Definitions

Ventricular tachycardia (VT) is defined as a tachycardia (rate > 100 beats per minute [bpm]) with three or more consecutive beats that originates in the ventricles. ^,

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  Accelerated idioventricular rhythm denotes a ventricular rhythm less than 100 bpm.

  
  
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  Sustained ventricular tachycardia lasts more than 30 seconds (unless requiring termination because of hemodynamic collapse), whereas nonsustained tachycardia terminates spontaneously within 30 seconds.

  
  
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  Monomorphic ventricular tachycardia has only one morphology during each episode ( Fig. 16.1 ).

  
  

  
  

  
  

  

  
  

  
  

  Types of ventricular tachycardia.

  
  
  
  
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  Pleomorphic ventricular tachycardia has more than one morphology of monomorphic VT during the same or different episodes of VT, but the QRS is not continuously changing. In patients with implantable cardioverter defibrillators (ICDs), pleomorphic VT is associated with increased risk.

  
  
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  In polymorphic ventricular tachycardia there is a constant change in QRS configuration indicating a changing ventricular activation sequence, usually at a heart rate less than 333 bpm (cycle length > 180 ms). Rapid polymorphic ventricular tachycardia cannot easily be distinguished from ventricular fibrillation.

  
  
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  Bidirectional ventricular tachycardia is a rare form of tachycardia with two alternating morphologies, usually right bundle branch block with alternating left and right axis deviation. This typically occurs in digitalis intoxication, catecholaminergic polymorphic ventricular tachycardia, or other conditions that predispose cardiac myocytes to delayed afterdepolarizations (DADs) and triggered activity.

  
  
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  Incessant VT denotes hemodynamically stable VT lasting hours.

  
  
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  VT storm indicates very frequent episodes of VT (more than three episodes in 24 hours), monomorphic or polymorphic, requiring cardioversion.

  
  
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  Torsades de pointes is a form of polymorphic ventricular tachycardia with characteristic beat-by-beat changes (twisting around the baseline) in the QRS complex associated with prolongation of the QT interval.

  
  
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  Ventricular flutter indicates a monomorphic, regular ventricular arrhythmia with a rate of approximately 300 bpm (cycle length 200 ms) with no isoelectric interval between QRS complexes.

  
  
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  Ventricular fibrillation (VF) usually has a rate greater than 300 bpm (cycle length ≤ 200 ms) and is a grossly irregular ventricular rhythm with marked variability in QRS morphology and amplitude. Fine VF is low-amplitude VF that superficially could mimic asystole.

Electrophysiologic mechanisms

Ventricular tachycardia

Monomorphic VT may be focal or macroreentrant. Focal VT has a point source of earliest ventricular activation with a spread of activation away in all directions from that site. The mechanism can be triggered activity, automaticity, or microreentry. The site of origin can be endocardial or epicardial with focal endocardial breakthrough (see Chapter 2 ). Macroreentry is due to myocardial scars secondary to prior myocardial infarction or other disease process.

Triggered activity as a result of delayed afterdepolarizations is the usual mechanism of idiopathic outflow tract tachycardias. Termination of idiopathic ventricular outflow tract tachycardias by an intravenous bolus of adenosine or infusion of a calcium channel blocker or by vagotonic maneuvers is consistent with triggered activity as the likely mechanism for some of these tachycardias. These tachycardias can be difficult to induce at electrophysiology testing; rapid-burst pacing and/or isoproterenol infusion is often required.

Automaticity that is provoked by adrenergic stimulation (not triggered) or disease processes that diminish cell-to-cell coupling may less commonly cause focal VT. This type of VT may become incessant under stress or during isoproterenol administration but cannot be initiated or terminated by programmed electrical stimulation; it can sometimes be suppressed by calcium channel blockers or beta blockers. Automaticity from damaged Purkinje fibers has been suggested as a mechanism for catecholamine-sensitive, focal origin VT. Automaticity can also occur in partially depolarized myocytes, as has been shown for VTs during the early phase of myocardial infarction and in some patients with ventricular scars. Automatic premature beats may, in addition, initiate reentrant VTs.

Reentry around a myocardial scar (scar-related reentry) characterized by regions of slow conduction and anatomic or functional unidirectional conduction block at some point in the reentry path is the cause of the majority of monomorphic VT in patients with heart disease. Myocardial scarring is identified from low-voltage regions on ventricular voltage maps, areas with fractionated electrograms, unexcitability during pace mapping, evidence of scarring on myocardial imaging, or from an area of surgical incision. Normal myocardium is typically characterized by bipolar voltage greater than 1.5 mV, dense scarring by bipolar voltage less than 0.5 mV, and border zone tissue by bipolar voltage of 0.5 to 1.5 mV. It should be noted, however, that voltage mapping has several limitations, include variation of bipolar and unipolar amplitudes as a result of wave front direction, electrode size and spacing, and annotation of multiple component signals to the largest peak. Prior myocardial infarction is the most common cause, but scar-related VT also occurs in cardiomyopathies and after cardiac surgery for congenital heart disease or valve replacement. Evidence supporting reentry includes initiation and termination by programmed stimulation (although this does not exclude triggered activity), demonstrable entrainment or resetting with fusion, continuous diastolic electrical activity, and isolated diastolic potentials that cannot be dissociated from VT by perturbations introduced by pacing.

After myocardial infarction, ion channel remodeling and regional reductions in I _Na and I _Ca are present within the scar, as well as reduced coupling between myocytes by increased collagen, alterations in gap junction distribution and function, and intervening patchy fibrosis resulting in a zigzag pattern of transverse conduction. Thus scar remodeling contributes to the formation of channels and regions where conduction time is prolonged, facilitating reentry. Many reentry circuits contain a protected isthmus or channel of variable length, isolated by arcs of conduction block ( Fig. 16.2 ). Typical isthmus sites are located in areas with low voltages, with dimensions ranging from 21 to 59 mm length by 15 to 47 mm width. Circuit exit sites, defined by local activation coincident with the onset of the QRS, are observed in the infarct border zone as described by voltage mapping. Multiple VT morphologies caused by multiple reentry circuits are often inducible in the same patient. The majority of reentrant circuits are located in the subendocardium, but subepicardial or intramyocardial reentry may also occur.

Activation map of reentrant ventricular tachycardias.

Activation maps of ventricular tachycardias (VT) in the anterior-septum of the left ventricle. The left panel shows a reentrant figure-eight circuit with a separate entrance, common channel, and exit. The entrance is characterized by convergence of the two activation wavefronts, forming a convex-shaped curvature with a wavefront propagating toward the common channel. The common channel “isthmus” is bounded by two lateral lines of block (or pseudoblock, allowing very slow conduction). The exit is characterized by concave-shaped curvature with divergence of wavefronts in front and lateral to the common-channel. The right panel is another example of figure-eight reentrant VT with an opposite axis. The arrowheads mark the proximal curvature (entrance) into the common channel.

(Anter E, Tschabrunn CM, Buxton AE, Josephson ME. High-resolution mapping of postinfarction reentrant ventricular tachycardia: electrophysiological characterization of the circuit. Circulation. 2016;134(4):314-327.

Macroreentry through the bundle branches occurs in patients with slowed conduction through the His-Purkinje system and is usually associated with severe left ventricular dysfunction as a result of dilated cardiomyopathy, valvular heart disease, and, less often, ischemic heart disease. ^, Although these tachycardias are usually unstable, the 12-lead electrocardiogram (ECG), when obtainable, may show either a left bundle branch block (LBBB) or right bundle branch block (RBBB) pattern. The necessary condition for bundle branch reentry is prolonged conduction in the His-Purkinje system, and this is reflected in the HV interval, which is prolonged during sinus rhythm and prolonged or equal to the baseline sinus rhythm during VT. The circuit involves the right and left brunch bundles with antegrade conduction occurring most of the time through the right bundle, and the HV interval during tachycardia is usually, but not invariably, equal to or greater than the HV interval measured during sinus rhythm. The HH interval variation usually precedes any VV interval variation, in contrast to what happens in microreentrant ventricular tachycardia with retrograde activation of the His bundle.

Left ventricular, fascicular, verapamil-sensitive VT occurs in patients without structural heart disease. The mechanism is reentry that appears to involve a portion of the Purkinje fibers, most often in the region of the left posterior fascicle, giving rise to a characteristic RBBB superior axis QRS configuration and a QRS duration that is only slightly prolonged. ^,

Diagnosis

With monomorphic VT the ECG displays a wide-QRS (>120 ms) tachycardia. A relatively narrow QRS (100 to 120 ms) may be seen in fascicular VT or in septal VT arising close to the His-Purkinje network. Prior MI, idiopathic VT, and arrhythmogenic cardiomyopathies (most often arrhythmogenic right ventricular cardiomyopathy/dysplasia [ARVC/D] ) are the most common causes.

Polymorphic VT is usually seen in the context of QT prolongation (in the form of torsades de pointes), in patients with other genetic channelopathies (Brugada syndrome, short QT, or early repolarization syndrome) and nonischemic cardiomyopathies, and in patients with acute ST-elevation myocardial infarction (STEMI) or myocardial ischemia. In STEMI, polymorphic VT may be seen during the acute phase or up to 8 days after the MI, and these patients are at high risk of developing arrhythmic storm.

Torsades de pointes occurs in most commonly in congenital long-QT syndrome (LQTS), drug-related QT prolongation, and metabolic abnormalities such as hypokalemia and during marked bradycardia in patients with third-degree atrioventricular (AV) block with premature ventricular contractions (PVCs).

Polymorphic VT/VF storm in a patient with coronary disease is strongly suggestive of acute myocardial ischemia; pauses may occur before polymorphic VT even in the absence of QT prolongation. Usually, severe underlying heart disease is present. More rarely, VT storm can occur in patients who have a structurally normal heart, such as in Brugada syndrome, LQTS, or catecholaminergic VT, or in drug overdoses.

The differential diagnosis of wide-QRS tachycardias is discussed in Chapter 11 .

Electrophysiology testing

Electrophysiology study may be required for establishment of the diagnosis in patients presenting with nonsustained ventricular rhythms. Indications include the need for differentiation from supraventricular tachycardia (SVT) with aberration, AF in the context of an accessory pathway, or other forms of aberration; risk stratification in patients with repaired tetralogy of Fallot or sarcoidosis; and programmed electrical stimulation for induction of VT.

Programmed electrical stimulation (PES) may also be used for risk stratification purposes. In postinfarction patients with nonsustained ventricular tachycardia (NSVT), the induction of sustained ventricular tachycardia is associated with a two- to threefold increased risk of arrhythmia-related death. In patients with reduced left ventricular ejection fraction (LVEF; <40%) and NSVT, inducibility of sustained monomorphic ventricular tachycardia at baseline PES is associated with a 2-year actuarial risk of sudden death or cardiac arrest of 50% compared with a 6% risk in patients without inducible ventricular tachycardia. Analysis of patients enrolled in the MUSTT (Multicenter UnSustained Tachycardia Trial) and of those in the registry revealed that noninducible patients have a significantly lower risk of cardiac arrest or sudden death compared with inducible patients at 2 and 5 years (12% vs 24% and 18% vs 32%, respectively). Noninducibility after VT ablation in patients with postinfarction VT is also independently associated with lower mortality during long-term follow-up. Still, as these results indicate, patients with noninducible sustained VT are not free of risk of sudden death, although in a recent trial, revascularized patents with noninducible arrhythmias 4 days after the infarction and an LVEF less than 30% had a similar long-term survival free of death or arrhythmia as patients with LVEF greater than 40%.

The MUSTT investigators have further analyzed the relationship of ejection fraction and inducible ventricular tachyarrhythmias to mode of death in 1791 patients who did not receive antiarrhythmic therapy. Total and arrhythmic mortality were higher in patients with an ejection fraction less than 30% compared with those whose ejection fractions were 30% to 40%. The relative contribution of arrhythmic events to total mortality was significantly higher in patients with inducible VT and among patients with an ejection fraction of 30% or greater. This study therefore suggested that the major utility of electrophysiologic testing may be restricted to patients having an ejection fraction between 30% and 40%. There has been some evidence that programmed stimulation performed as early as 3 days after myocardial infarction (MI) in patients with LVEF 40% or less induces VT in up to one-third of patients and may identify patients at high risk for spontaneous VT and sudden cardiac death. Noninducibility after VT ablation in patients with postinfarction VT is independently associated with lower mortality during long-term follow-up.

The ventricular stimulation protocol and the type of VT induced are important. Inducible monomorphic VT identifies patients at high risk of arrhythmia even when it is very fast (cycle length 200 to 250 ms, rate 240 to 300 bpm) ^, or is induced by three or four extrastimuli or by burst pacing. ^, Inducibility of ventricular fibrillation or flutter (usually with a cycle length less than 200 to 250 ms) has been considered a nonspecific finding, ^{, ,} especially when induced with three extrastimuli at very short coupling intervals. In the MUSTT, VF with one to two extrastimuli did confer an adverse prognostic significance.

These results should be considered in the context of evidence from analysis of stored ICD data that have shown little association between spontaneous and induced ventricular arrhythmias. The remodeling process after MI is ongoing, with a resultant low correlation between induced and clinically occurring VT in the long term.

In patients with coronary artery disease and relatively preserved left ventricular function (LVEF > 40%), the role of PES is not established, but there has been observational evidence that it may be of value for risk stratification. Inducible monomorphic VT might prompt catheter ablation and, if needed, an ICD, whereas inducibility of VF may be a nonspecific sign, especially if three extrastimuli are used. However, further investigations for ischemia, cardiomyopathies, or inherited channelopathies may be appropriate. The prognostic usefulness of programmed stimulation in patients with nonischemic dilated cardiomyopathy, including those with NSVT, remains controversial. ^, There has been some evidence that inducibility of ventricular arrhythmias, and especially polymorphic VT or VF, indicates increased likelihood of subsequent ICD therapies and might be considered a useful risk stratifier.

Inducible sustained monomorphic or polymorphic VT is an independent risk factor for subsequent events in patients with repaired tetralogy of Fallot and sarcoidosis.

Catheter ablation

Rationale

Catheter ablation is currently indicated for VT in various clinical settings either for eradication of the arrhythmia, as occurs in idiopathic VT, or for reducing the arrhythmia burden and consequent ICD shocks in patients with ischemic or structural heart disease. ^, ICD shocks are associated with diminished quality of life and increased mortality. ^, Antiarrhythmic drugs have an important role in shock reduction; however, these agents often have limited efficacy and significant side effects. ^, Amiodarone reduces VT recurrence and ICD shocks but may be associated with increased mortality in this respect. Thus, in cases of frequent monomorphic VT or VT storm in patients with ischemic cardiomyopathy who already have an ICD, ablation can reduce the number of ICD shocks and is preferable to drug therapy escalation (according to the VANISH, SMASH-VT, and VTACH randomized trials). Preventive VT ablation before ICD implantation does not reduce mortality or hospitalization for arrhythmia or worsening heart failure during 1 year of follow-up, but patients subjected to ablation have fewer ventricular arrhythmias and ICD interventions (per the BERLIN VT randomized trial).

In-hospital mortality rates for VT catheter ablation depend on the clinical condition of the patient. On average, they are 2.5% for ischemic heart disease, 1.5% for nonischemic structural heart disease, and 0.1% for patients without apparent heart disease, although no mortality has been reported for idiopathic VT ablation in experienced centers (see also specific VT entities, and Table 16.1 ). ^,

Although catheter ablation has not been proven to improve mortality in any randomized trial, retrospective cohort studies have provided evidence that successful ablation may be associated with both a higher rate of freedom from VT and also improved survival. A retrospective analysis of outcomes of VT ablation demonstrated that freedom from recurrent VT is associated with a significant reduction in all-cause mortality, independent of ejection fraction and heart failure status. A meta-analysis of 8 cohort studies with 928 postinfarction VT patients demonstrated that patients who have VT rendered noninducible by an ablation procedure have a lower VT recurrence rate compared with those who still have inducible arrhythmias after the ablation. Noninducibility translated to a significant reduction in all-cause mortality compared with partial success. In a multicenter observational study of postinfarction patients, noninducibility was associated with a 35% reduction in mortality. A similar finding has been reported in dilated cardiomyopathy patients.

Procedural considerations

Anticoagulation with intravenous heparin is necessary for all left ventricular (LV) procedures, as well as for right ventricular (RV) procedures in patients at high risk for thromboembolism. Endocardial mapping often is also done in epicardial procedures. In fully anticoagulated patients, pericardial access for epicardial mapping/ablation can be performed without interruption of anticoagulation ^, or after protamine reversal.

Most laboratories use general anesthesia (GA) for scar-related VTs and conscious sedation for idiopathic PVC/VT. Conscious sedation and GA can potentially suppress spontaneous or inducible arrhythmia by reducing sympathetic tone and is preferred for complex ablation procedures that can last for several hours, during which the patients are required to remain still to facilitate stability of the electroanatomic map. The frequency and depth of breathing play an important role in determining good catheter contact and stability. Epicardial access is often easier when respiratory motion can be controlled as under GA. However, patients with severe LV dysfunction can experience hemodynamic deterioration during prolonged procedures under GA.

Acute hemodynamic decompensation, defined as persistent hypotension despite vasopressors requiring mechanical support or discontinuation of the procedure, is reported to occur in 11% of patients and portends increased mortality. To identify patients at highest risk for hemodynamic decompensation, the PAAINESD (Pulmonary disease, Age older than 60 years, general Anesthesia, Ischemic cardiomyopathy, New York Heart Association class III or IV, LVEF < 25%, VT Storm, Diabetes mellitus), and the I-VT (LVEF, age, electrical storm, type of cardiomyopathy and diabetes mellitus [ www.vtscore.org ]) risk scores have been developed.

An inotropic agent, intraaortic balloon pump, or percutaneous LV assist device (LVAD) or extracorporeal membrane oxygenation (ECMO) have been used to maintain hemodynamic stability during VT ablation. ^, Although more complicated to use, ECMO provides maximal hemodynamic support (>4.5 L/min) and is of most benefit when placed preemptively in high-risk patients undergoing VT ablation or as a bailout measure when intraprocedural hemodynamic deterioration occurs. These devices maintain end-organ perfusion during prolonged periods of VT and may allow a longer time for detailed entrainment/activation mapping.

Electroanatomic mapping and multielectrode catheters (see Chapters 5 and 7 ) are now used for VT substrate mapping in most laboratories. They allow rapid acquisition of multiple sites at high spatial resolution, and the increased current density during pacing from smaller electrodes can achieve capture at relatively low pacing stimulus strength. However, various shapes of multielectrode configurations may induce ectopy, spatial sampling is not uniform, and none of them is well suited for mapping of papillary muscles or the epicardium.

Coronary angiography or imaging of the coronary ostia with intracardiac echocardiography in relevant cases is necessary for epicardial ablation and for ablation in the sinuses of Valsalva. A distance of more than 5 mm from the ablation catheter tip to an epicardial coronary artery and more than 10 mm of the catheter tip to the coronary ostium are considered safe for ablation.

Mapping techniques

Mapping during VT

12-lead ECG mapping.

A 12-lead ECG obtained during tachycardia may provide certain clues about the origin of the arrhythmia, as discussed in the Clinical Forms section.

Body surface mapping.

Electrocardiographic imaging (ECGI) integrates unipolar electrograms obtained during the arrhythmia while the patient is wearing a 256-electrode vest, with ventricular anatomy derived from a computed tomography (CT) or cardiac magnetic resonance (CMR) scan with the vest in place. An activation map during the arrhythmia is then mathematically derived using the inverse solution and is plotted on the epicardial surface as designated by the CT or CMR scan. ECGI maps have shown good correlations with endo- and epicardial mapping results in patients with and without ischemic cardiomyopathy, and outflow arrhythmias. ^, Their efficacy is diminished in reentrant VTs over myocardial scarring or over slowly conducting tissue. Clinical experience with this modality is limited.

Activation mapping.

During hemodynamically tolerated scar-related VT, the onset of the surface QRS corresponds temporally to the emergence of the diastolic VT circuit from the scar. Recordings from the exit site of a VT circuit with conventional catheters demonstrate electrograms that precede the onset of the surface QRS complexes. Electroanatomic activation mapping using multielectrode catheters (see Chapter 5 ) is now usually employed for identifying the VT exit site. Electroanatomic activation mapping involves the identification of the earliest site of electrical activation in a cardiac chamber compared with an arbitrary reference electrogram during VT. This information can be color coded and recorded on a three-dimensional (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 that location. Because electrical activity is continuous, activation mapping in reentrant VT is not useful to delineate early and late activation, but it can be used to identify VT exit sites along the scar border and identification of diastolic corridors (isthmuses) during VT. The VT reentry circuit isthmus is a critical component of the VT circuit and may not necessarily correspond to channels identified by electroanatomic voltage mapping. ^,

Electrograms at isthmus sites occur earlier during diastole, typically have very low voltage amplitude (<0.5 mV), and can have multiple components, but the mere presence of diastolic potentials during VT cannot discriminate between isthmus and bystander sites ( Fig. 16.3 ). The inability to dissociate a diastolic potential from the next ventricular electrogram by pacing maneuvers makes it more likely that the diastolic potential does originate in a critical isthmus. Diastolic potentials, together with the recording of bipolar myocardial signal amplitude less than 1.5 mV, allow orientation toward the areas where pace or entrainment mapping should be performed.

Myocardial scar and mechanism of reentrant VT.

(A) A VT circuit (red arrow) is dependent on slow and circuitous electrical activity through border zone tissue during the diastolic period (orange dashed lines) , which is recorded as diastolic electrograms (black asterisk) on the MAP. Locations distal to the VT circuit (orange asterisks) may also demonstrate diastolic electrograms as a result of passive activation (orange arrows) . Critical locations are identified only with entrainment and termination of VT with ablation. The QRS morphology of the VT is dependent on the exit site from border zone tissue to the normal myocardium (red star) . (B) Another VT circuit with a different exit site would demonstrate a different QRS morphology on electrocardiography. MAP, Mapping catheter; VT, ventricular tachycardia.

(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(23):2924-2941.)

Electrograms can also be fractionated and immediately precede the onset of the QRS complex at the exit site from a VT reentry circuit. Ablation at exit sites can terminate the tachycardia, but it may also result in a change of the tachycardia circuit and/or cycle length (CL) in which the diastolic pathway exits at different locations from the scar. Both central and exit sites have been the preferred ablation targets, but zones of slow conduction are more functionally relevant than the latest activated regions.

A limitation of endocardial activation mapping is that scar-related circuits, particularly in patients with a nonischemic substrate, can have intramural or epicardial components that might not be recorded on the surface.

VT Entrainment.

As discussed, electrogram timing alone is not entirely reliable as a guide to successful ablation sites due to the frequent presence of multiple conduction channels, some of which are bystanders, and entrainment techniques are used to determine relevance to the VT circuit. Entrainment principles are the same as discussed for any reentrant tachycardia (see Chapter 10 ) provided that we are dealing with one VT circuit. Responses to pacing from various sites in and around the circuit are indicated in Fig. 16.4 . Critical isthmus sites are defined by concealed entrainment—that is, no change of QRS morphology, S-QRS interval less than 70% of the VT cycle length (ideally equal to the electrogram to QRS during VT), and a postpacing interval–VT cycle length difference 30 ms or less (ideally equal to the VT cycle length).

Entrainment responses from components of reentrant VT circuit.

CL, Cycle length; PPI, postpacing interval; VT, ventricular tachycardia.

(Cronin EM, Bogun FM, Maury P, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias: Executive summary. Heart Rhythm. 2020;17(1):e155-e205.)

With pacing site outside the reentry circuit during VT, the stimulated wave front that propagates out from the pacing site collides with the orthodromically propagating wave front of the reentry circuit and produces a fused QRS complex (classic entrainment). During pacing from within a protected region or in a bystander site communicating with the critical isthmus near the reentry circuit, pacing entrains the VT without changing the QRS configuration (concealed entrainment or entrainment with concealed fusion).

The S-QRS interval is indicative of the conduction time from the pacing site to the point of the VT exit from the scar. A short S-QRS suggests a stimulus closer to the exit, whereas a long S-QRS indicates an entrance to the channel. If pacing is performed from a site in the circuit, the stimulus-QRS interval should be equal to the electrogram-QRS interval during VT. If pacing is performed from a bystander site, the stimulus-QRS interval is longer than the electrogram-QRS interval during tachycardia. ^, The stimulus-QRS/VTCL ratio is therefore a reflection of the pacing site location within the critical zone of the reentry circuit.

The postpacing interval (PPI) measures the interval from the pacing stimulus to the following nonstimulated depolarization recorded at the pacing site and is also used to verify whether the pacing site is within the circuit or is in a bystander area ( Fig. 16.5 ). To prove that a specific site is an integral part of the reentrant circuit (i.e., entrance, isthmus, or exit site), the PPI should approximate the tachycardia CL (<30 ms). Care is needed not to pace at a very fast rate that may result in slower conduction and erroneous prolongation of the PPI and to distinguish tachycardia depolarizations from far-field electrograms generated by remote tissue.

Entrainment of VT.

Pacing in the scar at a cycle length (CL) 20 ms shorter than the tachycardia CL accelerates all electrograms and QRS complexes to the paced CL. QRS complexes during pacing match those during ventricular tachycardia. The postpacing interval (blue arrow) approximates the tachycardia CL.

(Nof E, Stevenson WG, John RM. Catheter ablation for ventricular arrhythmias. Arrhythm Electrophysiol Rev. 2013;2(1):45-52.)

Successful entrainment mapping satisfying all criteria identifies critical isthmus sites where a few radiofrequency lesions can reliably eliminate VT. ^,

Mapping during sinus rhythm

Although entrainment mapping is the preferred method for characterizing the VT circuit, hemodynamic instability during tachycardia and the need to induce clinical VT may make this approach challenging. The presence of multiple VT morphologies also makes entrainment mapping cumbersome. In the Thermocool VT ablation trial, 54% of induced VT morphologies were unmappable, most commonly because of hemodynamic instability. Even in patients with well-tolerated clinical VT, approximately 70% will have at least one unmappable VT induced at electrophysiology (EP) study.

Late potentials and fractionated electrograms.

Diastolic activity is detected in the form of late or isolated potentials after the QRS complex and separated from the ventricular electrogram by an isoelectric interval of more than 20 ms or as fractionated electrograms with multiple components without an isoelectric segment and an amplitude 0.5 mV or less, a duration 130 ms or greater, and/or an amplitude/duration ratio 0.005 or less ( Fig. 16.6 ).

Example of an isolated potential recorded within a posterior left ventricular scar.

The isolated potential (arrow) is separated from the ventricular electrogram by an isoelectric segment of 120 ms. The amplitude of the isolated potential is 0.035 mV. The electrogram width is 260 ms. In this patient there were 11 different inducible ventricular tachycardias (VTs); after the ablation procedure and the displayed lesions, these VTs were no longer inducible. Map dist, distal electrode pair of the mapping catheter.

(Bogun F, Good E, Reich S, et al. Isolated potentials during sinus rhythm and pace-mapping within scars as guides for ablation of post-infarction ventricular tachycardia. J Am Coll Cardiol. 2006;47(10):2013-2019.)

Potentials within the QRS may also be identified with high-density mapping during sinus rhythm. These potentials are defined as local abnormal ventricular activations ( LAVAs ) and have been described as credible targets for VT ablation ( Figs. 16.7 and 16.8 ), although the absence of inducible VT at the end of the procedure was not predictive of VT-free survival in this study. Mapping of abnormal electrograms during RV pacing may be more sensitive than during normal sinus rhythm because of a change in the direction of the activation wave front ( Fig. 16.9 ). A limitation of fractionated electrograms and late potentials is that they are markedly influenced by factors such as the direction of wave front activation, catheter orientation, and electrode confiduration. ^,

Electrogram recordings from different patients to show various characteristics of local abnormal ventricular electrograms (LAVAs; arrows ).

1. The potential representing LAVA is fused with the terminal portion of the far-field ventricular signal, making it difficult to identify the LAVA as a separate signal. 2. LAVA potential occurs just after and with a slightly higher frequency than the far-field ventricular potential. LAVAs in 1 and 2 occur within the QRS complex. 3. LAVA is a double-component potential that closely follows the farfield ventricular signal. The early component is a high-frequency potential that is almost fused with the preceding far-field ventricular potential. It occurs within the terminal portion of the QRS complex. Another low-amplitude signal follows an isoelectric interval and represents the late component of LAVA, which occurs after the QRS complex. 4. LAVAs are represented by multicomponent signals without isoelectric intervals. These signals can be visualized distinctly from the preceding far-field ventricular signal. 5. Double-component LAVA signal. Although the early component is recorded just after the QRS complex, the late component is recorded after the inscription of the T wave on the surface ECG.

(Jais P, Maury P, Khairy P, et al. Elimination of local abnormal ventricular activities: a new end point for substrate modification in patients with scar-related ventricular tachycardia. Circulation. 2012;125(18):2184-2196.)

Myocardial scar and substrate for reentrant VT.

(Left) Electrical activation from the normal myocardium through border zone tissue is slow and delayed (red 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 VTs. LAVA, Local abnormal ventricular activity; MAP, mapping catheter; VT, ventricular tachycardia.

(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(23): 2924-2941.)

(A) Sinus rhythm electrograms (EGMs) demonstrating late potentials and multicomponent EGMs (arrows). (B) Right ventricular (RV) pacing used to expose late potentials (arrows) hidden within the QRS during sinus rhythm (left panel) and biventricular pacing (right panel). (C) Entrainment mapping with capture of the far field EGM (left panel). A reduction in pacing output (right panel) results in successful capture of the local EGM (arrow) and evidence of concealed entrainment. (D) EGMs recorded from abnormal substrate are poorly coupled to the rest of the myocardium. RV pacing results in separation of the late potential (hidden within the sinus QRS beat), and extrastimulus results in further delay.

(Sadek MM, Schaller RD, Supple GE, et al. Ventricular tachycardia ablation: the right approach for the right patient. Arrhythm Electrophysiol Rev. 2014;3(3):161-167.)

Scar identification.

Scar tissue identification is based on bipolar electrogram amplitude using a 4-mm-tip mapping catheter and 1-mm ring interelectrode spacing with a 2-mm ring filtered at 10 to 400 Hz. Normal ventricular tissue has a bipolar voltage more than 1.5 mV, dense scar is defined by voltages less than 0.5 mV, and a border zone is defined by voltages between 0.5 and 1.5 mV. However, unipolar pacing in the area of the so-called dense scar shows local capture, suggesting presence of viable myocardium, and a bipolar voltage of less than 0.1 mV has also been used to define electrical inexcitability. Changing the bipolar viability voltage range to 0.1 to 0.5 mV increases the heterogeneity within the area of previously defined “dense scar.” In patients with nonischemic cardiomyopathy in particular, heart biopsies have demonstrated that the amount of viable myocardium shows a linear association with both bipolar and unipolar voltage, in a way that any cutoff to delineate fibrosis is unreliable. In addition, bipolar voltage amplitude depends on several factors, as discussed in Chapter 5 (see Figs. 5.2 and 5.3 ). The addition of filtered unipolar to bipolar voltage mapping may be useful in this respect. ^,

Cardiac magnetic resonance is considered the gold standard for identification of scarring in the human myocardium, although its current resolution is limited for the purpose of reliable tissue characterization.

Pace mapping.

Pace mapping involves pacing at a rate close to the tachycardia CL from the site presumed to be close to the VT origin as judged on the 12-lead SCG during VT, in an attempt to match exactly the clinical VT morphology. Computer programs are now available that use template-matching algorithms to generate a correlation coefficient between VT morphology and pace maps.

Pace mapping can identify the site of origin of focal VTs and the tachycardia exit site in reentrant VTs. ^, Usually, pacing mapping within the scar reveals a paced QRS morphology similar to that during VT and a prolonged S-QRS interval (>40 ms). In particular, pace mapping at sites of isolated potentials detected during sinus rhythm (SR) in areas of scarring is helpful in identifying critical VT isthmuses. An abrupt transition between a paced QRS that matches the clinical VT (exit site) and a nonmatched paced QRS (entrance site) can also identify an isthmus. VT exit site pacing will yield a matched QRS with a short S-QRS, and entrance site pacing will often yield a nonmatched QRS because the stimulus wave front can exit antidromically in the opposite direction as the VT. Inherent limitations of pace mapping are that pacing in noncritical areas adjacent to the exit may also generate an adequate pace match that is similar in morphology to a pace map from the VT exit, whereas a perfect pace map can be observed at sites up to 2 cm away from the VT origin. ^, In addition, varying the pacing rate may alter the paced-QRS morphology. To minimize this, pacing should be conducted at the VT cycle length, and at the lowest possible pacing output to reduce the possibility of far field capture. For practical purposes, pacing is started at an output of 10 mA at 2 ms pulse width.

Ablation techniques

Epicardial ablation

Indications for epicardial mapping include an unsuccessful prior endocardial ablation procedure and VT unrelated to coronary artery disease (e.g., dilated cardiomyopathy [DCM], ARVC/D, hypertrophic cardiomyopathy [HCM], and Chagas cardiomyopathy) ( Fig. 16.10 ). The presence of midmyocardial or subepicardial scarring on CMR may be useful in identifying patients who are likely to require epicardial mapping for successful abolition of VT.

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