Lesson Eighty-one Catheterablation ofventricular tachycardia in postmyocardial infarction

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.

词 汇

prototypical adj.原型的，典型的

fibrils n.小纤维，原纤维

intersperse vt.点缀，散布

inert adj.惰性的，呆滞的，迟缓的，无效的

connexin n.接合素，联接蛋白

circuitous adj.迂曲的，绕行的，迂回线路的

convergent adj.收敛的，会聚性的，趋集于一点的

constrain vt.驱使，强迫，束缚

delineation n.描述，画轮廓

annotation n.注释，注解，释文

underappreciated adj.未受到充分赏识的，未得到正确评价的

superimpose vt.添加，重叠，附加，安装

inscribe vt.题写，题献，铭记，雕

注 释

1.The prototypical,and best understood,substrate for scarrelated reentrant VT is post-myocardial infarction （MI）VT中的substrate并非指基质，而是相当于example，瘢痕相关折返型室性心动过速的经典心脏疾病是陈旧性心肌梗死。其他心脏疾病如扩张型心肌病、致心律失常右心室心肌病、肥厚型心肌病和心脏结节病等也可发生瘢痕相关室性心动过速。

2.These areas of diastolic activation may or may not represent critical components of the VT circuit（isthmus vs.bystander sites）…指激动标测中标测到的舒张期电活动来源于边缘区，如该区域位于室性心动过速环路中，消融该部位能中止室性心动过速，证实为室性心动过速环路的峡部，但也可与室性心动过速环路相连，而不参与室性心动过速环路，该部位消融不能中止室性心动过速，称之为旁观者。

参考译文

第81课心肌梗死后室性心动过速射频消融

与发生于心脏结构正常的室性心动过速相比，发生于心肌梗死的室性心动过速使患者心性猝死风险增高，安置植入型心脏复律除颤器（ICD）是关键的治疗。对于这些个体，当抗心律失常药物无效或不理想时，导管消融可作为辅助治疗，或预防反复的ICD治疗。不过，对于那些因频发室性期前收缩或室性心动过速和心动过速心肌病者，在植入ICD前应考虑消融术，因为左心室功能可得以改善，随之心性猝死风险下降和免于植入ICD。

心肌梗死后室性心动过速的机制和基质

心肌梗死后室性心动过速是瘢痕相关折返型室性心动过速的原型，是最被了解的例子。心肌梗死后，心室肌可宽泛地分为正常、致密瘢痕或边缘区组织，后者由相互连接的存活心肌纤维组成，穿插于一片电绝缘的纤维化组织中。通过边缘区的缓慢而迂回的电传导，加上部分原因为联接蛋白43表达改变所致的细胞-细胞偶联减弱，促发折返型室性心动过速。另外，心脏自主神经支配的适应性和非适应性变化也促进室性心动过速的发生。进入聚集性局部环行神经元的交感和副交感神经传出纤维增加，而源于梗死组织的传入纤维较边缘区和正常组织减少，导致自主神经支配的非同质性，促进致心律失常基质的形成。

由于经常存在多条通路，电生理检查中常常出现众多环路并呈现多种可诱发性室性心动过速。每种室性心动过速12导联心电图上的形态决定于折返环进入正常组织的出口。虽然多数室性心动过速的出口位于心内膜，也有位于心肌中层和心外膜的。边缘区的存活组织可根据其异常的传导特性和特征性电图（如晚电位和碎裂电位，见图1）而加以识别，常为消融的靶点。

虽然自90年代中期以来，对心肌梗死后病理生理的根本认识没有变化，近来利用超高分辨率标测技术的心肌梗死后标测研究表明，这类患者可有极少区域局限的致心律失常边缘区。这些细小、解剖上固定的区域，显示方向依赖和速率依赖的缓慢传导速度，这与电压＜0.1mV区域中的高度弧形激动形式有关，消融这些相对细小的区域可引起室性心动过速中止及不可诱发。然而，这一观察的普遍性尚不得而知，并且需要另加研究。

除了瘢痕相关折返外，一些心肌梗死后患者出现与普肯野系统相关的室性心律失常。最初见于特发性多形性室性心动过速或心室颤动的描述，来自浦肯野纤维的局灶性室性期前收缩可促发这些心律失常的发生。相同的是心肌梗死后沿瘢痕边缘分布的存活普肯野纤维的促发活动可引起局灶性室性期前收缩，促发多形性室性心动过速或心室颤动。另外，急性缺血情况下，起源于浦肯野系统的局灶室性心动过速由促发活动和延迟后除极所致，这与心肌梗死久后导致的多形性室性心动过速的折返机制不同。对于这些浦肯野相关的不同室性心律失常可行导管消融。

导管消融技术

室性心动过速导管消融的通用方法涉及目标室性心动过速的特征，心律失常基质的勾画和心律失常组织的射频消融。目标室性心动过速包括所有临床发作的室性心动过速以及程控刺激诱发的室性心动过速。典型的程控刺激采用两个周长、多达3个期外刺激、以进行性缩短联律间期对心室2个部位进行刺激。当诱发出室性心动过速后，予以起搏中止或电复律，随后继续程控刺激及至诱发出同一类型室性心动过速或需多次电击复律。记录每一种室性心动过速的12导联心电图形态、速率（或周长）、束支传导阻滞形态、心电轴、胸导联移行及血流动力学影响。这不仅有助于室性心动过速出口的定位，也有助于选择下面阐述的消融术方案。

采用三维电解剖标测系统识别心肌瘢痕，该标测系统可以：（1）标测导管空间定位；（2）形成心室三维解剖图，基于标测导管记录到的电图电位振幅呈现彩色编码，有利于区别正常心肌与瘢痕或边缘区组织；（3）基于异常的电图特征、拖带或起搏标测编列心肌通道和潜在的室性心动过速环路峡部部位。正常心肌特征表现为＞1.5mV的双极电位，致密瘢痕表现为＜0.5mV的双极电位，而边缘区的双极电位在0.5～1.5mV之间。正如以前描述的，导致折返型室性心动过速的心肌通道位于边缘区内。这些通道具有特征性的双极电图，可分为碎裂电图或晚（或孤立）电位。碎裂电位呈多相，期间无等电位线，且振幅≤0.5mV，间期≥133ms，振幅/间期比≤0.005。晚或孤立电位发生于QRS波群之后，与心室电图相隔＞20ms的等电位间距（图1）。电压标测受限于波前方向引起的双极和单极振幅变化、电极大小和电极间距、以及对多成分信号与最大峰值的判读。

证实晚电位或孤立电位的部位与室性心动过速环路峡部的关键部分相关，是理想的消融靶点。窦性心律时碎裂电位和晚/孤立电位可能会被遗漏，只有在心室起搏下才得以表现出来。窦性心律时，这些电图证实隐于QRS波群中重叠的局部电激动和远场心室激动。心室起搏可引起局部电图延迟并与远场成分分开。这些异常电图，结合碎裂和晚/孤立电位，宽泛地列为局部异常心室激动（LAVA），也是室性心动过速的理想消融靶点。然而，应该注意的是慢传导或减速区比最晚的激动区更具功能相关性。

在诱发出室性心动过速且勾画出心律失常基质后，典型的消融方案包括结合拖带标测、激动标测、起搏标测及室性心动过速的基质的改造。一些证实碎裂电图、晚/孤立电位、或窦律时LAVA的部位在室性心动过速时可显示舒张期电活动。然而，不是所有这些部位对于维持室性心动过速是关键的，它们只是代表源于被动激动的舒张期电活动（图2）。确定激动通道关联性的最为可靠方法是室性心动过速发作时进行拖带操作，有关拖带的具体描述超出本文的范畴，简而言之，于室性心动过速发作时超速起搏某点以确定该部位是否是心动过速环的关键成分或是旁观者。针对完全符合室性心动过速环路峡部拖带标准的部位消融，室性心动过速中止率高。

激动标测涉及在室性心动过速发作时通过与人为的参考电图比较，确定心腔中最早的电活动部位。这种信息可由彩色编码并记录于三维电解剖图上，使得局部电活动的最早部位得以识别。这对局灶室性心动过速特别有用，局灶室性心动过速有一最早激动点并以此为中心向外激动。因为折返型室性心动过速的电活动是连续的，激动标测无助于勾画出早和晚激动，但是，可用于识别沿着瘢痕区的室性心动过速出口和室性心动过速时的舒张期廊道。这些舒张期激动区域可以是或不是室性心动过速环路的关键部分（峡部对旁观者），但常作为消融的靶点。

对于血流动力学不稳定的室性心动过速不宜行拖带和激动标测，69%缺血性心肌病患者室性心动过速消融中发生这种情况。窦性心律下勾画出瘢痕区，起搏标测是一种可用于不稳定室性心动过速靶点定位的方法，无需诱发室性心动过速。这包括沿瘢痕周边起搏去匹配起搏12导联心电图图形与临床室性心动过速图形，鉴别室性心动过速出口部位。接近出口部位，但进一步在瘢痕的起搏，可识辨潜在的室性心动过速峡部部位，特征为起搏刺激与起搏QRS波群之间有时差（起搏信号至QRS间期＞80ms）。作为替代方案，可进行瘢痕基质改造，消融目标涉及所有碎裂/晚电位和LAVA。

瘢痕相关室性心动过速消融的传统方法包括对血流动力学上能耐受的室性心动过速结合拖带/激动标测，对不稳定室性心动过速实施起搏标测和基质改造。

图1 折返型室性心动过速的心肌瘢痕和基质。（左）来自正常心肌的电活动通过边缘区时缓慢而延迟（深灰箭头）。多个心肌通道存在，可通过特征性电图识别，分为碎裂电图（上部，*），晚电位（中部，*），或局部异常心室激动（底部）。该患者LAVA在心室起搏下充分展示，心室起搏将局部异常电图（虚线箭头）与远场电图分开，证实到第3个综合波部位的局部传入阻滞。这些心肌通道可成为不同室性心动过速发作的潜在径路。LAVA＝局部异常心室激动；MAP＝标测电极。

图2 心肌瘢痕与折返型室性心动过速的机制。A：一种室性心动过速环路（深灰色箭头）依赖于舒张期经过边缘区组织缓慢而迂回的电激动（浅灰色点线），这在MAP上记录到舒张期电图（黑色*）。室性心动过速环路远端部位（浅灰色）也可证实源于被动激动（浅灰色箭标）的舒张期电图。关键的部位只能经拖带和消融中止室性心动过速而确定。室性心动过速的QRS形态决定于从边缘区到正常心肌组织的出口部位（深灰色★）。B：出口部位不同的另一种室性心动过速环路在心电图上呈现不同的QRS形态。MAP＝标测电极；VT＝室性心动过速。

[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.

（童鸿）