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Fascicular Ventricular Tachycardia
24 Fascicular Ventricular Tachycardia OUTLINE Pathophysiology, 858 Tachycardia Circuit, 858 Anatomy of the Left Fascicular System, 858 Epidemiology, 859 Clinical Presentation, 859 Initial Evaluation, 859 Principles of Management, 860 Acute Management, 860 Chronic Management, 860 Electrocardiographic Features, 860 Electrocardiogram During Normal Sinus Rhythm, 860 Electrocardiogram During Ventricular Tachycardia, 860 Electrophysiological Testing, 860 Induction of Tachycardia, 860
Diagnostic Maneuvers During Tachycardia, 861 Exclusion of Other Arrhythmia Mechanisms, 861 Mapping, 861 Activation Mapping, 861 Entrainment Mapping, 863 Pace Mapping, 863 Electroanatomic Mapping, 864 Noncontact Mapping, 864 Ablation, 864 Target of Ablation, 864 Ablation Technique, 866 Endpoints of Ablation, 867 Outcome, 867 Empirical Ablation of Noninducible Ventricular Tachycardia, 867
PATHOPHYSIOLOGY
activation propagates anterogradely (from basal to apical segments along the LV septum) over the abnormal Purkinje tissue with decremental conduction properties and verapamil sensitivity, which serves as the anterograde limb of the circuit and appears to be insulated from the nearby ventricular myocardium. The lower turnaround point of the reentrant circuit is located in the lower third of the septum, where the wavefront captures the fast conduction Purkinje tissue from or contiguous to the LPF, and retrograde activation occurs over the LPF from the apical to basal septum forming the retrograde limb of the reentrant circuit. In addition, at the lower turnaround point, anterograde activation occurs down the septum to break through (at the exit of the tachycardia circuit) in the posterior septal myocardium. The upper turnaround point of the reentrant circuit occurs over a zone of slow conduction located close to the main trunk of the left bundle branch (LB) in the basal interventricular septum (Fig. 24.1). The estimated distance between the entrance and exit of the circuit is approximately 2 cm.5,6
The His-Purkinje system plays an important role in the genesis of cardiac arrhythmias. The mechanisms of several types of monomorphic ventricular tachycardias (VTs) have been directly linked to the Purkinje system, including bundle branch reentrant VT, interfascicular reentrant VT, fascicular VT, and focal Purkinje VT. A subset of polymorphic VTs and ventricular fibrillation has also been linked to triggers originating from the Purkinje system. Most of those arrhythmias occur in patients with underlying structural heart disease; however, fascicular VT and a subset of focal Purkinje VTs are idiopathic, occurring in the absence of apparent cardiac disease.1,2 Idiopathic fascicular VT is a reentrant tachycardia involving the left fascicular Purkinje system. The reentry circuit is most commonly (90%) located in the territory of the left posterior fascicle (LPF), infrequently (5% to 10%) in the region of the left anterior fascicle (LAF), and rarely arise from fascicular locations high in the septum. Fascicular VT is also referred to as “verapamil-sensitive” VT, given its tendency to slow or terminate with intravenous verapamil.3,4
Tachycardia Circuit In the most common form (LPF-VT), the tachycardia circuit incorporates the LPF serving as one limb and abnormal Purkinje tissue with slow, decremental conduction serving as the other limb. The anterograde limb may be associated with longitudinal dissociation within the LPF or contiguous tissue that is directly coupled to the LPF (such as a false tendon) or, alternatively, has ventricular myocardium interposed. The zone of slow conduction appears to depend on the slow inward calcium current because the degree of slowing of tachycardia cycle length (TCL) in response to verapamil is entirely attributed to its negative dromotropic effects on the area of slow conduction.5,6 The entrance site to the slow conduction zone is thought to be located closer to the base of the left ventricle (LV) septum. From there,
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Anatomy of the Left Fascicular System The LB arises from the His bundle (HB) as numerous fine, intermingling fascicles that leave the left margin of the branching HB through most of its course along the crest of the muscular ventricular septum. The predivisional portion of the LB penetrates the membranous portion of the interventricular septum under the aortic ring and then divides under the septal endocardium into two branches: the LAF and the LPF. An estimated 65% of individuals have a third fascicle of the LB, the left median fascicle (LMF). The fascicles cascade down the LV septum in a fan-like configuration with extensive interconnections. Unlike the cord-like right bundle branch, the LB and its divisions are diffuse, fanlike structures that quickly arborize just beyond their origin. The LAF represents the superior (anterior) division of the LB, the LPF represents the inferior (posterior) division, and the LMF represents the septal (median) division.
CHAPTER 24 Fascicular Ventricular Tachycardia NSR
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VT
II
II
V1 DP
LPF
V1 His
A
His
B
Fig. 24.1 Schematic Illustration of the Reentrant Circuit in Fascicular Ventricular Tachycardia (VT). A block of the LV septum is depicted with the left posterior fascicle (LPF) and diastolic pathway (DP) running in parallel until they intersect at the bottom. A 10-pole catheter is shown recording between pathways; electrograms from each pair are shown along with surface electrocardiogram leads and His bundle recordings. (A) Activation sequence is shown during normal sinus rhythm (NSR), the dashed line denotes QRS onset. Note the direction and speed of propagation over the LPF while the DP is activated after the QRS and in both directions (arrows). (B) During VT complex, the DP is activated anterogradely and the LPF retrogradely (arrows). See text for discussion.
The LB subdivisions extend to the midportion of the septum before they detach from the underlying endocardium and form free-running false tendons that traverse the ventricular chamber, projecting predominantly toward the papillary muscles. The fascicles become ramified in the ventricular apex and extend back along the ventricular walls toward the cardiac base.7 The thin LAF crosses the anterobasal LV region toward the anterolateral papillary muscle and terminates in the Purkinje system of the anterolateral LV wall. The LPF appears as an extension of the main LB and is broad in its initial course. It then fans out extensively toward the posterior papillary muscle and terminates in the Purkinje system of the posteroinferior LV wall. The LMF runs to the interventricular septum; it arises in most cases from the LPF, less frequently from the LAF, or from both fascicles, and in a few cases it has an independent origin from the central part of the main LB at the site of its bifurcation.2
VT can be observed in 6% of patients. Spontaneous remission of the VT can occur with time.8
EPIDEMIOLOGY
INITIAL EVALUATION
Fascicular VT accounts for 10% to 15% of all idiopathic VTs. Age at presentation is typically 15 to 40 years (unusual after 55 years). Males are more commonly affected (60% to 80%). The clinical course is generally benign, and the prognosis is excellent. Sudden cardiac death is very rare. Tachycardia-induced cardiomyopathy precipitated by incessant
The diagnosis of fascicular VT is based on: (1) VT morphology on the surface electrocardiogram (ECG) (right bundle branch block [RBBB] with left or, less commonly, right axis deviation); (2) VT sensitivity to verapamil; and (3) absence of structural heart disease. Invasive electrophysiology (EP) testing is required to confirm the diagnosis. Evaluation
CLINICAL PRESENTATION Most patients present with mild to moderate symptoms of palpitations and lightheadedness. Occasionally, symptoms are debilitating and include fatigue, dyspnea, and presyncope. Syncope and cardiac arrest are rare. The VT is typically paroxysmal and can last for minutes to hours. Although fascicular VT can occur at rest, it is sensitive to catecholamines and often occurs during physical or emotional stress. Rarely, the VT can become incessant, sustained for a long period (days) and does not revert spontaneously to normal sinus rhythm (NSR). When incessant, fascicular VT can precipitate tachycardia-induced cardiomyopathy and heart failure.8
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CHAPTER 24 Fascicular Ventricular Tachycardia
to exclude structural heart disease is necessary and typically includes echocardiographic examination (that may show one or more prominent false tendons), stress testing, and coronary arteriography, depending on patient age and risk factors.8
Electrocardiogram During Ventricular Tachycardia
Oral verapamil or diltiazem is useful in mild cases; however, long-term efficacy is variable and the benefit of these drugs in management of patients with severe symptoms is often limited. Catheter ablation is highly effective (success rate of 85% to 90%) and is recommended for patients in whom drug therapy is not successful, not tolerated, or not preferred.3,8,9
Fascicular VT is characterized by relatively narrow QRS duration (127 ± 11 milliseconds) and short RS interval (the duration from the beginning of the QRS to the nadir of the S wave) in the precordial leads (60 to 80 milliseconds). The shorter QRS duration reflects the proximal exit of fascicular VTs from the His-Purkinje system (HPS). In addition, during fascicular VT, the interventricular septum is activated early with a left-to-right direction, resulting in an initial “r” waves in lead V1 and small “q” waves in leads I and aVL (similar to classic RBBB pattern). In addition, the rapid activation of the LV via the Purkinje system results in unopposed late activation of the right ventricular outflow tract (RVOT), leading to a large R′ amplitude in lead V1 (and r < R′).8,10 The VT rate is approximately 150 to 200 beats/min (range, 120 to 250 beats/min). Alternans in the TCL is frequently noted; otherwise, the VT rate is stable. According to the fascicular territory involved and, consequently, the QRS morphology, fascicular VTs are classified into three subtypes: (1) LPF VT (with the reentrant circuit exit in the inferoposterior septum) exhibits an RBBB and superior axis configuration (most common form); (2) LAF VT (with the reentrant circuit exit in the anterolateral wall of the LV) exhibits RBBB and right-axis deviation configuration; and (3) upper septal fascicular VT with a narrow QRS and normal axis configuration (rare form). In the most common form (LPF-VT), the QRS during VT typically has RBBB with LAF block configuration. The R/S ratio is less than 1 in leads V5 and V6 (Fig. 24.2). VTs arising more toward the middle at the region of the posterior papillary muscle have a left superior axis and RS in leads V5 and V6, whereas those arising closer to the apex have a right superior axis with a small “r” and deep S (or even QS) in leads V5 and V6.1,8
ELECTROCARDIOGRAPHIC FEATURES
ELECTROPHYSIOLOGICAL TESTING
Electrocardiogram During Normal Sinus Rhythm
Induction of Tachycardia
The resting ECG is usually normal. Symmetrical inferolateral T wave inversion can be observed after termination of the VT (cardiac memory).
Given the reentrant mechanism of fascicular VT, the arrhythmia is usually inducible by programmed electrical stimulation. In fact, fascicular
PRINCIPLES OF MANAGEMENT Acute Management Electrical cardioversion is required for VT termination in hemodynamically unstable patients. For stable patients with an established diagnosis of verapamil-sensitive fascicular VT, intravenous verapamil is the firstline treatment and is very successful in acutely terminating the VT. Intravenous verapamil slows the rate of VT progressively and then terminates it. Diltiazem is equally effective. Nonsustained VT may continue to occur for a while after termination.3 Response of VT to lidocaine, procainamide, amiodarone, sotalol, and beta-blockers is less consistent, and these drugs are usually ineffective. Carotid sinus massage and Valsalva maneuvers have no effect on the VT. Fascicular VT is generally unresponsive to adenosine; however, when catecholamine stimulation (isoproterenol infusion) is required for the initiation of VT (in the EP laboratory), the VT can become adenosine sensitive.8,9
Chronic Management
1
aVR
V1
V4
2
aVL
V2
V5
3
aVF
V3
V6
Fig. 24.2 Surface Electrocardiogram of Fascicular Ventricular Tachycardia (VT). Note the right bundle branch block and left anterior fascicle block pattern characteristic of these VTs.
CHAPTER 24 Fascicular Ventricular Tachycardia VT is characterized by its reproducible initiation and termination not just by ventricular stimulation but also by atrial pacing. Often, isoproterenol infusion facilitates VT induction. Consistent with a reentry mechanism, an inverse relationship is observed between the coupling interval of the initiating ventricular extrastimulation (VES) or ventricular pacing cycle length (PCL) and the first VT beat.6
Diagnostic Maneuvers During Tachycardia Entrainment
Entrainment of fascicular VT can usually be demonstrated with ventricular pacing at a PCL approximately 10 to 30 milliseconds shorter than the TCL. Manifest entrainment is more frequently achieved when pacing is performed from the RVOT because the RVOT is closer to the entrance site of the area of slow conduction in the reentrant circuit, located near the base of the LV septum. On the other hand, pacing from the RV apex is less likely to demonstrate entrainment and, when it does, it is unlikely to demonstrate manifest fusion because of the larger distance from the entrance site of the circuit and because of the narrow excitable gap of the reentrant circuit.
Resetting Fascicular VT can be reset by VES, with an increasing or mixed resetting response (characteristic of reentrant circuit with an excitable gap).
Termination VT can be reproducibly terminated with programmed atrial or ventricular stimulation.
Exclusion of Other Arrhythmia Mechanisms The differential diagnosis of fascicular VT includes interfascicular VT, supraventricular tachycardia (SVT) with aberrant conduction, and VT originating from the LV papillary muscles.
Interfascicular Ventricular Tachycardia Interfascicular VT has several characteristic features (see Chapter 26): (1) bifascicular block QRS morphology during VT, which is identical to that during NSR; (2) reversal of activation sequence of the HB and LB during VT; and (3) spontaneous oscillations in the TCL caused by changes in the LB-LB interval that precede and drive the TCL. Interfascicular VT terminates with VES or radiofrequency (RF) ablation that produces block in LAF or LPF.
Supraventricular Tachycardia When fascicular VT is associated with a 1 : 1 VA conduction and because of its responsiveness to verapamil and inducibility by atrial pacing, it can be misdiagnosed as SVT with bifascicular block aberrancy. During SVT (similar to NSR), the HB is activated in an anterograde direction with sequential activation of the HB and ventricles (see Chapter 21). In contrast, during fascicular VT, the HB is activated retrogradely, with parallel activation of the HB and ventricle. Thus the HV interval during SVT with aberrancy is equal to or slightly longer than that during NSR. On the other hand, the HV interval during fascicular VT is frequently negative (i.e., His potential is recorded after onset of the QRS). The His potential can also precede the QRS onset during fascicular VT (especially during upper septal fascicular VT); however, the HV interval during VT will be shorter than that during NSR. In addition, unlike fascicular VT, aberrantly conducted SVTs are typically responsive to adenosine, beta-blockers, and Valsalva maneuvers.
Papillary Muscle Ventricular Tachycardia Papillary muscle VTs typically manifest as premature ventricular complexes (PVCs) rather than sustained monomorphic VT and are more
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likely to occur in older patients with structural heart disease. VTs arising from the LV papillary muscles exhibit a QRS morphology that can mimic fascicular VT. However, compared with fascicular VT, papillary muscle VTs have a broader QRS complex (150 ± 15 milliseconds vs. 127 ± 11 milliseconds). In addition, VTs originating from the papillary muscles (which are farther away from the septum) lack the rsR′ pattern in lead V1; rather, those VTs often have a qR pattern (or, less commonly, a monophasic R wave) in lead V1. Furthermore, spontaneous variations in QRS morphology occur relatively frequently during VTs originating from the LV papillary muscles, a feature that can help distinguish these VTs from LV fascicular VT; the latter being a reentrant tachycardia with a consistent QRS morphology.8,10 Unlike patients with fascicular VAs, papillary muscle VAs are typically not inducible with programmed electrical stimulation, which is consistent with a nonreentrant mechanism of papillary muscle VTs.
Focal Purkinje Ventricular Tachycardia Idiopathic focal VTs can arise from the Purkinje system in either ventricle and can present as PVCs, accelerated idioventricular rhythm, or VT. Focal Purkinje VTs arising from the left Purkinje network exhibit an RBBB pattern with either left- or right-axis deviation and can be difficult to distinguish from fascicular VT. In contrast to the reentrant idiopathic fascicular VT, focal Purkinje VTs are most likely related to abnormal automaticity. These VTs are sensitive to autonomic tone and frequently display chronotropic properties. Focal Purkinje VTs are typically induced by exercise and catecholamines and slowed or terminated by beta-blockers (and hence classified as “propranolol-sensitive” VTs) and lidocaine. Unlike fascicular VT, focal Purkinje VTs are not responsive to verapamil and cannot be induced or terminated by programmed electrical stimulation. In addition, these VTs are transiently suppressed by adenosine and with overdrive pacing.11
MAPPING Activation Mapping Activation mapping is performed during sustained VT and is specifically directed toward sites with His or Purkinje potentials (PPs) extending from LV basal septal sites with HB recordings to most apical sites with presystolic PPs. Activation mapping is used to identify sites with the earliest ventricular activation and earliest presystolic PPs, as well as late diastolic potentials (LDPs).6,8 Mapping is performed along the LV inferior septum (for LPF VT), along the anterolateral LV (for LAF VT), or the basal LV septum (for left upper septal VT). Strategies for mapping and ablation of LPF VT, the most common type of fascicular VT, are discussed here in detail. The same principles can be applied for the two other types of fascicular VT. When the VT is not inducible or not sustained, mapping can be performed during NSR to record the PPs along the posterior aspect of the LV septum, identifying the course of the LPF.
Site of Earliest Ventricular Activation The site of earliest ventricular activation during VT (which represents the exit of the reentrant circuit) is in the region of the LPF (inferoposterior LV septum) in 90% of fascicular VTs (explaining the RBBB–superior axis configuration of the QRS), and in the region of the LAF (anterosuperior LV septum) in 5% to 10% of fascicular VTs (explaining the RBBB–right axis configuration of the QRS). In most cases, ventricular electrograms at the site of earliest activation are discrete during both NSR and VT. The HB is not a component of the reentrant circuit; in fact, a retrograde His potential is often recorded 20 to 40 milliseconds after the earliest ventricular activation (Fig. 24.3).12
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CHAPTER 24 Fascicular Ventricular Tachycardia
I II III
V1 V6
Hisdist RVA RVOT Abluni
Abldist Ablprox 200 msec
Fig. 24.3 Idiopathic Fascicular Ventricular Tachycardia. The blue arrow shows late diastolic small potential, 45 milliseconds prior to QRS onset. Distinct Purkinje-like potentials (blue arrow) are evident before the dotted line denoting QRS onset, as well as in the proximal ablation electrogram. The red arrow indicates retrograde His potential. Note the unipolar QS configuration just coinciding with QRS onset. Abldist, Distal ablation; Ablprox, proximal ablation; Abluni, unipolar ablation; Hisdist, distal His bundle; RVA, right ventricular apex; RVOT, right ventricular outflow tract.
I II III V1 V6 HRA Hisprox Hisdist RVA Abldist 200 msec
Fig. 24.4 Sinus Rhythm Recordings at a Successful Ablation Site for Fascicular Ventricular Tachycardia. The left arrow points to a Purkinje-like potential just prior to the local electrogram (also slightly preceding the onset of the QRS); the right arrow shows a sharp, delayed diastolic potential, purportedly from the slowconducting limb of the circuit. Abldist, Distal ablation; Hisdist, distal His bundle; Hisprox, proximal His bundle; HRA, high right atrium; RVA, right ventricular apex.
Purkinje Potential The PP (also referred to as “P2” in literature) is a discrete, high-frequency potential that precedes the site of earliest ventricular activation by 15 to 42 milliseconds and is recorded in the posterior third of the LV septum during VT, as well as during NSR (see Figs. 24.3 and 24.4). Because this
potential also precedes ventricular activation during NSR, it is believed to originate from activation of a segment of the LPF and to represent the lower turnaround point in the reentrant circuit. The earliest ventricular activation site (exit) during VT is identified more distally (apically) in the septum than the region with the earliest recorded PP.12
CHAPTER 24 Fascicular Ventricular Tachycardia
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Late Diastolic Potential
Entrainment Mapping
The LDP, also referred to as “P1” or “pre-PP,” is a discrete potential that precedes the PP during VT and is recorded at the basal, middle, or apical LV septum. During NSR, the LDP is inscribed after the QRS. The LDP is thought to originate from activation at the entrance to the abnormal Purkinje tissue (the specialized, verapamil-sensitive zone), which is thought to serve as the anterograde limb of the reentrant circuit and is isolated from surrounding muscle (allowing it to have a discrete diastolic activation time). The LDP differs in morphology from the PP and has a relatively small amplitude and low-frequency component. The area with LDP recording is confined to a small region (0.5 to 1.0 cm2) and is included in the larger area where the PP is recorded (2 to 3 cm2); hence the LDP often is recorded simultaneously with the PP by the same electrode. The LDP is recorded within an area proximal to the earliest PP recording site and is activated from the basal to apical septum toward the earliest PP site. The relative activation times of the LDP, PP, and local ventricular potential at the LDP recording site to the onset of QRS complex are −50.4 ± 18.9, −15.2 ± 9.6, and 3.0 ± 13.3 milliseconds, respectively (see Fig. 24.3). The earliest ventricular activation site (exit) during VT is identified at the posteroapical septum and is more apical in the septum than the region with LDP.12
Analysis of entrainment from different ventricular sites helps to identify the relationship of those sites to the VT circuit (Box 24.1). Entrainment with concealed fusion and a PPI that approximates the TCL helps to identify the diastolic slow zone (isthmus) of the reentrant circuit. Notably, because of the overlap between the fascicular tissue and the ventricular myocardium, pacing from the isthmus of the VT circuit may not produce concealed fusion, because pacing frequently results in local myocardial capture outside that region, producing manifest fusion.13 During entrainment, the LDP (representing the entrance of the circuit) is orthodromically captured and, as the pacing rate is increased, the LDP-PP interval (representing an area of decremental Purkinje tissue) prolongs, whereas the stimulus-to-LDP and PP-QRS intervals typically remain constant.12
Ventricular Activation Sequence During NSR, conduction propagates anterogradely (proximal to distal or basal to apical) and rapidly down the LPF, generating an anterograde PP followed by ventricular activation (see Fig. 24.1). In parallel, the impulse slowly conducts anterogradely over the abnormal Purkinje tissue, and such slow conduction (or block) in the proximal segment allows the anterograde wavefront traveling rapidly over the LPF to conduct retrogradely up the slow pathway, resulting in fusion of delayed (late) ascending and descending potentials that follow (or are buried in) local ventricular depolarization, which likely represent the LDPs recorded during VT (see Fig. 24.4). Those late potentials have been found only in patients with fascicular VT but not in control subjects and have been recorded in the midinferior septum within or contiguous to the LPF. During ventricular pacing, the LPF is activated retrogradely, generating a retrograde PP. In parallel, the impulse produces bidirectional activation of the abnormal Purkinje pathway in a manner similar but in reverse direction to that during NSR. During VT, activation propagates anterogradely (from the basal to the apical site of the LV septum) over the abnormal Purkinje tissue, giving rise to an anterograde LDP; hence the earliest LDP is seen in the basal septum and the latest LDP is seen in the apical septum. The reentrant wavefront then turns around in the lower third of the septum and activates the fast conduction Purkinje fibers along the LPF, generating a retrograde PP. From the lower turnaround point, the wavefront propagates anterogradely down the septum to exit the reentrant circuit and activate the posterior septal myocardium, and retrogradely over the LPF from apical to basal septum, forming the retrograde limb of the tachycardia, with an upper turnaround point of the reentrant wavefront occurring over a zone of slow conduction (between LDP and PP areas) located close to the main trunk of the LB (see Fig. 24.1). For a VES to initiate VT, retrograde block must occur in the abnormal Purkinje tissue, and the paced wavefront is retrogradely conducted up the LPF (generating a retrograde PP) with some delay and then down the abnormal Purkinje tissue (generating an anterograde LDP) to initiate reentry. Thus, during VT, the LDP precedes PP, which in turn precedes ventricular activation. Verapamil significantly prolongs the TCL, LDP-PP interval, and PP-LDP interval during VT. However, the interval from PP to the onset of the QRS complex remains unchanged.
Pace Mapping Pace mapping is not very reliable in identifying the optimal target site for ablation of fascicular VT. Pace mapping during NSR that matches the QRS morphology during VT can help to identify the exit site (i.e., the myocardial breakthrough site) of the VT circuit, but the exit site does not represent an effective ablation target. Pacing at successful ablation sites (within the slow diastolic zone of the VT circuit) often captures both the Purkinje fiber system and adjacent local myocardial tissue (away from the exit of the reentrant circuit) and also result in antidromic
BOX 24.1 Entrainment Mapping of
Verapamil-Sensitive Left Ventricle Ventricular Tachycardia
Pacing From Sites Outside VT Circuit (RV Apex or RVOT) • Manifest ventricular fusion on the surface ECG (fixed fusion at a single PCL and progressive fusion on progressively shorter PCLs) or fully paced QRS morphology • PPI − TCL > 30 ms • Interval between stimulus artifact to onset of QRS on surface ECG is greater than the interval between local ventricular electrogram on pacing lead to onset of QRS on surface ECG Pacing From Sites Inside VT Circuit (Posteroinferior LV Septum) • Manifest ventricular fusion on the surface ECG (fixed fusion at a single PCL and progressive fusion on progressively shorter PCLs) • PPI − TCL < 30 ms • Interval between stimulus artifact to onset of QRS on surface ECG equals the interval between local ventricular electrogram on pacing lead to onset of QRS on surface ECG (±20 ms) Pacing From Protected Isthmus Inside VT Circuit (Site Where Both PP and LDP Are Recorded) • Concealed ventricular fusion (i.e., paced QRS is identical to the VT QRS) • PPI − TCL < 30 ms • Interval between stimulus artifact to onset of QRS on surface ECG equals the interval between PP to onset of QRS on surface ECG (±20 ms) • Stimulus-to-LDP interval is long, and LDP is orthodromically captured from proximal to distal sites during activation CL, Cycle length; ECG, electrocardiogram; LDP, late diastolic potential; LV, left ventricle; PP, Purkinje potential; PPI, post-pacing interval; RV, right ventricle; RVOT, right ventricular outflow tract; VT, ventricular tachycardia.
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CHAPTER 24 Fascicular Ventricular Tachycardia
activation of the isthmus of the VT circuit, generating a QRS morphology that can be significantly different from the VT morphology.1,8
Electroanatomic Mapping Electroanatomic three-dimensional (3-D) mapping (CARTO mapping system [Biosense Webster, Diamond Bar, CA, United States] or EnSite NavX system [St. Jude Medical, St. Paul, MN, United States]) can facilitate mapping of the left fascicular system and is of particular value when mapping is performed during NSR. After the LV geometry is created, activation mapping is performed during NSR along the LV septum to trace the conduction system from the site of recording of His potential just under the aortic valve and moving progressively distally (apically) until no fascicular/PP can be recorded. These sites, as well as the sinus breakout point, are tagged as special landmarks on the electroanatomic map to help identify ablation targets (Fig. 24.5). Once sustained VT is induced, activation mapping is performed during VT, with particular attention to sites with earliest ventricular activation, sites with presystolic PPs, as well as sites with LDPs. These sites are tagged on the electroanatomic map to identify the different components of the reentry circuit in relation to the fascicular system identified during NSR.14,15
Noncontact Mapping The EnSite 3000 noncontact mapping system (St. Jude Medical) may be used to identify the sinus breakout point (i.e., the LV site with the earliest local activation during NSR), and that point has been used to guide linear ablation perpendicular to the conduction direction of LPF. Particular attention is paid to the geometric detail in the areas of the HB, septum, and apex of the LV. After the ventricular geometry has been generated, the system can then calculate electrograms from more than 3000 endocardial points simultaneously by reconstructing far-field
signals to create the isopotential map of sinus rhythm using a single cardiac cycle. The HB, LB, fascicles, and sinus breakout point are tagged as special landmarks in the geometry. The sinus breakout point is located in the midposterior septum and the local virtual electrogram presents with QS morphology (Fig. 24.6). Virtual electrograms at points from the HB down to the sinus breakout point show a sharp, low-amplitude potential preceding the ventricular potential. The interval between these two potentials becomes progressively shorter as the activation propagates from the HB to the sinus breakout point, until the two potentials finally fuse together at the sinus breakout point.16
ABLATION Target of Ablation Definition of the appropriate ablation target has evolved with better understanding of the anatomical substrate of fascicular VT. Initially, the ablation target site was defined as the site where the earliest endocardial ventricular activation time and the best pace map could be obtained during VT (which represents the exit of the reentrant circuit). Subsequently, in combination with pace mapping, the earliest PP preceding QRS onset during VT (considered to be the lower turnaround point of the reentrant circuit) in the posterior third of the LV septum was reported to be a marker for successful ablation. Successful ablation is achieved at sites where PP is recorded 30 to 40 milliseconds before QRS onset (Fig. 24.7). Entrainment mapping at this location helps to confirm the relationship to the reentrant circuit. Of note, this area is located more basally than the LV area that shows the earliest ventricular activation during VT (the exit point of the circuit into the ventricular septum), suggesting that the location of the earliest ventricular activation during tachycardia is not an ideal site for ablation of this arrhythmia. Later on, the LDP recorded during VT, which likely reflects
Fig. 24.5 Three-dimensional Electroanatomic (ESI NavX) Map of the Left Ventricle With Its Conduction System Obtained During Sinus Rhythm. Green markers denote His bundle and left bundle branch (LB) recording site; red markers denote posterior fascicle and Purkinje potential recording site; white marker denotes target for radiofrequency (RF) catheter ablation. (From Kataria V, Yaduvanshi A, Kumar M, Nair M. Demonstration of posterior fascicle to myocardial conduction block during ablation of idiopathic left ventricular tachycardia: an electrophysiological predictor of long-term success. Heart Rhythm. 2013;10:638–645.)
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CHAPTER 24 Fascicular Ventricular Tachycardia
AV
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H
Fig. 24.6 Noncontact Mapping During Normal Sinus Rhythm (NSR). Shown is an animated propagation map of the left ventricle (LV) from frames A to G in the right anterior oblique view during NSR. Note that the sinus activation propagates down from the His bundle (AV) to the left bundle branch (LB) and then bifurcates into left anterior and left posterior fascicles before the entire LV is finally activated. The activation breakout point is at the midposterior septum and marked sinus breakout point (SBO) on the map. The thick black line indicates the propagation direction of the wavefronts from AV down to SBO. (H) Right anterior oblique orientation of the images. Ant., Anterior; Inf., inferior; Sep., septal. (From Chen M, Yang B, Zou J, et al. Non-contact mapping and linear ablation of the left posterior fascicle during sinus rhythm in the treatment of idiopathic left ventricular tachycardia. Europace. 2005;7:138.)
I II III V1 V6
Fig. 24.7 Ablation of Idiopathic Fascicular Ventricular Tachycardia. Radiofrequency (RF) delivery is begun (blue arrow) at the site of the diastolic Purkinje potential during fascicular ventricular tachycardia. Within less than 1 second, the tachycardia terminates. The red arrow indicates probable Purkinje potentials. Abldist, Distal ablation; Ablprox, proximal ablation; CSprox, proximal coronary sinus; CSdist, distal coronary sinus; Hisdist, distal His bundle; Hisprox, proximal His bundle; HRA, high right atrium; RFwatts, radiofrequency watts; RVA, right ventricular apex.
Abldist Ablprox HRA Hisprox Hisdist CSprox CSdist RVA RFwatts Time
RF on 300 msec
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CHAPTER 24 Fascicular Ventricular Tachycardia
the excitation within the critical slow conduction area participating in the reentry circuit, was reported to be a useful marker in guiding successful ablation. Currently, ablation is targeted to a site over the middle or inferoapical portion of the LV septum where the earliest PP and LDP are recorded (Fig. 24.8). Verification of these sites can be achieved with entrainment mapping demonstrating concealed fusion and progressive prolongation of the LDP-PP interval with increasing pacing rate. In addition, pressure applied to the catheter tip at the LDP region occasionally results in VT termination with conduction block between LDP and PP. Pace mapping can also be used as an adjunct to verify this site but, because of poor sensitivity, is less helpful than in focal VTs. It is important to recognize that successful ablation is not necessarily predicted by targeting the earliest (most proximal) LDP. Success can be achieved by ablating an LDP distal to the earliest potential (within the apical third of the septum). This approach is preferred to help reduce the risk of damaging the trunk of the LB. If such an LDP cannot be detected, the site with the earliest PP may then be targeted by ablation.1,6 One report showed a high success rate of an ablation strategy targeting the distal most fascicular potentials of the LPF, close to the Purkinjemyocardial interface, as guided by electroanatomic mapping of the left fascicular system. Ablation is extended progressively distal linearly to the surrounding myocardium until conduction block is achieved between the LV myocardium and the distal posterior fascicle/Purkinje network. At successful ablation sites, the fascicular potential typically preceded the local ventricular electrogram by an interval of 12 ± 1.7 milliseconds, which is less presystolic than the earliest PP targeted in other ablation
VT
strategies. Myocardium-fascicular conduction block during NSR was defined as the prolongation of the interval between the local ventricular electrogram and the fascicular/PP just proximal to the ablation site (duration of >100 milliseconds) or a higher degree of myocardiumfascicular block is recorded. Notably, this ablation approach did not result in LPF block or left axis deviation given the site of ablation being distal to LPF itself.14
Ablation Technique Ablation is usually performed through the retrograde transaortic approach using a standard 4-mm-tip catheter. The catheter is advanced by prolapsing into the LV and directed to the LV septum. Mapping is initially concentrated at the inferoapical septum. If an ideal site is not found in this area, the ablation catheter is moved upward to the midseptal area. It is important to move the catheter slowly and carefully to avoid mechanical trauma to the circuit. Endocardial activation mapping and entrainment mapping are performed to define the target site of ablation.1 Once the target site is identified, a test RF current is applied during VT for 20 seconds with an initial power of 20 to 35 W, targeting a temperature of 60°C. If the VT is terminated or slowed within 15 seconds, additional current is applied for another 60 to 120 seconds and power is increased up to 40 W to reach the target temperature if necessary. If the test RF current is ineffective despite adequate catheter contact, ablation is directed to another site after additional mapping, usually targeting a more proximal site with the earlier LDP. This approach helps to limit RF damage to the area of LPF and LB. Rarely, if ever, does one need
NSR
I II III
V1 V6 HRA Hisprox Hisdist RVA Abluni
Abldist Ablprox 300 msec
Fig. 24.8 Ablation of Fascicular Ventricular Tachycardia (VT). Shown are recordings during VT (left) and normal sinus rhythm (NSR; right) from a successful ablation site for idiopathic left ventricular tachycardia. Red arrows indicate probable Purkinje potentials, activated distal-to-proximal during VT and proximal-to-distal during sinus. Blue arrows show His potentials, occurring after QRS onset during VT. Abldist, Distal ablation; Ablprox, proximal ablation; Abluni, unipolar ablation; Hisdist, distal His bundle; Hisprox, proximal His bundle; HRA, high right atrium; RVA, right ventricular apex..
CHAPTER 24 Fascicular Ventricular Tachycardia more than 50 W or the use of irrigated or large-tip electrodes to ablate these VTs successfully.1 During the RF application, successful ablation sites often display progressive prolongation of the LDP-PP interval, with termination of VT coincident with conduction block between the two potentials. After successful ablation, the LDP can no longer be recorded during NSR.
867
fascicular VT is vulnerable to mechanical injury because of catheter manipulation, which can render the tachycardia noninducible. In these cases, substrate mapping and ablation during NSR have been suggested to eradicate fascicular VT.1,8 Three approaches have been used for substrate-based ablation during sinus rhythm: (1) ablation of the slow conduction zone adjacent to the LPF; (2) anatomical linear ablation to transect the middle to distal portion of the LPF; and (3) ablation of the most distal LPF fibers at the Purkinje-myocardial interface.18 The first approach involves identifying areas of the slow conduction zone that is adjacent to the LPF, which might represent the anterograde limb of the VT reentry circuit. The location of this region is suggested by recording low-amplitude electrograms visible after the sinus QRS complex (presumably resulting from delayed retrograde activation of abnormal Purkinje fibers) in conjunction with more prominent PP (which is generated by anterograde conduction down the LPF). At these locations the low-amplitude signals occur 15 to 45 milliseconds after the PP, and the PP precedes the QRS onset by a relatively short interval (13 ± 8 milliseconds). A major limitation of this ablation strategy is the inability to identify the low-amplitude signals in a sizable proportion of patients. In addition, in another subset of patients, similar nonspecific low-amplitude signals are recorded over a sizeable area of the septum; targeting all those regions would increase the risk of injury to the conducting system.8 The second approach involves creation of an ablation line perpendicular to the activation direction of LPF and 1 cm above the sinus breakout point, as defined by electroanatomic or noncontact mapping during NSR (Fig. 24.9). The ablation line typically extends for approximately 2.0 ± 0. 4 cm in the region of the mid to midinferior LV septum and is guided by recording a small PP preceding the ventricular activation at its starting and ending points. A significant rightward shift of the QRS axis in the surface limb leads can be observed after the ablation procedure.16 The third approach involves targeting the distal most fascicular potentials of the LPF, close to the Purkinje-myocardial junction, as described previously. This approach can be used both for inducible or noninducible VT cases.14
Endpoints of Ablation Successful ablation is defined as the lack of inducibility of VT, with and without isoproterenol administration (using the best method for induction documented before ablation), at least 30 minutes after ablation. Importantly, creation of LPF block is not an effective endpoint for ablation and does not prevent arrhythmia recurrence.
Outcome The acute success rate is more than 90%, even when different mapping methods and ablation strategies are used. The recurrence rate is approximately 7% to 15%, with most recurrences occurring in the first 24 to 48 hours after the ablation procedure. Arrhythmia recurrences after an initially successful ablation are caused most commonly by recurrent fascicular VT involving the same fascicle and by new onset of upper septal VT in one third of patients. Of note, the development of new LPF block after fascicular VT ablation was associated with more basal ablations and did not protect against VT recurrence.6 Complications are rare and include different degrees of fascicular block (most likely because of inadvertent collateral damage to the LPF, particularly when ablation is delivered more basally), LBBB, cardiac tamponade, aortic regurgitation, and mitral regurgitation caused by torn chordae that may result from entrapment of the ablation catheter in a chorda of the mitral leaflet.17
Empirical Ablation of Noninducible Ventricular Tachycardia Conventional activation mapping, guided by either the earliest PP or the LDP, although effective, depends on the inducibility of sustained and hemodynamically stable fascicular VT. However, the VT may not be inducible in the EP laboratory. In addition, the critical substrate of
AV .LB
.Ant. .24
.25
.23 SBO .Sep. .APEX .Inf.
Fig. 24.9 Noncontact Mapping of Fascicular Ventricular Tachycardia During Normal Sinus Rhythm. A linear ablation lesion was created perpendicular to the wavefront propagation direction and 1 cm above the sinus breakout point (SBO). Both the starting and ending lesion points have a small Purkinje potential preceding the ventricular activation. Ant., Anterior; AV, His recording area; Inf., inferior; LB, left bundle branch; Sep., septal. (From Chen M, Yang B, Zou J, et al. Non-contact mapping and linear ablation of the left posterior fascicle during sinus rhythm in the treatment of idiopathic left ventricular tachycardia. Europace. 2005;7:138.)
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REFERENCES 1. Nogami A. Purkinje-related arrhythmias. J. Arrhythmia. 2011;27:6–27. 2. Scheinman MM. Role of the His-Purkinje system in the genesis of cardiac arrhythmia. Heart Rhythm. 2009;6:1050–1058. 3. Tsuchiya T, et al. Effects of verapamil and lidocaine on two components of the re-entry circuit of verapamil-senstitive idiopathic left ventricular tachycardia. J Am Coll Cardiol. 2001;37:1415–1421. 4. Talib AK, et al. Verapamil-sensitive upper septal idiopathic left ventricular tachycardia prevalence, mechanism, and electrophysiological characteristics. JACC Clin Electrophysiol. 2015;1:369–380. 5. Nogami A, et al. Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia. J Am Coll Cardiol. 2000;36:811–823. 6. Liu Y, et al. Catheter ablation of fascicular ventricular tachycardia: long-term clinical outcomes and mechanisms of recurrence. Circ Arrhythmia Electrophysiol. 2015;8:1443–1451. 7. Dobrzynski H, et al. Structure, function and clinical relevance of the cardiac conduction system, including the atrioventricular ring and outflow tract tissues. Pharmacol Ther. 2013;139:260–288. 8. Latchamsetty R, Bogun F. Fascicular tachycardia. Card Electrophysiol. Clin. 2014;6:567–579. 9. Collins KK, et al. Fascicular and nonfascicular left ventricular tachycardias in the young: an international multicenter study. J Cardiovasc Electrophysiol. 2013;24:640–648.
10. Al’Aref SJ, et al. Differentiation of papillary muscle from fascicular and mitral annular ventricular arrhythmias in patients with and without structural heart disease. Circ Arrhythmia Electrophysiol. 2015;8:616–624. 11. Sadek MM, et al. Idiopathic ventricular arrhythmias originating from the moderator band: electrocardiographic characteristics and treatment by catheter ablation. Heart Rhythm. 2015;12:67–75. 12. Sung RK, et al. Diagnosis and ablation of multiform fascicular tachycardia. J Cardiovasc Electrophysiol. 2013;24:297–304. 13. Ma W, et al. Mapping and ablation of ventricular tachycardia from the left upper fascicle: how to make the most of the fascicular potential? Circ Arrhythmia Electrophysiol. 2013;6:47–51. 14. Kataria V, Yaduvanshi A, Kumar M, et al. Demonstration of posterior fascicle to myocardial conduction block during ablation of idiopathic left ventricular tachycardia: an electrophysiological predictor of long-term success. Heart Rhythm. 2013;10:638–645. 15. Zhan XZ, et al. A new electrophysiologic observation in patients with idiopathic left ventricular tachycardia. Heart Rhythm. 2016;13:1460–1467. 16. Chen M, et al. Non-contact mapping and linear ablation of the left posterior fascicle during sinus rhythm in the treatment of idiopathic left ventricular tachycardia. Europace. 2005;7:138–144. 17. Li D, Guo J, Xu Y, et al. The surface electrocardiographic changes after radiofrequency catheter ablation in patients with idiopathic left ventricular tachycardia. Int J Clin Pract. 2004;58:11–18. 18. Chen H, et al. A novel method to identify the origin of ventricular tachycardia from the left fascicular system. Heart Rhythm. 2016;13: 686–694.
Diagnostic Maneuvers During Tachycardia, 861 Exclusion of Other Arrhythmia Mechanisms, 861 Mapping, 861 Activation Mapping, 861 Entrainment Mapping, 863 Pace Mapping, 863 Electroanatomic Mapping, 864 Noncontact Mapping, 864 Ablation, 864 Target of Ablation, 864 Ablation Technique, 866 Endpoints of Ablation, 867 Outcome, 867 Empirical Ablation of Noninducible Ventricular Tachycardia, 867
PATHOPHYSIOLOGY
activation propagates anterogradely (from basal to apical segments along the LV septum) over the abnormal Purkinje tissue with decremental conduction properties and verapamil sensitivity, which serves as the anterograde limb of the circuit and appears to be insulated from the nearby ventricular myocardium. The lower turnaround point of the reentrant circuit is located in the lower third of the septum, where the wavefront captures the fast conduction Purkinje tissue from or contiguous to the LPF, and retrograde activation occurs over the LPF from the apical to basal septum forming the retrograde limb of the reentrant circuit. In addition, at the lower turnaround point, anterograde activation occurs down the septum to break through (at the exit of the tachycardia circuit) in the posterior septal myocardium. The upper turnaround point of the reentrant circuit occurs over a zone of slow conduction located close to the main trunk of the left bundle branch (LB) in the basal interventricular septum (Fig. 24.1). The estimated distance between the entrance and exit of the circuit is approximately 2 cm.5,6
The His-Purkinje system plays an important role in the genesis of cardiac arrhythmias. The mechanisms of several types of monomorphic ventricular tachycardias (VTs) have been directly linked to the Purkinje system, including bundle branch reentrant VT, interfascicular reentrant VT, fascicular VT, and focal Purkinje VT. A subset of polymorphic VTs and ventricular fibrillation has also been linked to triggers originating from the Purkinje system. Most of those arrhythmias occur in patients with underlying structural heart disease; however, fascicular VT and a subset of focal Purkinje VTs are idiopathic, occurring in the absence of apparent cardiac disease.1,2 Idiopathic fascicular VT is a reentrant tachycardia involving the left fascicular Purkinje system. The reentry circuit is most commonly (90%) located in the territory of the left posterior fascicle (LPF), infrequently (5% to 10%) in the region of the left anterior fascicle (LAF), and rarely arise from fascicular locations high in the septum. Fascicular VT is also referred to as “verapamil-sensitive” VT, given its tendency to slow or terminate with intravenous verapamil.3,4
Tachycardia Circuit In the most common form (LPF-VT), the tachycardia circuit incorporates the LPF serving as one limb and abnormal Purkinje tissue with slow, decremental conduction serving as the other limb. The anterograde limb may be associated with longitudinal dissociation within the LPF or contiguous tissue that is directly coupled to the LPF (such as a false tendon) or, alternatively, has ventricular myocardium interposed. The zone of slow conduction appears to depend on the slow inward calcium current because the degree of slowing of tachycardia cycle length (TCL) in response to verapamil is entirely attributed to its negative dromotropic effects on the area of slow conduction.5,6 The entrance site to the slow conduction zone is thought to be located closer to the base of the left ventricle (LV) septum. From there,
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Anatomy of the Left Fascicular System The LB arises from the His bundle (HB) as numerous fine, intermingling fascicles that leave the left margin of the branching HB through most of its course along the crest of the muscular ventricular septum. The predivisional portion of the LB penetrates the membranous portion of the interventricular septum under the aortic ring and then divides under the septal endocardium into two branches: the LAF and the LPF. An estimated 65% of individuals have a third fascicle of the LB, the left median fascicle (LMF). The fascicles cascade down the LV septum in a fan-like configuration with extensive interconnections. Unlike the cord-like right bundle branch, the LB and its divisions are diffuse, fanlike structures that quickly arborize just beyond their origin. The LAF represents the superior (anterior) division of the LB, the LPF represents the inferior (posterior) division, and the LMF represents the septal (median) division.
CHAPTER 24 Fascicular Ventricular Tachycardia NSR
859
VT
II
II
V1 DP
LPF
V1 His
A
His
B
Fig. 24.1 Schematic Illustration of the Reentrant Circuit in Fascicular Ventricular Tachycardia (VT). A block of the LV septum is depicted with the left posterior fascicle (LPF) and diastolic pathway (DP) running in parallel until they intersect at the bottom. A 10-pole catheter is shown recording between pathways; electrograms from each pair are shown along with surface electrocardiogram leads and His bundle recordings. (A) Activation sequence is shown during normal sinus rhythm (NSR), the dashed line denotes QRS onset. Note the direction and speed of propagation over the LPF while the DP is activated after the QRS and in both directions (arrows). (B) During VT complex, the DP is activated anterogradely and the LPF retrogradely (arrows). See text for discussion.
The LB subdivisions extend to the midportion of the septum before they detach from the underlying endocardium and form free-running false tendons that traverse the ventricular chamber, projecting predominantly toward the papillary muscles. The fascicles become ramified in the ventricular apex and extend back along the ventricular walls toward the cardiac base.7 The thin LAF crosses the anterobasal LV region toward the anterolateral papillary muscle and terminates in the Purkinje system of the anterolateral LV wall. The LPF appears as an extension of the main LB and is broad in its initial course. It then fans out extensively toward the posterior papillary muscle and terminates in the Purkinje system of the posteroinferior LV wall. The LMF runs to the interventricular septum; it arises in most cases from the LPF, less frequently from the LAF, or from both fascicles, and in a few cases it has an independent origin from the central part of the main LB at the site of its bifurcation.2
VT can be observed in 6% of patients. Spontaneous remission of the VT can occur with time.8
EPIDEMIOLOGY
INITIAL EVALUATION
Fascicular VT accounts for 10% to 15% of all idiopathic VTs. Age at presentation is typically 15 to 40 years (unusual after 55 years). Males are more commonly affected (60% to 80%). The clinical course is generally benign, and the prognosis is excellent. Sudden cardiac death is very rare. Tachycardia-induced cardiomyopathy precipitated by incessant
The diagnosis of fascicular VT is based on: (1) VT morphology on the surface electrocardiogram (ECG) (right bundle branch block [RBBB] with left or, less commonly, right axis deviation); (2) VT sensitivity to verapamil; and (3) absence of structural heart disease. Invasive electrophysiology (EP) testing is required to confirm the diagnosis. Evaluation
CLINICAL PRESENTATION Most patients present with mild to moderate symptoms of palpitations and lightheadedness. Occasionally, symptoms are debilitating and include fatigue, dyspnea, and presyncope. Syncope and cardiac arrest are rare. The VT is typically paroxysmal and can last for minutes to hours. Although fascicular VT can occur at rest, it is sensitive to catecholamines and often occurs during physical or emotional stress. Rarely, the VT can become incessant, sustained for a long period (days) and does not revert spontaneously to normal sinus rhythm (NSR). When incessant, fascicular VT can precipitate tachycardia-induced cardiomyopathy and heart failure.8
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CHAPTER 24 Fascicular Ventricular Tachycardia
to exclude structural heart disease is necessary and typically includes echocardiographic examination (that may show one or more prominent false tendons), stress testing, and coronary arteriography, depending on patient age and risk factors.8
Electrocardiogram During Ventricular Tachycardia
Oral verapamil or diltiazem is useful in mild cases; however, long-term efficacy is variable and the benefit of these drugs in management of patients with severe symptoms is often limited. Catheter ablation is highly effective (success rate of 85% to 90%) and is recommended for patients in whom drug therapy is not successful, not tolerated, or not preferred.3,8,9
Fascicular VT is characterized by relatively narrow QRS duration (127 ± 11 milliseconds) and short RS interval (the duration from the beginning of the QRS to the nadir of the S wave) in the precordial leads (60 to 80 milliseconds). The shorter QRS duration reflects the proximal exit of fascicular VTs from the His-Purkinje system (HPS). In addition, during fascicular VT, the interventricular septum is activated early with a left-to-right direction, resulting in an initial “r” waves in lead V1 and small “q” waves in leads I and aVL (similar to classic RBBB pattern). In addition, the rapid activation of the LV via the Purkinje system results in unopposed late activation of the right ventricular outflow tract (RVOT), leading to a large R′ amplitude in lead V1 (and r < R′).8,10 The VT rate is approximately 150 to 200 beats/min (range, 120 to 250 beats/min). Alternans in the TCL is frequently noted; otherwise, the VT rate is stable. According to the fascicular territory involved and, consequently, the QRS morphology, fascicular VTs are classified into three subtypes: (1) LPF VT (with the reentrant circuit exit in the inferoposterior septum) exhibits an RBBB and superior axis configuration (most common form); (2) LAF VT (with the reentrant circuit exit in the anterolateral wall of the LV) exhibits RBBB and right-axis deviation configuration; and (3) upper septal fascicular VT with a narrow QRS and normal axis configuration (rare form). In the most common form (LPF-VT), the QRS during VT typically has RBBB with LAF block configuration. The R/S ratio is less than 1 in leads V5 and V6 (Fig. 24.2). VTs arising more toward the middle at the region of the posterior papillary muscle have a left superior axis and RS in leads V5 and V6, whereas those arising closer to the apex have a right superior axis with a small “r” and deep S (or even QS) in leads V5 and V6.1,8
ELECTROCARDIOGRAPHIC FEATURES
ELECTROPHYSIOLOGICAL TESTING
Electrocardiogram During Normal Sinus Rhythm
Induction of Tachycardia
The resting ECG is usually normal. Symmetrical inferolateral T wave inversion can be observed after termination of the VT (cardiac memory).
Given the reentrant mechanism of fascicular VT, the arrhythmia is usually inducible by programmed electrical stimulation. In fact, fascicular
PRINCIPLES OF MANAGEMENT Acute Management Electrical cardioversion is required for VT termination in hemodynamically unstable patients. For stable patients with an established diagnosis of verapamil-sensitive fascicular VT, intravenous verapamil is the firstline treatment and is very successful in acutely terminating the VT. Intravenous verapamil slows the rate of VT progressively and then terminates it. Diltiazem is equally effective. Nonsustained VT may continue to occur for a while after termination.3 Response of VT to lidocaine, procainamide, amiodarone, sotalol, and beta-blockers is less consistent, and these drugs are usually ineffective. Carotid sinus massage and Valsalva maneuvers have no effect on the VT. Fascicular VT is generally unresponsive to adenosine; however, when catecholamine stimulation (isoproterenol infusion) is required for the initiation of VT (in the EP laboratory), the VT can become adenosine sensitive.8,9
Chronic Management
1
aVR
V1
V4
2
aVL
V2
V5
3
aVF
V3
V6
Fig. 24.2 Surface Electrocardiogram of Fascicular Ventricular Tachycardia (VT). Note the right bundle branch block and left anterior fascicle block pattern characteristic of these VTs.
CHAPTER 24 Fascicular Ventricular Tachycardia VT is characterized by its reproducible initiation and termination not just by ventricular stimulation but also by atrial pacing. Often, isoproterenol infusion facilitates VT induction. Consistent with a reentry mechanism, an inverse relationship is observed between the coupling interval of the initiating ventricular extrastimulation (VES) or ventricular pacing cycle length (PCL) and the first VT beat.6
Diagnostic Maneuvers During Tachycardia Entrainment
Entrainment of fascicular VT can usually be demonstrated with ventricular pacing at a PCL approximately 10 to 30 milliseconds shorter than the TCL. Manifest entrainment is more frequently achieved when pacing is performed from the RVOT because the RVOT is closer to the entrance site of the area of slow conduction in the reentrant circuit, located near the base of the LV septum. On the other hand, pacing from the RV apex is less likely to demonstrate entrainment and, when it does, it is unlikely to demonstrate manifest fusion because of the larger distance from the entrance site of the circuit and because of the narrow excitable gap of the reentrant circuit.
Resetting Fascicular VT can be reset by VES, with an increasing or mixed resetting response (characteristic of reentrant circuit with an excitable gap).
Termination VT can be reproducibly terminated with programmed atrial or ventricular stimulation.
Exclusion of Other Arrhythmia Mechanisms The differential diagnosis of fascicular VT includes interfascicular VT, supraventricular tachycardia (SVT) with aberrant conduction, and VT originating from the LV papillary muscles.
Interfascicular Ventricular Tachycardia Interfascicular VT has several characteristic features (see Chapter 26): (1) bifascicular block QRS morphology during VT, which is identical to that during NSR; (2) reversal of activation sequence of the HB and LB during VT; and (3) spontaneous oscillations in the TCL caused by changes in the LB-LB interval that precede and drive the TCL. Interfascicular VT terminates with VES or radiofrequency (RF) ablation that produces block in LAF or LPF.
Supraventricular Tachycardia When fascicular VT is associated with a 1 : 1 VA conduction and because of its responsiveness to verapamil and inducibility by atrial pacing, it can be misdiagnosed as SVT with bifascicular block aberrancy. During SVT (similar to NSR), the HB is activated in an anterograde direction with sequential activation of the HB and ventricles (see Chapter 21). In contrast, during fascicular VT, the HB is activated retrogradely, with parallel activation of the HB and ventricle. Thus the HV interval during SVT with aberrancy is equal to or slightly longer than that during NSR. On the other hand, the HV interval during fascicular VT is frequently negative (i.e., His potential is recorded after onset of the QRS). The His potential can also precede the QRS onset during fascicular VT (especially during upper septal fascicular VT); however, the HV interval during VT will be shorter than that during NSR. In addition, unlike fascicular VT, aberrantly conducted SVTs are typically responsive to adenosine, beta-blockers, and Valsalva maneuvers.
Papillary Muscle Ventricular Tachycardia Papillary muscle VTs typically manifest as premature ventricular complexes (PVCs) rather than sustained monomorphic VT and are more
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likely to occur in older patients with structural heart disease. VTs arising from the LV papillary muscles exhibit a QRS morphology that can mimic fascicular VT. However, compared with fascicular VT, papillary muscle VTs have a broader QRS complex (150 ± 15 milliseconds vs. 127 ± 11 milliseconds). In addition, VTs originating from the papillary muscles (which are farther away from the septum) lack the rsR′ pattern in lead V1; rather, those VTs often have a qR pattern (or, less commonly, a monophasic R wave) in lead V1. Furthermore, spontaneous variations in QRS morphology occur relatively frequently during VTs originating from the LV papillary muscles, a feature that can help distinguish these VTs from LV fascicular VT; the latter being a reentrant tachycardia with a consistent QRS morphology.8,10 Unlike patients with fascicular VAs, papillary muscle VAs are typically not inducible with programmed electrical stimulation, which is consistent with a nonreentrant mechanism of papillary muscle VTs.
Focal Purkinje Ventricular Tachycardia Idiopathic focal VTs can arise from the Purkinje system in either ventricle and can present as PVCs, accelerated idioventricular rhythm, or VT. Focal Purkinje VTs arising from the left Purkinje network exhibit an RBBB pattern with either left- or right-axis deviation and can be difficult to distinguish from fascicular VT. In contrast to the reentrant idiopathic fascicular VT, focal Purkinje VTs are most likely related to abnormal automaticity. These VTs are sensitive to autonomic tone and frequently display chronotropic properties. Focal Purkinje VTs are typically induced by exercise and catecholamines and slowed or terminated by beta-blockers (and hence classified as “propranolol-sensitive” VTs) and lidocaine. Unlike fascicular VT, focal Purkinje VTs are not responsive to verapamil and cannot be induced or terminated by programmed electrical stimulation. In addition, these VTs are transiently suppressed by adenosine and with overdrive pacing.11
MAPPING Activation Mapping Activation mapping is performed during sustained VT and is specifically directed toward sites with His or Purkinje potentials (PPs) extending from LV basal septal sites with HB recordings to most apical sites with presystolic PPs. Activation mapping is used to identify sites with the earliest ventricular activation and earliest presystolic PPs, as well as late diastolic potentials (LDPs).6,8 Mapping is performed along the LV inferior septum (for LPF VT), along the anterolateral LV (for LAF VT), or the basal LV septum (for left upper septal VT). Strategies for mapping and ablation of LPF VT, the most common type of fascicular VT, are discussed here in detail. The same principles can be applied for the two other types of fascicular VT. When the VT is not inducible or not sustained, mapping can be performed during NSR to record the PPs along the posterior aspect of the LV septum, identifying the course of the LPF.
Site of Earliest Ventricular Activation The site of earliest ventricular activation during VT (which represents the exit of the reentrant circuit) is in the region of the LPF (inferoposterior LV septum) in 90% of fascicular VTs (explaining the RBBB–superior axis configuration of the QRS), and in the region of the LAF (anterosuperior LV septum) in 5% to 10% of fascicular VTs (explaining the RBBB–right axis configuration of the QRS). In most cases, ventricular electrograms at the site of earliest activation are discrete during both NSR and VT. The HB is not a component of the reentrant circuit; in fact, a retrograde His potential is often recorded 20 to 40 milliseconds after the earliest ventricular activation (Fig. 24.3).12
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CHAPTER 24 Fascicular Ventricular Tachycardia
I II III
V1 V6
Hisdist RVA RVOT Abluni
Abldist Ablprox 200 msec
Fig. 24.3 Idiopathic Fascicular Ventricular Tachycardia. The blue arrow shows late diastolic small potential, 45 milliseconds prior to QRS onset. Distinct Purkinje-like potentials (blue arrow) are evident before the dotted line denoting QRS onset, as well as in the proximal ablation electrogram. The red arrow indicates retrograde His potential. Note the unipolar QS configuration just coinciding with QRS onset. Abldist, Distal ablation; Ablprox, proximal ablation; Abluni, unipolar ablation; Hisdist, distal His bundle; RVA, right ventricular apex; RVOT, right ventricular outflow tract.
I II III V1 V6 HRA Hisprox Hisdist RVA Abldist 200 msec
Fig. 24.4 Sinus Rhythm Recordings at a Successful Ablation Site for Fascicular Ventricular Tachycardia. The left arrow points to a Purkinje-like potential just prior to the local electrogram (also slightly preceding the onset of the QRS); the right arrow shows a sharp, delayed diastolic potential, purportedly from the slowconducting limb of the circuit. Abldist, Distal ablation; Hisdist, distal His bundle; Hisprox, proximal His bundle; HRA, high right atrium; RVA, right ventricular apex.
Purkinje Potential The PP (also referred to as “P2” in literature) is a discrete, high-frequency potential that precedes the site of earliest ventricular activation by 15 to 42 milliseconds and is recorded in the posterior third of the LV septum during VT, as well as during NSR (see Figs. 24.3 and 24.4). Because this
potential also precedes ventricular activation during NSR, it is believed to originate from activation of a segment of the LPF and to represent the lower turnaround point in the reentrant circuit. The earliest ventricular activation site (exit) during VT is identified more distally (apically) in the septum than the region with the earliest recorded PP.12
CHAPTER 24 Fascicular Ventricular Tachycardia
863
Late Diastolic Potential
Entrainment Mapping
The LDP, also referred to as “P1” or “pre-PP,” is a discrete potential that precedes the PP during VT and is recorded at the basal, middle, or apical LV septum. During NSR, the LDP is inscribed after the QRS. The LDP is thought to originate from activation at the entrance to the abnormal Purkinje tissue (the specialized, verapamil-sensitive zone), which is thought to serve as the anterograde limb of the reentrant circuit and is isolated from surrounding muscle (allowing it to have a discrete diastolic activation time). The LDP differs in morphology from the PP and has a relatively small amplitude and low-frequency component. The area with LDP recording is confined to a small region (0.5 to 1.0 cm2) and is included in the larger area where the PP is recorded (2 to 3 cm2); hence the LDP often is recorded simultaneously with the PP by the same electrode. The LDP is recorded within an area proximal to the earliest PP recording site and is activated from the basal to apical septum toward the earliest PP site. The relative activation times of the LDP, PP, and local ventricular potential at the LDP recording site to the onset of QRS complex are −50.4 ± 18.9, −15.2 ± 9.6, and 3.0 ± 13.3 milliseconds, respectively (see Fig. 24.3). The earliest ventricular activation site (exit) during VT is identified at the posteroapical septum and is more apical in the septum than the region with LDP.12
Analysis of entrainment from different ventricular sites helps to identify the relationship of those sites to the VT circuit (Box 24.1). Entrainment with concealed fusion and a PPI that approximates the TCL helps to identify the diastolic slow zone (isthmus) of the reentrant circuit. Notably, because of the overlap between the fascicular tissue and the ventricular myocardium, pacing from the isthmus of the VT circuit may not produce concealed fusion, because pacing frequently results in local myocardial capture outside that region, producing manifest fusion.13 During entrainment, the LDP (representing the entrance of the circuit) is orthodromically captured and, as the pacing rate is increased, the LDP-PP interval (representing an area of decremental Purkinje tissue) prolongs, whereas the stimulus-to-LDP and PP-QRS intervals typically remain constant.12
Ventricular Activation Sequence During NSR, conduction propagates anterogradely (proximal to distal or basal to apical) and rapidly down the LPF, generating an anterograde PP followed by ventricular activation (see Fig. 24.1). In parallel, the impulse slowly conducts anterogradely over the abnormal Purkinje tissue, and such slow conduction (or block) in the proximal segment allows the anterograde wavefront traveling rapidly over the LPF to conduct retrogradely up the slow pathway, resulting in fusion of delayed (late) ascending and descending potentials that follow (or are buried in) local ventricular depolarization, which likely represent the LDPs recorded during VT (see Fig. 24.4). Those late potentials have been found only in patients with fascicular VT but not in control subjects and have been recorded in the midinferior septum within or contiguous to the LPF. During ventricular pacing, the LPF is activated retrogradely, generating a retrograde PP. In parallel, the impulse produces bidirectional activation of the abnormal Purkinje pathway in a manner similar but in reverse direction to that during NSR. During VT, activation propagates anterogradely (from the basal to the apical site of the LV septum) over the abnormal Purkinje tissue, giving rise to an anterograde LDP; hence the earliest LDP is seen in the basal septum and the latest LDP is seen in the apical septum. The reentrant wavefront then turns around in the lower third of the septum and activates the fast conduction Purkinje fibers along the LPF, generating a retrograde PP. From the lower turnaround point, the wavefront propagates anterogradely down the septum to exit the reentrant circuit and activate the posterior septal myocardium, and retrogradely over the LPF from apical to basal septum, forming the retrograde limb of the tachycardia, with an upper turnaround point of the reentrant wavefront occurring over a zone of slow conduction (between LDP and PP areas) located close to the main trunk of the LB (see Fig. 24.1). For a VES to initiate VT, retrograde block must occur in the abnormal Purkinje tissue, and the paced wavefront is retrogradely conducted up the LPF (generating a retrograde PP) with some delay and then down the abnormal Purkinje tissue (generating an anterograde LDP) to initiate reentry. Thus, during VT, the LDP precedes PP, which in turn precedes ventricular activation. Verapamil significantly prolongs the TCL, LDP-PP interval, and PP-LDP interval during VT. However, the interval from PP to the onset of the QRS complex remains unchanged.
Pace Mapping Pace mapping is not very reliable in identifying the optimal target site for ablation of fascicular VT. Pace mapping during NSR that matches the QRS morphology during VT can help to identify the exit site (i.e., the myocardial breakthrough site) of the VT circuit, but the exit site does not represent an effective ablation target. Pacing at successful ablation sites (within the slow diastolic zone of the VT circuit) often captures both the Purkinje fiber system and adjacent local myocardial tissue (away from the exit of the reentrant circuit) and also result in antidromic
BOX 24.1 Entrainment Mapping of
Verapamil-Sensitive Left Ventricle Ventricular Tachycardia
Pacing From Sites Outside VT Circuit (RV Apex or RVOT) • Manifest ventricular fusion on the surface ECG (fixed fusion at a single PCL and progressive fusion on progressively shorter PCLs) or fully paced QRS morphology • PPI − TCL > 30 ms • Interval between stimulus artifact to onset of QRS on surface ECG is greater than the interval between local ventricular electrogram on pacing lead to onset of QRS on surface ECG Pacing From Sites Inside VT Circuit (Posteroinferior LV Septum) • Manifest ventricular fusion on the surface ECG (fixed fusion at a single PCL and progressive fusion on progressively shorter PCLs) • PPI − TCL < 30 ms • Interval between stimulus artifact to onset of QRS on surface ECG equals the interval between local ventricular electrogram on pacing lead to onset of QRS on surface ECG (±20 ms) Pacing From Protected Isthmus Inside VT Circuit (Site Where Both PP and LDP Are Recorded) • Concealed ventricular fusion (i.e., paced QRS is identical to the VT QRS) • PPI − TCL < 30 ms • Interval between stimulus artifact to onset of QRS on surface ECG equals the interval between PP to onset of QRS on surface ECG (±20 ms) • Stimulus-to-LDP interval is long, and LDP is orthodromically captured from proximal to distal sites during activation CL, Cycle length; ECG, electrocardiogram; LDP, late diastolic potential; LV, left ventricle; PP, Purkinje potential; PPI, post-pacing interval; RV, right ventricle; RVOT, right ventricular outflow tract; VT, ventricular tachycardia.
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CHAPTER 24 Fascicular Ventricular Tachycardia
activation of the isthmus of the VT circuit, generating a QRS morphology that can be significantly different from the VT morphology.1,8
Electroanatomic Mapping Electroanatomic three-dimensional (3-D) mapping (CARTO mapping system [Biosense Webster, Diamond Bar, CA, United States] or EnSite NavX system [St. Jude Medical, St. Paul, MN, United States]) can facilitate mapping of the left fascicular system and is of particular value when mapping is performed during NSR. After the LV geometry is created, activation mapping is performed during NSR along the LV septum to trace the conduction system from the site of recording of His potential just under the aortic valve and moving progressively distally (apically) until no fascicular/PP can be recorded. These sites, as well as the sinus breakout point, are tagged as special landmarks on the electroanatomic map to help identify ablation targets (Fig. 24.5). Once sustained VT is induced, activation mapping is performed during VT, with particular attention to sites with earliest ventricular activation, sites with presystolic PPs, as well as sites with LDPs. These sites are tagged on the electroanatomic map to identify the different components of the reentry circuit in relation to the fascicular system identified during NSR.14,15
Noncontact Mapping The EnSite 3000 noncontact mapping system (St. Jude Medical) may be used to identify the sinus breakout point (i.e., the LV site with the earliest local activation during NSR), and that point has been used to guide linear ablation perpendicular to the conduction direction of LPF. Particular attention is paid to the geometric detail in the areas of the HB, septum, and apex of the LV. After the ventricular geometry has been generated, the system can then calculate electrograms from more than 3000 endocardial points simultaneously by reconstructing far-field
signals to create the isopotential map of sinus rhythm using a single cardiac cycle. The HB, LB, fascicles, and sinus breakout point are tagged as special landmarks in the geometry. The sinus breakout point is located in the midposterior septum and the local virtual electrogram presents with QS morphology (Fig. 24.6). Virtual electrograms at points from the HB down to the sinus breakout point show a sharp, low-amplitude potential preceding the ventricular potential. The interval between these two potentials becomes progressively shorter as the activation propagates from the HB to the sinus breakout point, until the two potentials finally fuse together at the sinus breakout point.16
ABLATION Target of Ablation Definition of the appropriate ablation target has evolved with better understanding of the anatomical substrate of fascicular VT. Initially, the ablation target site was defined as the site where the earliest endocardial ventricular activation time and the best pace map could be obtained during VT (which represents the exit of the reentrant circuit). Subsequently, in combination with pace mapping, the earliest PP preceding QRS onset during VT (considered to be the lower turnaround point of the reentrant circuit) in the posterior third of the LV septum was reported to be a marker for successful ablation. Successful ablation is achieved at sites where PP is recorded 30 to 40 milliseconds before QRS onset (Fig. 24.7). Entrainment mapping at this location helps to confirm the relationship to the reentrant circuit. Of note, this area is located more basally than the LV area that shows the earliest ventricular activation during VT (the exit point of the circuit into the ventricular septum), suggesting that the location of the earliest ventricular activation during tachycardia is not an ideal site for ablation of this arrhythmia. Later on, the LDP recorded during VT, which likely reflects
Fig. 24.5 Three-dimensional Electroanatomic (ESI NavX) Map of the Left Ventricle With Its Conduction System Obtained During Sinus Rhythm. Green markers denote His bundle and left bundle branch (LB) recording site; red markers denote posterior fascicle and Purkinje potential recording site; white marker denotes target for radiofrequency (RF) catheter ablation. (From Kataria V, Yaduvanshi A, Kumar M, Nair M. Demonstration of posterior fascicle to myocardial conduction block during ablation of idiopathic left ventricular tachycardia: an electrophysiological predictor of long-term success. Heart Rhythm. 2013;10:638–645.)
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CHAPTER 24 Fascicular Ventricular Tachycardia
AV
AV
.23 .24 .LB .25 .26
.Sep.
AV
.23 .24 .LB .25
.Ant.
.26
.24 .LB
.26
.24 .LB .25
.24 .LB .25
.Ant.
.26 .26
.APEX
.Inf.
.Inf. E
F
.23 .24 .LB .25
.Ant.
.26
.27 .27 .Sep. .SBO .SBO
.27 .Sep. .SBO
.APEX .Inf. D
AV
.23
.Ant.
.27 .Sep. .SBO
C AV
.26
.Inf.
B AV .23
.25
.Ant.
.APEX
.Inf.
A
.23 .24 .LB
.27 .Sep. .SBO .APEX
.APEX .Inf.
.26
.25
.Ant.
.27 .Sep. .SBO
.27 .SBO
AV
.23
.Ant.
.27 .Sep. .SBO .APEX
.APEX .Inf. G
H
Fig. 24.6 Noncontact Mapping During Normal Sinus Rhythm (NSR). Shown is an animated propagation map of the left ventricle (LV) from frames A to G in the right anterior oblique view during NSR. Note that the sinus activation propagates down from the His bundle (AV) to the left bundle branch (LB) and then bifurcates into left anterior and left posterior fascicles before the entire LV is finally activated. The activation breakout point is at the midposterior septum and marked sinus breakout point (SBO) on the map. The thick black line indicates the propagation direction of the wavefronts from AV down to SBO. (H) Right anterior oblique orientation of the images. Ant., Anterior; Inf., inferior; Sep., septal. (From Chen M, Yang B, Zou J, et al. Non-contact mapping and linear ablation of the left posterior fascicle during sinus rhythm in the treatment of idiopathic left ventricular tachycardia. Europace. 2005;7:138.)
I II III V1 V6
Fig. 24.7 Ablation of Idiopathic Fascicular Ventricular Tachycardia. Radiofrequency (RF) delivery is begun (blue arrow) at the site of the diastolic Purkinje potential during fascicular ventricular tachycardia. Within less than 1 second, the tachycardia terminates. The red arrow indicates probable Purkinje potentials. Abldist, Distal ablation; Ablprox, proximal ablation; CSprox, proximal coronary sinus; CSdist, distal coronary sinus; Hisdist, distal His bundle; Hisprox, proximal His bundle; HRA, high right atrium; RFwatts, radiofrequency watts; RVA, right ventricular apex.
Abldist Ablprox HRA Hisprox Hisdist CSprox CSdist RVA RFwatts Time
RF on 300 msec
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the excitation within the critical slow conduction area participating in the reentry circuit, was reported to be a useful marker in guiding successful ablation. Currently, ablation is targeted to a site over the middle or inferoapical portion of the LV septum where the earliest PP and LDP are recorded (Fig. 24.8). Verification of these sites can be achieved with entrainment mapping demonstrating concealed fusion and progressive prolongation of the LDP-PP interval with increasing pacing rate. In addition, pressure applied to the catheter tip at the LDP region occasionally results in VT termination with conduction block between LDP and PP. Pace mapping can also be used as an adjunct to verify this site but, because of poor sensitivity, is less helpful than in focal VTs. It is important to recognize that successful ablation is not necessarily predicted by targeting the earliest (most proximal) LDP. Success can be achieved by ablating an LDP distal to the earliest potential (within the apical third of the septum). This approach is preferred to help reduce the risk of damaging the trunk of the LB. If such an LDP cannot be detected, the site with the earliest PP may then be targeted by ablation.1,6 One report showed a high success rate of an ablation strategy targeting the distal most fascicular potentials of the LPF, close to the Purkinjemyocardial interface, as guided by electroanatomic mapping of the left fascicular system. Ablation is extended progressively distal linearly to the surrounding myocardium until conduction block is achieved between the LV myocardium and the distal posterior fascicle/Purkinje network. At successful ablation sites, the fascicular potential typically preceded the local ventricular electrogram by an interval of 12 ± 1.7 milliseconds, which is less presystolic than the earliest PP targeted in other ablation
VT
strategies. Myocardium-fascicular conduction block during NSR was defined as the prolongation of the interval between the local ventricular electrogram and the fascicular/PP just proximal to the ablation site (duration of >100 milliseconds) or a higher degree of myocardiumfascicular block is recorded. Notably, this ablation approach did not result in LPF block or left axis deviation given the site of ablation being distal to LPF itself.14
Ablation Technique Ablation is usually performed through the retrograde transaortic approach using a standard 4-mm-tip catheter. The catheter is advanced by prolapsing into the LV and directed to the LV septum. Mapping is initially concentrated at the inferoapical septum. If an ideal site is not found in this area, the ablation catheter is moved upward to the midseptal area. It is important to move the catheter slowly and carefully to avoid mechanical trauma to the circuit. Endocardial activation mapping and entrainment mapping are performed to define the target site of ablation.1 Once the target site is identified, a test RF current is applied during VT for 20 seconds with an initial power of 20 to 35 W, targeting a temperature of 60°C. If the VT is terminated or slowed within 15 seconds, additional current is applied for another 60 to 120 seconds and power is increased up to 40 W to reach the target temperature if necessary. If the test RF current is ineffective despite adequate catheter contact, ablation is directed to another site after additional mapping, usually targeting a more proximal site with the earlier LDP. This approach helps to limit RF damage to the area of LPF and LB. Rarely, if ever, does one need
NSR
I II III
V1 V6 HRA Hisprox Hisdist RVA Abluni
Abldist Ablprox 300 msec
Fig. 24.8 Ablation of Fascicular Ventricular Tachycardia (VT). Shown are recordings during VT (left) and normal sinus rhythm (NSR; right) from a successful ablation site for idiopathic left ventricular tachycardia. Red arrows indicate probable Purkinje potentials, activated distal-to-proximal during VT and proximal-to-distal during sinus. Blue arrows show His potentials, occurring after QRS onset during VT. Abldist, Distal ablation; Ablprox, proximal ablation; Abluni, unipolar ablation; Hisdist, distal His bundle; Hisprox, proximal His bundle; HRA, high right atrium; RVA, right ventricular apex..
CHAPTER 24 Fascicular Ventricular Tachycardia more than 50 W or the use of irrigated or large-tip electrodes to ablate these VTs successfully.1 During the RF application, successful ablation sites often display progressive prolongation of the LDP-PP interval, with termination of VT coincident with conduction block between the two potentials. After successful ablation, the LDP can no longer be recorded during NSR.
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fascicular VT is vulnerable to mechanical injury because of catheter manipulation, which can render the tachycardia noninducible. In these cases, substrate mapping and ablation during NSR have been suggested to eradicate fascicular VT.1,8 Three approaches have been used for substrate-based ablation during sinus rhythm: (1) ablation of the slow conduction zone adjacent to the LPF; (2) anatomical linear ablation to transect the middle to distal portion of the LPF; and (3) ablation of the most distal LPF fibers at the Purkinje-myocardial interface.18 The first approach involves identifying areas of the slow conduction zone that is adjacent to the LPF, which might represent the anterograde limb of the VT reentry circuit. The location of this region is suggested by recording low-amplitude electrograms visible after the sinus QRS complex (presumably resulting from delayed retrograde activation of abnormal Purkinje fibers) in conjunction with more prominent PP (which is generated by anterograde conduction down the LPF). At these locations the low-amplitude signals occur 15 to 45 milliseconds after the PP, and the PP precedes the QRS onset by a relatively short interval (13 ± 8 milliseconds). A major limitation of this ablation strategy is the inability to identify the low-amplitude signals in a sizable proportion of patients. In addition, in another subset of patients, similar nonspecific low-amplitude signals are recorded over a sizeable area of the septum; targeting all those regions would increase the risk of injury to the conducting system.8 The second approach involves creation of an ablation line perpendicular to the activation direction of LPF and 1 cm above the sinus breakout point, as defined by electroanatomic or noncontact mapping during NSR (Fig. 24.9). The ablation line typically extends for approximately 2.0 ± 0. 4 cm in the region of the mid to midinferior LV septum and is guided by recording a small PP preceding the ventricular activation at its starting and ending points. A significant rightward shift of the QRS axis in the surface limb leads can be observed after the ablation procedure.16 The third approach involves targeting the distal most fascicular potentials of the LPF, close to the Purkinje-myocardial junction, as described previously. This approach can be used both for inducible or noninducible VT cases.14
Endpoints of Ablation Successful ablation is defined as the lack of inducibility of VT, with and without isoproterenol administration (using the best method for induction documented before ablation), at least 30 minutes after ablation. Importantly, creation of LPF block is not an effective endpoint for ablation and does not prevent arrhythmia recurrence.
Outcome The acute success rate is more than 90%, even when different mapping methods and ablation strategies are used. The recurrence rate is approximately 7% to 15%, with most recurrences occurring in the first 24 to 48 hours after the ablation procedure. Arrhythmia recurrences after an initially successful ablation are caused most commonly by recurrent fascicular VT involving the same fascicle and by new onset of upper septal VT in one third of patients. Of note, the development of new LPF block after fascicular VT ablation was associated with more basal ablations and did not protect against VT recurrence.6 Complications are rare and include different degrees of fascicular block (most likely because of inadvertent collateral damage to the LPF, particularly when ablation is delivered more basally), LBBB, cardiac tamponade, aortic regurgitation, and mitral regurgitation caused by torn chordae that may result from entrapment of the ablation catheter in a chorda of the mitral leaflet.17
Empirical Ablation of Noninducible Ventricular Tachycardia Conventional activation mapping, guided by either the earliest PP or the LDP, although effective, depends on the inducibility of sustained and hemodynamically stable fascicular VT. However, the VT may not be inducible in the EP laboratory. In addition, the critical substrate of
AV .LB
.Ant. .24
.25
.23 SBO .Sep. .APEX .Inf.
Fig. 24.9 Noncontact Mapping of Fascicular Ventricular Tachycardia During Normal Sinus Rhythm. A linear ablation lesion was created perpendicular to the wavefront propagation direction and 1 cm above the sinus breakout point (SBO). Both the starting and ending lesion points have a small Purkinje potential preceding the ventricular activation. Ant., Anterior; AV, His recording area; Inf., inferior; LB, left bundle branch; Sep., septal. (From Chen M, Yang B, Zou J, et al. Non-contact mapping and linear ablation of the left posterior fascicle during sinus rhythm in the treatment of idiopathic left ventricular tachycardia. Europace. 2005;7:138.)
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REFERENCES 1. Nogami A. Purkinje-related arrhythmias. J. Arrhythmia. 2011;27:6–27. 2. Scheinman MM. Role of the His-Purkinje system in the genesis of cardiac arrhythmia. Heart Rhythm. 2009;6:1050–1058. 3. Tsuchiya T, et al. Effects of verapamil and lidocaine on two components of the re-entry circuit of verapamil-senstitive idiopathic left ventricular tachycardia. J Am Coll Cardiol. 2001;37:1415–1421. 4. Talib AK, et al. Verapamil-sensitive upper septal idiopathic left ventricular tachycardia prevalence, mechanism, and electrophysiological characteristics. JACC Clin Electrophysiol. 2015;1:369–380. 5. Nogami A, et al. Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia. J Am Coll Cardiol. 2000;36:811–823. 6. Liu Y, et al. Catheter ablation of fascicular ventricular tachycardia: long-term clinical outcomes and mechanisms of recurrence. Circ Arrhythmia Electrophysiol. 2015;8:1443–1451. 7. Dobrzynski H, et al. Structure, function and clinical relevance of the cardiac conduction system, including the atrioventricular ring and outflow tract tissues. Pharmacol Ther. 2013;139:260–288. 8. Latchamsetty R, Bogun F. Fascicular tachycardia. Card Electrophysiol. Clin. 2014;6:567–579. 9. Collins KK, et al. Fascicular and nonfascicular left ventricular tachycardias in the young: an international multicenter study. J Cardiovasc Electrophysiol. 2013;24:640–648.
10. Al’Aref SJ, et al. Differentiation of papillary muscle from fascicular and mitral annular ventricular arrhythmias in patients with and without structural heart disease. Circ Arrhythmia Electrophysiol. 2015;8:616–624. 11. Sadek MM, et al. Idiopathic ventricular arrhythmias originating from the moderator band: electrocardiographic characteristics and treatment by catheter ablation. Heart Rhythm. 2015;12:67–75. 12. Sung RK, et al. Diagnosis and ablation of multiform fascicular tachycardia. J Cardiovasc Electrophysiol. 2013;24:297–304. 13. Ma W, et al. Mapping and ablation of ventricular tachycardia from the left upper fascicle: how to make the most of the fascicular potential? Circ Arrhythmia Electrophysiol. 2013;6:47–51. 14. Kataria V, Yaduvanshi A, Kumar M, et al. Demonstration of posterior fascicle to myocardial conduction block during ablation of idiopathic left ventricular tachycardia: an electrophysiological predictor of long-term success. Heart Rhythm. 2013;10:638–645. 15. Zhan XZ, et al. A new electrophysiologic observation in patients with idiopathic left ventricular tachycardia. Heart Rhythm. 2016;13:1460–1467. 16. Chen M, et al. Non-contact mapping and linear ablation of the left posterior fascicle during sinus rhythm in the treatment of idiopathic left ventricular tachycardia. Europace. 2005;7:138–144. 17. Li D, Guo J, Xu Y, et al. The surface electrocardiographic changes after radiofrequency catheter ablation in patients with idiopathic left ventricular tachycardia. Int J Clin Pract. 2004;58:11–18. 18. Chen H, et al. A novel method to identify the origin of ventricular tachycardia from the left fascicular system. Heart Rhythm. 2016;13: 686–694.