. Certain sites demonstrating fractionated electrograms,late/isolated potentials,or LAVA in sinus rhythm may show diastolic electrogram activity during VT.However,not all of these locations will be critical for maintaining VT;they may simply represent diastolic activity due to passive activation （Figure 2）.The most reliable method for determining the relevance of a channel of activation is to utilize entrainment maneuvers during VT.A detailed description of entrainment is beyond the scope of this paper;briefly,it involves overdrive pacing of VT from a site to determine whether that site is a critical component of the tachycardia circuit or is a bystander site.Targeting of the sites that fulfill entrainment criteria for VT circuit isthmus sites has a high incidence of terminating VT.

Activation mapping involves the identification of the earliest site of electrical activation in a cardiac chamberin comparison to an arbitraryreference electrogram during VT.This information can be color coded and recorded on a 3D electroanatomic map so that the earliest site of local electrical activation can be identified.This is particularly useful for focal VT that has a single earliest site with centrifugal activation away from thatlocation.Because electricalactivity is continuous,activation mapping in re-entrant VT is not useful to delineate early and late activation;however,it can be used to identify VT exit sites along the scar border and identification of diastolic corridors during VT.These areas of diastolic activation may or may not represent critical components of the VT circuit（isthmus vs.bystander sites）but are often targeted for ablation.2

Figure 1 Myocardial Scar and Substrate for Re-Entrant VT.（Left）Electrical activation from the normal myocardium through border zone tissue is slow and delayed （dark grey arrows）.Multiple myocardial channels are present and can be identified by characteristic electrograms that can be classified as fractionated electrograms （top,asterisk）,late potentials（middle,asterisk）,or local abnormal ventricular activity（bottom）.In this case,LAVA is best appreciated with ventricular pacing,which separates the local abnormal electrogram （dashed arrow）from the far-field electrogram with demonstration of local entrance block to the site with the third complex.These myocardial channels may all serve as potential pathways for different ventricular tachycardias.LAVA＝local abnormal ventricular activity;MAP＝mapping catheter.

Figure 2 Myocardial Scar and Mechanism of Re-Entrant VT.（A）A VT circuit（dark grey arrow） is dependent upon slow and circuitous electrical activity through border zone tissue during the diastolic period （light grey dashed lines）,which are recorded as diastolic electrograms（black asterisk）on the MAP.Locations distal to the VT circuit（light grey asterisks）may also demonstrate diastolic electrograms due to passive activation（light grey arrows）.Critical locations are identified only with entrainment and termination of VT with ablation.The QRS morphology of the VT is dependent upon the exit site from border zone tissue to the normal myocardium（dark grey star）.（B）Another VT circuit with a different exit site would demonstrate a different QRS morphology on electrocardiography.MAP＝mapping catheter;VT＝ventricular tachycardia.

Entrainment and activation mapping cannot be per- formed in the presence of hemodynamically unstable VT,which is reported to occur in 69%of patients with ischemic cardiomyopathy undergoing VT ablation.After scar delineation in sinus rhythm,pace mapping is a methodology utilized to target these unstable VTs without requiring VT induction.This involves pacing along the scar periphery to match the paced 12-lead ECG morphology with the clinical VT morphology,thereby identifying the VT exit sites.Pacing adjacent to the exit site,but further within the scar,may identify potential VT isthmus sites,characterized by latency between the pacing stimulus and the paced QRS（stimulation to QRS interval＞80 ms）.Alternatively,substrate modification of the scar can be performed that targets all fractionated/late potentials and LAVA.

The traditional approach to ablation of scar-related VT has involved using a combination of entrainment/activation mapping for hemodynamically tolerated VT and pace mapping and substrate modification for unstable VT.

詞 匯

prototypical adj.原型的，典型的

fibrils n.小纖維，原纖維

intersperse vt.點綴，散布

inert adj.惰性的，呆滯的，遲緩的，無效的

connexin n.接合素，聯(lián)接蛋白

circuitous adj.迂曲的，繞行的，迂回線路的

convergent adj.收斂的，會聚性的，趨集于一點的

constrain vt.驅(qū)使，強迫，束縛

delineation n.描述，畫輪廓

annotation n.注釋，注解，釋文

underappreciated adj.未受到充分賞識的，未得到正確評價的

superimpose vt.添加，重疊，附加，安裝

inscribe vt.題寫，題獻，銘記，雕

注 釋

1.The prototypical,and best understood,substrate for scarrelated reentrant VT is post-myocardial infarction （MI）VT中的substrate并非指基質(zhì)，而是相當于example，瘢痕相關(guān)折返型室性心動過速的經(jīng)典心臟疾病是陳舊性心肌梗死。其他心臟疾病如擴張型心肌病、致心律失常右心室心肌病、肥厚型心肌病和心臟結(jié)節(jié)病等也可發(fā)生瘢痕相關(guān)室性心動過速。

2.These areas of diastolic activation may or may not represent critical components of the VT circuit（isthmus vs.bystander sites）…指激動標測中標測到的舒張期電活動來源于邊緣區(qū)，如該區(qū)域位于室性心動過速環(huán)路中，消融該部位能中止室性心動過速，證實為室性心動過速環(huán)路的峽部，但也可與室性心動過速環(huán)路相連，而不參與室性心動過速環(huán)路，該部位消融不能中止室性心動過速，稱之為旁觀者。

參考譯文

第81課心肌梗死后室性心動過速射頻消融

與發(fā)生于心臟結(jié)構(gòu)正常的室性心動過速相比，發(fā)生于心肌梗死的室性心動過速使患者心性猝死風險增高，安置植入型心臟復律除顫器（ICD）是關(guān)鍵的治療。對于這些個體，當抗心律失常藥物無效或不理想時，導管消融可作為輔助治療，或預防反復的ICD治療。不過，對于那些因頻發(fā)室性期前收縮或室性心動過速和心動過速心肌病者，在植入ICD前應考慮消融術(shù)，因為左心室功能可得以改善，隨之心性猝死風險下降和免于植入ICD。

心肌梗死后室性心動過速的機制和基質(zhì)

心肌梗死后室性心動過速是瘢痕相關(guān)折返型室性心動過速的原型，是最被了解的例子。心肌梗死后，心室肌可寬泛地分為正常、致密瘢痕或邊緣區(qū)組織，后者由相互連接的存活心肌纖維組成，穿插于一片電絕緣的纖維化組織中。通過邊緣區(qū)的緩慢而迂回的電傳導，加上部分原因為聯(lián)接蛋白43表達改變所致的細胞-細胞偶聯(lián)減弱，促發(fā)折返型室性心動過速。另外，心臟自主神經(jīng)支配的適應性和非適應性變化也促進室性心動過速的發(fā)生。進入聚集性局部環(huán)行神經(jīng)元的交感和副交感神經(jīng)傳出纖維增加，而源于梗死組織的傳入纖維較邊緣區(qū)和正常組織減少，導致自主神經(jīng)支配的非同質(zhì)性，促進致心律失?；|(zhì)的形成。

由于經(jīng)常存在多條通路，電生理檢查中常常出現(xiàn)眾多環(huán)路并呈現(xiàn)多種可誘發(fā)性室性心動過速。每種室性心動過速12導聯(lián)心電圖上的形態(tài)決定于折返環(huán)進入正常組織的出口。雖然多數(shù)室性心動過速的出口位于心內(nèi)膜，也有位于心肌中層和心外膜的。邊緣區(qū)的存活組織可根據(jù)其異常的傳導特性和特征性電圖（如晚電位和碎裂電位，見圖1）而加以識別，常為消融的靶點。

雖然自90年代中期以來，對心肌梗死后病理生理的根本認識沒有變化，近來利用超高分辨率標測技術(shù)的心肌梗死后標測研究表明，這類患者可有極少區(qū)域局限的致心律失常邊緣區(qū)。這些細小、解剖上固定的區(qū)域，顯示方向依賴和速率依賴的緩慢傳導速度，這與電壓＜0.1mV區(qū)域中的高度弧形激動形式有關(guān)，消融這些相對細小的區(qū)域可引起室性心動過速中止及不可誘發(fā)。然而，這一觀察的普遍性尚不得而知，并且需要另加研究。

除了瘢痕相關(guān)折返外，一些心肌梗死后患者出現(xiàn)與普肯野系統(tǒng)相關(guān)的室性心律失常。最初見于特發(fā)性多形性室性心動過速或心室顫動的描述，來自浦肯野纖維的局灶性室性期前收縮可促發(fā)這些心律失常的發(fā)生。相同的是心肌梗死后沿瘢痕邊緣分布的存活普肯野纖維的促發(fā)活動可引起局灶性室性期前收縮，促發(fā)多形性室性心動過速或心室顫動。另外，急性缺血情況下，起源于浦肯野系統(tǒng)的局灶室性心動過速由促發(fā)活動和延遲后除極所致，這與心肌梗死久后導致的多形性室性心動過速的折返機制不同。對于這些浦肯野相關(guān)的不同室性心律失?？尚袑Ч芟?。

導管消融技術(shù)

室性心動過速導管消融的通用方法涉及目標室性心動過速的特征，心律失?；|(zhì)的勾畫和心律失常組織的射頻消融。目標室性心動過速包括所有臨床發(fā)作的室性心動過速以及程控刺激誘發(fā)的室性心動過速。典型的程控刺激采用兩個周長、多達3個期外刺激、以進行性縮短聯(lián)律間期對心室2個部位進行刺激。當誘發(fā)出室性心動過速后，予以起搏中止或電復律，隨后繼續(xù)程控刺激及至誘發(fā)出同一類型室性心動過速或需多次電擊復律。記錄每一種室性心動過速的12導聯(lián)心電圖形態(tài)、速率（或周長）、束支傳導阻滯形態(tài)、心電軸、胸導聯(lián)移行及血流動力學影響。這不僅有助于室性心動過速出口的定位，也有助于選擇下面闡述的消融術(shù)方案。

采用三維電解剖標測系統(tǒng)識別心肌瘢痕，該標測系統(tǒng)可以：（1）標測導管空間定位；（2）形成心室三維解剖圖，基于標測導管記錄到的電圖電位振幅呈現(xiàn)彩色編碼，有利于區(qū)別正常心肌與瘢痕或邊緣區(qū)組織；（3）基于異常的電圖特征、拖帶或起搏標測編列心肌通道和潛在的室性心動過速環(huán)路峽部部位。正常心肌特征表現(xiàn)為＞1.5mV的雙極電位，致密瘢痕表現(xiàn)為＜0.5mV的雙極電位，而邊緣區(qū)的雙極電位在0.5～1.5mV之間。正如以前描述的，導致折返型室性心動過速的心肌通道位于邊緣區(qū)內(nèi)。這些通道具有特征性的雙極電圖，可分為碎裂電圖或晚（或孤立）電位。碎裂電位呈多相，期間無等電位線，且振幅≤0.5mV，間期≥133ms，振幅/間期比≤0.005。晚或孤立電位發(fā)生于QRS波群之后，與心室電圖相隔＞20ms的等電位間距（圖1）。電壓標測受限于波前方向引起的雙極和單極振幅變化、電極大小和電極間距、以及對多成分信號與最大峰值的判讀。

證實晚電位或孤立電位的部位與室性心動過速環(huán)路峽部的關(guān)鍵部分相關(guān)，是理想的消融靶點。竇性心律時碎裂電位和晚/孤立電位可能會被遺漏，只有在心室起搏下才得以表現(xiàn)出來。竇性心律時，這些電圖證實隱于QRS波群中重疊的局部電激動和遠場心室激動。心室起搏可引起局部電圖延遲并與遠場成分分開。這些異常電圖，結(jié)合碎裂和晚/孤立電位，寬泛地列為局部異常心室激動（LAVA），也是室性心動過速的理想消融靶點。然而，應該注意的是慢傳導或減速區(qū)比最晚的激動區(qū)更具功能相關(guān)性。

在誘發(fā)出室性心動過速且勾畫出心律失常基質(zhì)后，典型的消融方案包括結(jié)合拖帶標測、激動標測、起搏標測及室性心動過速的基質(zhì)的改造。一些證實碎裂電圖、晚/孤立電位、或竇律時LAVA的部位在室性心動過速時可顯示舒張期電活動。然而，不是所有這些部位對于維持室性心動過速是關(guān)鍵的，它們只是代表源于被動激動的舒張期電活動（圖2）。確定激動通道關(guān)聯(lián)性的最為可靠方法是室性心動過速發(fā)作時進行拖帶操作，有關(guān)拖帶的具體描述超出本文的范疇，簡而言之，于室性心動過速發(fā)作時超速起搏某點以確定該部位是否是心動過速環(huán)的關(guān)鍵成分或是旁觀者。針對完全符合室性心動過速環(huán)路峽部拖帶標準的部位消融，室性心動過速中止率高。

激動標測涉及在室性心動過速發(fā)作時通過與人為的參考電圖比較，確定心腔中最早的電活動部位。這種信息可由彩色編碼并記錄于三維電解剖圖上，使得局部電活動的最早部位得以識別。這對局灶室性心動過速特別有用，局灶室性心動過速有一最早激動點并以此為中心向外激動。因為折返型室性心動過速的電活動是連續(xù)的，激動標測無助于勾畫出早和晚激動，但是，可用于識別沿著瘢痕區(qū)的室性心動過速出口和室性心動過速時的舒張期廊道。這些舒張期激動區(qū)域可以是或不是室性心動過速環(huán)路的關(guān)鍵部分（峽部對旁觀者），但常作為消融的靶點。

對于血流動力學不穩(wěn)定的室性心動過速不宜行拖帶和激動標測，69%缺血性心肌病患者室性心動過速消融中發(fā)生這種情況。竇性心律下勾畫出瘢痕區(qū)，起搏標測是一種可用于不穩(wěn)定室性心動過速靶點定位的方法，無需誘發(fā)室性心動過速。這包括沿瘢痕周邊起搏去匹配起搏12導聯(lián)心電圖圖形與臨床室性心動過速圖形，鑒別室性心動過速出口部位。接近出口部位，但進一步在瘢痕的起搏，可識辨潛在的室性心動過速峽部部位，特征為起搏刺激與起搏QRS波群之間有時差（起搏信號至QRS間期＞80ms）。作為替代方案，可進行瘢痕基質(zhì)改造，消融目標涉及所有碎裂/晚電位和LAVA。

瘢痕相關(guān)室性心動過速消融的傳統(tǒng)方法包括對血流動力學上能耐受的室性心動過速結(jié)合拖帶/激動標測，對不穩(wěn)定室性心動過速實施起搏標測和基質(zhì)改造。

圖1 折返型室性心動過速的心肌瘢痕和基質(zhì)。（左）來自正常心肌的電活動通過邊緣區(qū)時緩慢而延遲（深灰箭頭）。多個心肌通道存在，可通過特征性電圖識別，分為碎裂電圖（上部，*），晚電位（中部，*），或局部異常心室激動（底部）。該患者LAVA在心室起搏下充分展示，心室起搏將局部異常電圖（虛線箭頭）與遠場電圖分開，證實到第3個綜合波部位的局部傳入阻滯。這些心肌通道可成為不同室性心動過速發(fā)作的潛在徑路。LAVA＝局部異常心室激動；MAP＝標測電極。

圖2 心肌瘢痕與折返型室性心動過速的機制。A：一種室性心動過速環(huán)路（深灰色箭頭）依賴于舒張期經(jīng)過邊緣區(qū)組織緩慢而迂回的電激動（淺灰色點線），這在MAP上記錄到舒張期電圖（黑色*）。室性心動過速環(huán)路遠端部位（淺灰色）也可證實源于被動激動（淺灰色箭標）的舒張期電圖。關(guān)鍵的部位只能經(jīng)拖帶和消融中止室性心動過速而確定。室性心動過速的QRS形態(tài)決定于從邊緣區(qū)到正常心肌組織的出口部位（深灰色★）。B：出口部位不同的另一種室性心動過速環(huán)路在心電圖上呈現(xiàn)不同的QRS形態(tài)。MAP＝標測電極；VT＝室性心動過速。

[1] Dukkipati SR,Koruth JS,Choudry S,et al.Catheter Ablation of Ventricular Tachycardia in Structural Heart Disease:Indications,Strategies,and Outcomes-Part II.J Am Coll Cardiol,2017,70:2924-2941.doi:10.1016/j.jacc.2017.10.030.

（童鴻）