Abstract
Idiopathic ventricular tachycardias (VTs) usually occur in specific locations and have specific QRS morphologies. The most common idiopathic VT is VT from the outflow tract of the right ventricle (RV). Other idiopathic RV-VT is tricuspid annular VT. In idiopathic left VTs, there are left ventricular (LV) outflow tract VT, mitral annular VT, papillary muscle VT, crux VT, verapamil-sensitive left fascicular VT, and nonreentrant fascicular VT. The mechanism of mitral and tricuspid annular VTs is nonreentry. Radiofrequency catheter ablation (RFCA) of mitral annular VT is highly successful. RFCA eliminates approximately 90% of the free wall tricuspid annular VT, but only 57% of the septal tricuspid VT. RFCA of papillary muscle is challenging because catheter stability is very difficult because of papillary muscle contractions. Crux VT is rare and may arise from the epicardium. Ablation may be performed within the proximal coronary sinus or proximal middle cardiac vein, or by a pericardial approach. The mechanism of verapamil-sensitive idiopathic fascicular VT is reentry, and there are several subtypes. Ablation targets are the diastolic potential in the VT circuit, and the RFCA success rate is greater than 90% for the common type of fascicular VT. The mechanism of nonreentrant fascicular VT is abnormal automaticity from the distal Purkinje system. The recurrence rate after ablation for nonreentrant fascicular VT is much higher than that of reentrant fascicular VT.
Keywords
ablation, atrioventricular annulus, crux, fascicle, nonreentry, papillary muscle, Purkinje
Key Points
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The mechanism of idiopathic mitral and tricuspid annular ventricular tachycardias (VTs) is nonreentry (triggered activity or automaticity).
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Mitral annular VT has a right bundle branch block (RBBB) pattern and monophasic R or Rs in leads V 2 to V 6 . Catheter ablation of mitral annular VT is highly successful.
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Tricuspid annular VT exhibits a left bundle branch block pattern, R (r) in lead I, and the presence of an R (r) in lead aV L . Catheter ablation eliminates approximately 90% of VTs arising from the free wall portion of the tricuspid annulus, but only 57% of those from the septal portions.
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Papillary muscle VT appears to be based on a focal (nonreentrant) mechanism.
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Activation mapping seems to be most useful for ablation of papillary muscle VTs. They typically do not exhibit any recordings of diastolic potentials during sinus rhythm or VT. Catheter ablation is challenging because catheter stability is very difficult because of papillary muscle contractions. Successful catheter ablation usually requires irrigated ablation catheters, and intracardiac echocardiography to visualize the direct contact with the papillary muscle.
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VTs originating from the crux of the heart are rare and may arise by a focal mechanism from the epicardium; they may be induced with programmed stimulation or burst pacing from the right ventricle, and often require isoproterenol (catecholamine sensitive). Ablation may be performed within the proximal coronary sinus or proximal middle cardiac vein, or by a pericardial approach.
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The mechanism of verapamil-sensitive idiopathic left fascicular VT is reentry.
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Diagnosis is based on demonstration of RBBB and superior axis configuration (common type); RBBB and inferior axis configuration (uncommon type); or a relatively narrow QRS and inferior axis configuration (rare type), together with dependence on left ventricular fascicular activation and verapamil sensitivity (termination or slowing of the tachycardia). In some cases, the reentrant circuit of VT can involve the Purkinje network lying around the papillary muscles.
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Ablation targets are the diastolic potential in the VT circuit or the presystolic fused Purkinje potential at the VT exit. The success rate of ablation is greater than 90% for verapamil-sensitive idiopathic left VT.
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The mechanism of nonreentrant fascicular VT is abnormal automaticity from the distal Purkinje system. It is difficult to distinguish this VT from verapamil-sensitive idiopathic left fascicular VT by 12-lead electrocardiogram. The ablation target is the earliest Purkinje activation during VT. The recurrence rate after ablation for nonreentrant fascicular VT is much higher than that of verapamil-sensitive idiopathic left fascicular VT.
Sustained monomorphic ventricular tachycardia (VT) is most often related to myocardial structural heart disease, including healed myocardial infarction and cardiomyopathies. However, no apparent structural abnormality is identified in approximately 10% of all sustained monomorphic VTs in the United States and 20% of those in Japan. These VTs are referred to as idiopathic. Idiopathic VTs usually occur in specific locations and have specific QRS morphologies, whereas VTs associated with structural heart disease have a QRS morphology that tends to indicate the location of the scar. Idiopathic VT comprises multiple discrete subtypes that are best differentiated by their mechanism, QRS morphology, and site of origin. The most common idiopathic VT originates from a focus in the outflow tract of the right ventricle (RV) (see Chapter 28 ), and its mechanism is most likely triggered activity. In idiopathic left VT, the following four types exist: left ventricular outflow tract VT, VT from the mitral annulus, papillary muscle VT, VT arising from ventricular crux, verapamil-sensitive left fascicular VT, and nonreentrant fascicular VT ( Box 29.1 ). This chapter focuses on the assessment and nonpharmacologic treatment of idiopathic left and right VTs and left fascicular VTs.
Outflow Tract VTs ( triggered activity, reentry, or automaticity )
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Left ventricular outflow tract, aortic sinus of Valsalva, or epicardial VT
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Right ventricular outflow tract or pulmonary artery VT
Mitral Annular VT ( triggered activity, reentry, or automaticity )
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Anterolateral, anteromedial (aorto-mitral continuity), lateral, posterior, or posteroseptal mitral annular origin
Tricuspid Annular VT ( triggered activity, reentry, or automaticity )
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Posterior–posterolateral, anterior–anterolateral, posteroseptum, anteroseptal (parahissian), or midseptal mitral annular origin
Papillary Muscle VT ( triggered activity, reentry, or automaticity)
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Left posterior papillary muscle, left anterior papillary muscle, or right papillary muscle origin
VT Arising From Ventricular Crux ( triggered activity, reentry, or automaticity )
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Middle cardiac vein approach or epicardial approach
Left Ventricular Reentrant Fascicular VTs (reentry)
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Left posterior septal fascicular VT
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Left posterior papillary muscle fascicular VT
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Left anterior septal fascicular VT
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Left anterior papillary muscle fascicular VT
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Left upper septal fascicular VT
Nonreentrant Fascicular VT (triggered activity or automaticity)
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Left Purkinje origin
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Right Purkinje origin
VT, Ventricular tachycardia.
Mitral Annular Ventricular Tachycardia
Mitral annular VTs are found in 5% of symptomatic, idiopathic VTs/premature ventricular complexes (PVCs) and occur with equal frequency in both sexes or with a male predominance (male, 53%–69%). Mitral annular VTs were noted in 5% of all cases of idiopathic VT ; however, a previous study showed that mitral annular VT accounts for 49% of idiopathic repetitive monomorphic VTs arising from the left ventricle (LV; other sites included the coronary cusps and inferoseptal region).
Pathophysiology
Classification
Mitral annular VT can be classified by the anatomic location. The majority originate from the anterolateral portion of the mitral annulus (in close proximity to the aorto-mitral continuity), and less commonly the lateral, posterior, or posteroseptal annulus ( Fig. 29.1 ). The anterior and anteromedial portion of the mitral annulus, that is the aorto-mitral continuity, may also be the origin of the VT.
Mechanism
The mechanism of this arrhythmia appears to be nonreentry, and it may be a triggered activity based on the response to adenosine, verapamil, and pacing maneuvers. It has been proposed that a remnant of the atrioventricular conduction system close to the aorto-mitral continuity, such as a dead-end tract, might be important in the genesis of the nonreentrant mechanism for the tachycardia. The close proximity of the anterolateral mitral valve to the right ventricular outflow tract, left ventricular outflow tract, and left ventricular epicardial myocardium near the left coronary cusp suggests that idiopathic VT from these sites could likely originate from a single focus, with different exit points or activation of alternate pathways between the VT focus and an exit point.
Diagnostic Criteria
Surface Electrocardiogram
The electrocardiogram (ECG) in mitral annular VT has a right bundle branch block (RBBB) pattern and a monophasic R or Rs in leads V 2 to V 6 (see Fig. 29.1 ). Further, an ECG analysis can precisely distinguish among the different subtypes by the polarity of the QRS complex in the inferior and lateral leads. In anterolateral VTs, the polarity of the QRS complex in leads I and aV L is negative and positive in the inferior leads. Posterior VTs and posteroseptal VTs have a negative polarity in the inferior leads and positive polarity in leads I and aV L . VT arising from the free wall portion of the annulus, such as an anterolateral VT or posterior VT, has a longer QRS duration (sometimes also described as a δ-wave–like morphology ) and notching in the late phase of the R wave/Q wave in the inferior leads. This feature is not observed in posteroseptal, anterior, or anteromedial VTs. Notching of the late phase of the QRS complex in the inferior leads and widening of the QRS complex observed in these VTs may result from phased excitation from the LV free wall to the RV. Posterior VTs have a dominant R in V 1 , whereas posteroseptal VTs have a negative QRS component in V 1 (qR, qr, rs, rS, or QS). The Q wave amplitude ratio of lead III to lead II is greater in posteroseptal VTs than in posterior VTs. Anterior and anteromedial VTs arising from the aorto-mitral continuity exhibit an absence of S waves in lead V 6 and RBBB or left bundle branch block (LBBB) with an early transition as noted in aortic cusp VTs ( Fig. 29.2 ). A proposed algorithm to predict the precise focus of a VT/premature ventricular contractions originating from the mitral annulus is shown in Fig. 29.3 .
Mapping and Ablation
Catheter ablation using radiofrequency (RF) energy to cure patients with mitral annular VT is associated with a high success rate because of the focal origin of this form of VT ( Figs. 29.4 and 29.5 ). The 12-lead ECG is a useful initial guide to localize the site of the origin of the tachycardia. Intracardiac mapping to select the optimal site for ablation (see Figs. 29.4 and 29.5 ) includes activation mapping (earliest local intracardiac electrogram that precedes the onset of surface QRS during VT) and pace mapping (pacing the ventricle from a selected site during sinus rhythm to match the 12-lead morphology of the spontaneous or induced VT). All successful ablation sites have atrial and ventricular electrogram amplitudes satisfying the criteria for a mitral annular origin, with a ratio of the atrial to ventricular electrograms of less than 1 and an amplitude of the atrial and ventricular electrograms of more than 0.08 and 0.5 mV, respectively, at the successful ablation site. Some patients have a potential noted before the local ventricular electrogram. The use of 3-dimensional electroanatomic mapping systems may reduce the fluoroscopic exposure and improve the efficacy of the catheter ablation by providing activation maps during VT that identify the site of origin and also provide the ability to maneuver the ablation catheter easily to recorded sites of interest.
Success and Recurrence Rates
Catheter ablation is highly successful with ablation delivered at the site of the earliest ventricular activation or sites with a 12/12 pace-map match. However, there was a recurrence rate of 8% in one series. Most cases may be successfully ablated by an endocardial approach, but ablation in the coronary venous system, specifically the great cardiac vein, has been described. Comparing the morphology of the coronary sinus ECG with that at the site of ablation on the mitral annulus may be helpful for determining the optimal ablation site.
Tricuspid Annular Ventricular Tachycardia
Tricuspid annular VTs are found in 8% of all the cases of idiopathic VTs/PVCs (including right- and left-sided VT/PVC) and approximately 5% of all patients with a right-sided VT origin. A recent study reported that tricuspid annular VT arising from the free wall portion is more common in males than in females (male/female ratio, 1.83), whereas the incidence of that arising from the septum is distributed almost equally between males and females.
Pathophysiology
Classification
Tricuspid annular VT can be classified by the anatomic location. Septal sites were more common than free wall sites in a previous study (74%) and less common in the series presented by another study (43%). Of the septal locations, the majority were anteroseptal or parahissian (72%).
Mechanism
The mechanism of this arrhythmia appears to be nonreentrant based on the findings that it typically occurs spontaneously and cannot easily be induced by pacing maneuvers.
Diagnostic Criteria
Surface Electrocardiogram
All VT/PVCs arising from the tricuspid annulus demonstrate an LBBB QRS morphology and positive QRS polarity in leads I, V 5 , and V 6 ( Figs. 29.6 and 29.7 ). No negative component of the QRS complex is found in lead I. The R wave in lead I is usually greater because the tricuspid annulus is more rightward and inferior to the right ventricular outflow tract. A positive component (any r or R) is recorded in lead aV L in 95% of patients, and the overall polarity in aV L is positive in 89%.
Among all tricuspid annular VTs, the QRS duration and Q wave amplitude in each of leads V 1 to V 3 were greater in VT/PVCs arising from the free wall of the tricuspid annulus compared with the septum. The septal VTs have an early transition in the precordial leads (V 3 ), narrower QRS complexes, and Qs in lead V 1 with the absence of notching in the inferior leads, whereas the free wall VTs are associated with a late precordial transition (>V 3 ), wider QRS complexes, absence of Q waves in lead V 1 , and notching in the inferior leads (the timing of the second peak of the notched QRS complex in the inferior leads corresponds precisely with the left ventricular free wall activation). These ECG characteristics are confirmed by pace mapping. A proposed algorithm to predict the precise focus of a VT/premature ventricular contractions originating from the tricuspid annulus is shown in Fig. 29.8 .
Mapping and Ablation
The 12-lead ECG is a useful initial guide to localize the site of origin of the tachycardia. Intracardiac mapping to select the optimal site for ablation ( Fig. 29.9 ; see Fig. 29.7 ) includes activation mapping (earliest local intracardiac electrogram that precedes the onset of surface QRS during VT) and pace mapping (pacing the ventricle from a selected site during sinus rhythm to match the 12-lead morphology of the spontaneous or induced VT). All successful ablation sites had atrial and ventricular electrogram amplitudes satisfying the criteria for a tricuspid annular origin, with a ratio of the atrial to ventricular electrograms at the ablation site of less than 1, and the amplitudes of the atrial and ventricular electrograms are 0.03 or more and less than 0.35 mV at the ablation site, respectively. VTs originating from near the His bundle have a similar ECG and electrophysiologic characteristics as those from the right coronary cusp or noncoronary cusp adjacent to the membranous septum (see Fig. 29.7 ). Therefore when right ventricular mapping shows the earliest ventricular activation near the His bundle, mapping in the right coronary cusp and noncoronary cusp should be added to identify the origin. The use of 3-dimensional electroanatomic mapping systems may reduce the fluoroscopic exposure and improve the efficacy of catheter ablation by providing activation maps during VT that identify the site of the origin and also provide the ability to maneuver the ablation catheter easily to recorded sites of interest. The use of these systems is especially useful for ablating VTs arising from the anteroseptal or parahissian portion (see Fig. 29.7 ). Confirmation of the distance between the ablation site and His-bundle recording site is important to avoid impairing atrioventricular conduction during RF energy applications.
Success and Recurrence Rates
In one series, RF catheter ablation was more often successful for the free wall (90%) than the septal (57%) group. The low success rate in the septal tricuspid annular group was thought to be caused by concern for impairing atrioventricular conduction with RF ablation. This is in contrast to the 100% acute success rate in another series.
Complications
In the case of catheter ablation of VTs originating from near the His bundle, careful attention has to be paid because of its proximity to the atrioventricular node and His bundle region.
Papillary Muscle Ventricular Tachycardia
Idiopathic ventricular arrhythmias (VAs) that originate from papillary muscles account for 4% to 12% of idiopathic VAs, and patients with papillary muscle VTs seem to be older. Syncope and cardiac arrest are rare, but several cases of PVCs from papillary muscles triggering ventricular fibrillation (VF) have been reported. Frequent papillary PVCs can also induce cardiomyopathy that is reversible if suppression of the PVCs is successful.
Pathophysiology
Classification
The chordal apparatus of both mitral leaflets inserts into two groups of papillary muscles. The anterior papillary muscle and posterior papillary muscle arise from the middle to apical aspect of the anterior or inferior wall of the LV, respectively ( Fig. 29.10 ). Papillary muscle VAs originate more commonly from the posterior papillary muscle than from the anterior papillary muscle and are less likely to be sustained compared with fascicular tachycardias. This kind of VA can occur from papillary muscles or the parietal band in the RV.
Mechanism
Papillary muscle VTs appear to be based on a focal (nonreentrant) mechanism. Papillary muscle VT is usually exercise-induced and is catecholamine sensitive, often requiring isoproterenol or epinephrine for induction. This VT cannot be entrained, and lacks late potentials during sinus rhythm at the site of ablation.
Diagnostic Criteria
Surface Electrocardiogram
VTs from the papillary muscles have an RBBB pattern (see Fig. 29.10 and Fig. 29.11 ). The QRS width is significantly greater in papillary muscle arrhythmias compared with idiopathic left verapamil-sensitive VTs (150 ± 15 vs. 127 ± 11 ms). Papillary muscle VT often exhibits multiple QRS morphologies, with subtle changes seen spontaneously or during ablation. These subtle morphologic changes are thought to be from preferential conduction to different exit sites or multiple regions of origins within the complex structure of the papillary muscles (see Fig. 29.10 ).
Subtle ECG differences can help differentiate papillary muscle VT from fascicular VT. Papillary muscle VT usually has a wider QRS; it does not have Purkinje potentials preceding the QRS during VT; and if present, Purkinje potentials will be late in sinus rhythm compared with pre-QRS with fascicular VTs. The V 1 morphology of posterior papillary muscle VTs typically has a qR morphology or R compared with an rsR′ for fascicular VTs, and will notably have an absence of Q waves in leads I and aV L .
Mapping and Ablation
Activation mapping seems to be most useful in the ablation of papillary muscle VTs (see Fig. 29.11 ). They typically do not show recordings of diastolic potentials during sinus rhythm or VT, which suggests that the Purkinje network is not involved in these kinds of arrhythmias. Successful catheter ablation usually requires irrigated ablation catheters and intracardiac echocardiography (ICE) to visualize adequacy of catheter contact with the papillary muscle.
RF catheter ablation is challenging because catheter stability is very difficult to achieve as a result of papillary muscle contractions. In addition, the myocardium at the base of the papillary muscles is relatively thick. The creation of a deep lesion may be necessary for long-term success because of the distance between the VT origin and endocardial surface.
Successful catheter ablation usually requires irrigated ablation catheters and ICE to visualize the degree of contact with the papillary muscle. Detailed 3-dimensional reconstruction of the ventricles, image integration by ICE and/or multi-detector computed tomography, and the use of contact sensing ablation catheters are also useful and important for a successful ablation. Furthermore, a transseptal approach may be required to obtain good contact of the ablation catheter with the LV papillary muscles. A relatively wide area (approximately half) of the papillary muscle circumference and multiple ablation lesions may need to be targeted because of the potential for a deep intramural focus with multiple exits. A recent study reported that cryoablation has been used when traditional radiofrequency ablation has failed, and may be more effective than radiofrequency ablation because of the improved contact stability.
Success and Recurrence Rates
Acute procedural success of ablation of papillary muscle arrhythmias originating from anterior and posterior papillary muscles (i.e., elimination of targeted PVCs/VTs during the procedure) is generally fair (60%–100%). However, recurrence rates are 71% and 50%, respectively, which are greater than that for left anterior fascicular (LAF; 25%) and left posterior fascicular (LPF; 13%) VTs, and are most likely caused by poor catheter stability.
Complications
Gradual titration of the power, careful manipulation of the catheter, and detailed observation using real-time ICE imaging are important to avoid any complications. Postablation follow-up should include echocardiography to rule out mitral regurgitation, but despite extensive ablation on papillary muscles, its incidence is low.
Ventricular Tachycardia Arising from the Crux of the Heart
Recent studies have reported VTs arising from the crux of the heart. A recent study reported that crux VTs were found in 15 patients (1.8%) out of 1021 cases with idiopathic VTs/PVCs undergoing RF catheter ablation. Fifteen patients (83%) had sustained VT and three required an implantable cardioverter defibrillator implantation because of syncope.
Pathophysiology
Classification
Crux VT can be classified by the anatomic location using fluoroscopic images and 3-dimensional activation maps, that is, those with apical crux VT ( n = 9) and those with basal crux VT ( n = 9). Basal crux VTs were defined as those VTs with a successful ablation region in the proximal coronary sinus (CS) or proximal middle cardiac vein (MCV) within 2 cm of the MCV ostium. Apical crux VTs were defined as those VTs that the earliest activation or successful ablation region was in the middle MCV, more than 2 cm from the MCV ostium or epicardial space over the cardiac crux.
Anatomy
The cardiac crux is a pyramidal space of the posteroseptal region, which is formed by the AV annulus and interventricular groove, and it represents the confluence of all four cardiac chambers and the CS in their nearest proximity and has a pyramidal space. The basal crux area lies in close proximity to the ostium of the MCV, whereas the apical crux area lies near the posterior interventricular artery, more inferior and epicardial as compared with the basal crux area.
Mechanism
This type of VT appears to have a focal mechanism from the epicardium and is initiated with programmed stimulation or burst pacing from the RV, and often requires isoproterenol (catecholamine sensitive).
Diagnostic Criteria
Surface Electrocardiogram
The ECG demonstrates a superior axis and QS pattern in leads II and III and a maximum deflection index, determined by the analysis of the QRS complex, of 0.55 or more ( Fig. 29.12 ). Most patients (89%) had an R>S wave in V 2 and pseudodelta wave duration of more than 34 ms. In apical crux VTs, V 6 exhibited either a QS or rS pattern, and aVR presented with an R>S wave in most cases. Those with an RBBB pattern had a prominent R wave in V 1 with a transition to an rS or qS pattern in V 6 . Those with an LBBB pattern had an early transition in V 2 with a late transition to an rS or qS in V 6 . Furthermore, the QRS morphology often changed spontaneously from an RBBB to LBBB in 44% of the patients with apical crux VTs. On the other hand, basal crux VTs were either negative or isoelectric in V 1 , positive in V 6 , and had an early transition in V 2 . A proposed algorithm to predict the precise focus of a VT/PVCs originating from the crux is shown in Fig. 29.13 .
Mapping and Ablation
Activation mapping and pace mapping in the CS or MCV are used for the determination of ablation sites. For apical crux VTs, the success rate of RF catheter ablation within the MCV is low, and VT recurrence is high. However, the success rate of epicardial ablation over the cardiac crux is high. In basal crux VTs, the success rate of RF catheter ablation within the CS or MCV is high, and VT recurrence is low.
Complications
Perforation of the CS or impairment of a coronary artery (posterior descending artery) may occur with catheter ablation from the CS or MCV or if a percutaneous epicardial approach is performed.
Reentrant Left Fascicular Ventricular Tachycardia
Pathophysiology and Classification
Verapamil-sensitive fascicular VT is the most common form of idiopathic left VT. It was first recognized as an electrocardiographic entity in 1979 by Zipes and colleagues, who identified the following characteristic diagnostic triad: (1) induction with atrial pacing; (2) RBBB and left-axis configuration; and (3) manifestation in patients without structural heart disease. In 1981 Belhassen and associates were the first to demonstrate the verapamil sensitivity of the tachycardia, a fourth identifying feature. Ohe and colleagues reported another type of this tachycardia, with RBBB and a right-axis configuration, in 1988. Finally, my colleague and I reported the upper septal fascicular tachycardia variant. According to the QRS morphology, we first divided verapamil-sensitive left fascicular VT into three subgroups, namely: (1) LPF VT, in which the QRS morphology exhibits an RBBB configuration and a superior axis ( Fig. 29.14 ); (2) LAF VT, in which the QRS morphology exhibits an RBBB configuration and inferior axis ( Fig. 29.15 ); and (3) upper septal fascicular VT, in which the QRS morphology exhibits a narrow QRS configuration and normal or right-axis deviation ( Fig. 29.16 ). LPF VT is common, LAF VT is uncommon, and left upper septal fascicular VT is very rare. Left upper septal fascicular VT sometimes occurred after previous catheter ablation of other fascicular VTs.
The reentrant circuit of verapamil-sensitive fascicular VT can involve the Purkinje network lying around the papillary muscles. Recently, my colleagues and I reported distinct subtype of verapamil-sensitive reentrant fascicular VT: papillary muscle fascicular VT. In addition to the current classification with three subtypes, papillary muscle fascicular VT is another identifiable verapamil-sensitive fascicular VT ( Fig. 29.17 ). Papillary muscle fascicular VT and VT from myocardium of papillary are basically different entities, while there must be some overlap.
Substrate and Anatomy
The anatomic basis of this tachycardia has provoked considerable interest. Some data suggest that the tachycardia may originate from a false tendon or fibromuscular band in the LV. Suwa et al. described a false tendon in the LV of a patient with idiopathic VT in whom the VT was eliminated by surgical resection of the tendon. Using transthoracic and transesophageal echocardiography, Thakur and colleagues found false tendons extending from the posteroinferior LV to the basal septum in 15 of 15 patients with idiopathic left VT but in only 5% of control patients. Maruyama and associates reported a case with the recording of sequential diastolic potentials bridging the entire diastolic period and a false tendon extending from the midseptum to the inferoapical septum. Lin and colleagues found that 17 of 18 patients with idiopathic VT had this fibromuscular band but also found it in 35 of 40 control patients. They concluded that the band was a common echocardiographic finding and was not a specific arrhythmogenic substrate for this tachycardia, although they could not exclude the possibility that the band was a potential substrate of the VT. Small fibromuscular bands, trabeculae carneae, and small papillary muscles cannot be detected by transthoracic echocardiography. The Purkinje networks in these small anatomic structures are important when considering the mechanism of left fascicular VT. In the papillary muscle fascicular VTs, fibromuscular bands near papillary muscles can be the substrate of the VT circuit. An autopsy specimen of the human heart shows the anatomic connection between the anterior and posterior papillary muscles ( Fig. 29.18 ), and the possible electrical connection between them may explain the changes in QRS axis during ablation of this VT. Recently, Haïssaguerre et al. proposed three kinds of Purkinje reentry in their review article about VAs and His-Purkinje system. The fascicular VT in their schema seems to be the septal fascicular VT, and the distal Purkinje-muscle reentrant tachycardia seems to be papillary muscle fascicular tachycardia ( Fig. 29.19 ).
Mechanism of Tachycardia
The mechanism of verapamil-sensitive left VT is reentry because it can be induced, entrained, and terminated by programmed ventricle or atrial stimulation. To confirm its reentry circuit and the mechanism, my colleagues and I performed left ventricular septal mapping using an octapolar electrode catheter in 20 patients with LPF VT ( Fig. 29.20 ). In 15 of 20 patients (75%), two distinct potentials, P1 and P2, were recorded during the VT at the midseptum ( Fig. 29.21 ). Although the mid-diastolic potential (P1) was recorded earlier from the proximal rather than the distal electrodes, the fused presystolic Purkinje potential (P2) was recorded earlier from the distal electrodes. During sinus rhythm, recording at the same site demonstrated P2, which was recorded after the His bundle potential and before the onset of the QRS complex, suggesting P2 as potentials of LFP. The sequence of the P2 during sinus rhythm was the reverse of that seen during VT. VT could be entrained from the atrium ( Fig. 29.22 ) and from the ventricle. Entrainment pacing from the atrium or ventricle captured P1 orthodromically and reset the VT ( Figs. 29.23 and 29.24 ). The interval from the stimulus to P1 was prolonged as the pacing rate increased. The effect of verapamil on P1 and P2 is shown in Fig. 29.25 . Intravenous administration of 1.5 mg of verapamil significantly prolonged the cycle length of the VT, from 305 to 350 ms. Both the P1–P2 and P2–P1 intervals were proportionally prolonged after verapamil administration. These findings demonstrated that P1 is a critical potential in the circuit of the verapamil-sensitive LPF VT and suggested the presence of a macroreentry circuit involving the normal Purkinje system and abnormal Purkinje tissue with decremental properties and verapamil sensitivity. Although P1 has proved to be a critical potential in the VT circuit, whether the left posterior fascicle or Purkinje fiber (P2) is involved in the retrograde limb of the reentrant circuit was controversial. Morishima and associates reported a case with negative participation of the proximal left posterior fascicle (P2) to the LPF VT circuit. Selective capture of left posterior fascicle (P2) by a sinus complex did not affect the cycle length of VT, suggesting P2 as a bystander ( Fig. 29.26A ). And the postpacing interval after the entrainment from left ventricular septal myocardium was equal to the cycle length of VT, suggesting left ventricular septal myocardium as the retrograde limb (see Fig. 29.26B ). Maeda and associates also reported a case of left posterior fascicle (P2) in a bystander circuit of LPF VT. Although RF energy application at the site with P1 and P2 changed the activation sequence of P2 and the surface QRS morphology, VT did not terminate and the activation sequence of P1 remained unchanged ( Fig. 29.27 ). Ouyang and coworkers suggested that idiopathic left VT reentry might be a small macroreentry circuit consisting of one anterograde Purkinje fiber with a Purkinje potential, one retrograde Purkinje fiber with retrograde Purkinje potentials, and the ventricular myocardium as the bridge.
