Ablation of Scar-Related Ventricular Tachycardia

VT CIRCUIT

The primary mechanism underlying scar-related VT is macroreentry. Ventricles scarred by disease (e.g., infarction) or surgery (e.g., repaired tetralogy of Fallot) contain islands of surviving myocyte bundles interspersed among electrically unexcitable scar (EUS) creating isthmuses or zones of slow conduction that facilitate reentrant excitation.¹,²,³,⁴ Integral to the VT reentrant circuit is this critical isthmus of slow conduction protected by anatomical and/or functional barriers and is the primary target site for ablation.¹

CIRCUIT MODEL

A two-dimensional model provides a working framework to guide ablation that centers around the critical isthmus (Fig. 20-1).²,⁴ At the proximal end of the isthmus is an excitable point of entry called the entrance site. At its distal end, the exit site provides continuity between the circuit and the rest of the ventricle. The circuit is completed by dominant inner or outer loops connecting both ends of the isthmus allowing reentry—one type of which is figure of 8 reentry (Fig. 20-2). The difference between inner and outer loops is that outer loops connect entrance and exit sites around the periphery of scar, while inner loops travel within the scar and are, therefore, electrically isolated. During VT, the isthmus is activated from entrance to exit after which the wavefront leaves the circuit to activate the ventricle. The VT morphology, therefore, reflects the location of the isthmus exit site. Adjacent bystander sites are blind channels or alleys within scar that are passively activated during tachycardia and not essential to the reentrant circuit. Remote bystanders are noncritical sites located outside the circuit. The isthmus is a critical component of the circuit and, therefore, the target site for ablation. Each circuit site is identified by specific entrainment mapping criteria.

In contrast to a simple two-dimensional working construct, actual VT circuits are complex, three-dimensional structures that can involve endocardial, mid-myocardial, and epicardial layers. The circuit for certain diseases (e.g., myocardial infarction) shows a predilection for the endocardium, while others (e.g., nonischemic cardiomyopathy, arrhythmogenic right ventricular [RV] cardiomyopathy, sarcoidosis) show a predilection for the mid-myocardium and epicardium.⁵ For infarct VT, the macroreentrant circuit can span several centimeters with the length of isthmuses averaging approximately 3 cm. Exit sites tend to be located at the infarct border zone (defined by voltages = 0.5 mV − 1.5 mV), while central isthmus and entrance sites are located within dense scar (<0.5 mV).⁶,⁷

12-LEAD ECG DURING VT

The 12-lead ECG provides the approximate location of the VT exit site.⁸ Because VT arises from the border zone of an infarct, Q waves are preserved during tachycardia and reflect both infarct location and exit site. The terminal QRS forces in lead V1 determine VT bundle branch block (BBB) morphology. Left bundle branch block (LBBB) VT (negative terminal forces in V1) identifies either a left septal or RV tachycardia. Right bundle branch block (RBBB) VT (positive terminal forces in V1) indicates a left ventricular (LV) tachycardia. VT with a superior axis arises from the inferior wall of the ventricle, while an inferior axis identifies an anterior or outflow tract origin. VT associated with inferior infarctions shows predilection for the LV base between the infarct border and the mitral annulus (submitral VT) with a zone of slow conduction running parallel to the mitral
annulus and showing two characteristic morphologies: LBBB/LS axis (septal exit) and RBBB/RS axis (lateral exit).⁹ Positive precordial concordance (all positive QRS complexes across the precordium) indicates a basal VT near the mitral valve. Negative precordial concordance (all negative QRS complexes across the precordium) identifies an apical VT (Figs. 20-3 and 20-4).

FIGURE 20-1 Figure of 8 (double loop) reentry. The protected isthmus is a region of slow conduction critical to the circuit. Proximal and distal isthmus sites are the entrance and exit, respectively. The exit site is the point where the activation wavefront leaves the circuit to depolarize the ventricles and, therefore, determines the VT morphology. Bystander sites are passively activated and not integral to tachycardia.

MAPPING AND ABLATION

Ventricular mapping can be performed either during VT (entrainment mapping) or sinus/paced rhythm (substrate-based ablation). Because the mechanism of scar-mediated VT is macroreentry, discrete electrograms can be recorded during the entire VT cycle length. The target of ablation is the critical isthmus: proximal (entrance), mid (central), and distal (exit) isthmus sites, which generate low-amplitude/fractionated early, mid-, and late diastolic potentials, respectively, during VT. While mid-diastolic potentials representing the central isthmus

are important to identify, they are not specific for the critical isthmus and can be recorded from adjacent bystander sites. Therefore, entrainment mapping coupled with activation mapping should be performed to determine the value of the recording site to the reentrant circuit.

FIGURE 20-2 Figure of 8 (double loop) reentry. A large inferior scar (gray tags) creates a critical isthmus of slow conduction allowing figure of 8 reentry. Early (red) meets late (purple) on the lateral and septal sides of the mitral annulus. Long, fragmented mid-diastolic potential (arrows) representing slow asynchronous activation is recorded from the isthmus (zigzag line) where radiofrequency (RF) energy terminated VT.

FIGURE 20-3 LV apical VT (negative precordial concordance). Electro-anatomic LV voltage map shows a large apical aneurysm with apical ballooning (arrowheads). Pacemapping within the aneurysm generates a long St-QRS interval and 12-lead ECG match to VT. Ablation lesions (red tags) are delivered to these sites and circumferentially around the border zone of the aneurysm. Gray tags denote EUS.

FIGURE 20-4 LV apical VT (negative precordial concordance). Electro-anatomic LV voltage map shows a large apical aneurysm. Pacemapping from the LV apex generates a long St-QRS interval with negative precordial concordance despite lack of a visible electrogram during sinus rhythm. Ablation lesions (red tags) are delivered to this site and throughout the aneurysm. Gray tags denote EUS, and black tags denote late potentials (LPs).

ENTRAINMENT MAPPING

Entrainment mapping is a valuable pacing maneuver that identifies functional components of the tachycardia circuit and differentiates them from bystander sites (Fig. 20-5).¹⁰,¹¹,¹²,¹³ During VT, pacing stimuli are delivered at a cycle length 10-20 ms shorter than the VT cycle length. It is imperative to confirm that pacing stimuli truly capture the ventricle and accelerate VT to the pacing cycle length (Fig. 20-6). Stimuli penetrating the circuit and entraining tachycardia give rise to orthodromic and antidromic wavefronts. The antidromic wavefront of the first stimulus collides with tachycardia, while its orthodromic counterpart advances the circuit. With continuation of pacing, the orthodromic wavefront of each pacing stimulus (n) advances the tachycardia and collides with the antidromic wavefront of the subsequent (n + 1) stimulus (continuous resetting). When pacing stops, the last orthodromic wavefront has no antidromic wavefront with which to collide and completes one revolution around the circuit, and tachycardia continues.

FIGURE 20-5 Diagram illustrating the six different entrainment sites. Entrance site stimulation shows concealed fusion, long St-QRS = egm-QRS, and PPI = TCL. Exit site stimulation produces concealed fusion, short St-QRS = egm-QRS, and PPI = TCL. Outer loop site stimulation causes manifest fusion but PPI = TCL. Inner loop site stimulation shows concealed fusion, very long St-QRS = egm-QRS, and PPI = TCL. Adjacent bystander site stimulation generates concealed fusion, long St-QRS ≠ egm-QRS, and PPI ≠ TCL. (The St-QRS [a + b] > egm-QRS intervals [b − a] and the PPI = TCL + 2a provided that the conduction times in and out of the bystander pathway are equal. The letter a denotes bystander pathway conduction time, and b denotes conduction time from junction between bystander and isthmus to exit site.) Remote bystander site stimulation shows manifest fusion and PPI ≠ TCL. (The PPI = VTCL + 2c provided that the conduction times to and from the circuit are equal. The letter c denotes conduction time between pacing site and circuit.)

Entrainment Criteria

Three criteria define each mapped site relative to the circuit: 1) paced QRS relative to tachycardia QRS morphology, 2) stimulus (St)-QRS relative to electrogram (egm)-QRS interval, and 3) post-pacing interval (PPI) relative to tachycardia cycle length (TCL). The St-QRS − egm-QRS and PPI-TCL are complementary to each other.

Concealed versus Manifest Fusion

Entrainment from isthmus (entrance, central, and exit), inner loop, and adjacent bystander sites activates the ventricle from the isthmus exit site so that paced QRS morphologies are identical to tachycardia (entrainment with concealed fusion) (Figs. 20-7, 20-8, 20-9, 20-10, 20-11, 20-12, 20-13, 20-14, 20-15 and 20-16). Collision between orthodromic and antidromic wavefronts occurs “upstream” to the pacing site within the circuit resulting in local fusion that is undetectable on the
12-lead ECG (hence, the term “concealed”). Entrainment from outer loop and remote bystander sites produces paced QRS morphologies different from tachycardia (entrainment with manifest fusion) (Figs. 20-17, 20-18, 20-19 and 20-20).

FIGURE 20-6 Pseudo-entrainment (noncapture). At first glance, it appears that the ventricle is entrained with concealed fusion, St-QRS (33% TCL) − egm-QRS = 101 ms, and PPI − TCL = 100 ms suggesting an adjacent bystander site. Close inspection, however, reveals that pacing stimuli fail to capture the ventricle (prolonging St-QRS intervals). Asterisks denote far-field electrograms. Arrows denote the putative near-field electrograms.

St-QRS versus egm-QRS Interval

The St-QRS interval is measured from the pacing artifact to onset of the QRS complex. Entrance, central, and exit site stimulation produce long (51-70% VTCL), intermediate (31-50% VTCL), and short (≤30% VTCL) St-QRS intervals, respectively (Figs. 20-7, 20-8, 20-9, 20-10, 20-11, 20-12 and 20-13). Because the inner loop is within scar proximal to the critical isthmus, stimulation from this site generates very long St-QRS intervals (>70% VTCL) (Fig. 20-14). The St-QRS intervals for outer loop and remote bystander sites are generally short because myocardial tissue outside the circuit is directly depolarized by the pacing stimulus unless stimulation occurs within remote scar (Figs. 20-17, 20-18, 20-19 and 20-20). In contrast, the St-QRS intervals for adjacent bystander sites are typically long and equals the conduction time over the bystander pathway plus the conduction time from its junction with the isthmus to the exit site (Figs. 20-15 and 20-16).

The egm-QRS interval represents the activation time from the mapping site to onset of the QRS complex. It is very long for inner loop sites and becomes progressively shorter as the mapping catheter heads toward entrance, central, and exit sites. Electrograms from the isthmus are typically low amplitude; fractionated; and occur during early (entrance), mid (central), or late (“presystolic”) (exit) diastole.¹⁴ Diastolic electrograms are not isthmus specific and can be recorded from bystander sites. Therefore, the egm-QRS relative to St-QRS intervals differentiates isthmus from bystander sites. Isthmus (entrance to exit) and dominant inner loop sites demonstrate matching St-QRS and egm-QRS intervals (≤20 ms) because they are participants in the reentrant circuit, while bystander sites (adjacent, remote) do not (>20 ms). The St-QRS interval for an adjacent bystander site is the conduction time out of the bystander pathway plus the conduction time from its junction with the isthmus to the exit site, while the egm-QRS interval is the difference between them. The St-QRS interval for a remote bystander site is generally 0 (unless in noncircuit scar) and does not match the corresponding egm-QRS interval, which is the conduction time from the exit to the remote bystander site. The St-QRS and egm-QRS intervals for outer loop sites depend on pacing location relative to the exit site and also generally do not match unless near the exit (“exit zone”).

Post-pacing Interval-Tachycardia Cycle Length

The PPI is measured from the last pacing stimulus to the onset of the first spontaneous near-field electrogram recorded on

the mapping catheter. This near-field electrogram of interest is differentiated from far-field electrograms by its disappearance during pacing due to direct local capture at the stimulation site.¹³ Far-field electrograms remain visible during entrainment and separate from the pacing stimulus. Analysis of orthodromically captured electrograms from neighboring dipoles (e.g., Abl px) can provide additional confirmation. Because the revolution time around the circuit equals the TCL, entrainment from a site within the circuit (isthmus, dominant inner and outer loop) results in PPI − TCL ≤30 ms. Entrainment from bystander sites (adjacent, remote) produces PPI − TCL >30 ms. The PPI for an adjacent bystander site is the conduction time out of the bystander pathway, once around the circuit, and back to the bystander pathway. Assuming that conduction times in and out of the pathway are equal, the PPI = TCL + 2 (bystander pathway conduction time). The PPI for a remote bystander site is the conduction time from pacing site to the circuit, once around the circuit, and back again to the pacing site. Assuming that the conduction times to and from the circuit are equal, the PPI = TCL + 2 (conduction time between pacing site and circuit). The PPI can be unexpectedly short if 1) high pacing output captures distant tissue (large virtual electrode), 2) entrainment momentarily accelerates VT, 3) pacing “short circuits” the actual circuit (e.g., transient conduction around a smaller nondominant inner loop), or 4) the near-field electrogram is orthodromically (not directly) captured (far-field ventricular capture outside the circuit penetrates and orthodromically entrains the near-field electrogram inside the circuit in which case it occurs at the pacing cycle length).¹⁵

FIGURE 20-7 Exit site. Paced and VT complexes are identical (concealed fusion). The St-QRS (25% TCL) − egm-QRS = 3 ms. The PPI − TCL = 15 ms. Radiofrequency (RF) delivery terminates tachycardia in 11.1 sec.

FIGURE 20-8 Exit site. Paced and VT complexes are identical (concealed fusion). The St-QRS (21% TCL) − egm-QRS = 1 ms. The PPI − TCL = 3 ms. Radiofrequency (RF) delivery terminates tachycardia in 0.8 sec. The ablation catheter records a split potential—the first component (asterisks) of which is not captured by pacing stimuli and, therefore, not used for PPI measurement. The second component (arrows) is the near-field electrogram of interest and also seen as a LP during ventricular paced rhythm.

FIGURE 20-9 Exit site. Paced and VT complexes are identical (concealed fusion). The St-QRS (22% TCL) − egm-QRS = 0 ms. The PPI − TCL = 2 ms. Radiofrequency (RF) delivery terminates tachycardia.

FIGURE 20-10 Central isthmus site. Paced and VT complexes are identical (concealed fusion) with subtle beat-tobeat alternation in QRS morphology (a form of multiple exit site (MES) stimulation (see below)). The St-QRS interval (48% TCL) − egm-QRS interval = 4 ms. The PPI − TCL = 17 ms. Application of radiofrequency (RF) energy terminates tachycardia in 3.1 sec. Asterisks denote far-field ventricular potentials not captured by pacing. Arrows denote the near-field electrograms of interest.

FIGURE 20-11 Central isthmus site. Paced and VT complexes are identical (concealed fusion). The St-QRS interval (39% TCL) − egm-QRS interval = 10 ms. The PPI − TCL = 10 ms. Application of radiofrequency (RF) energy terminates tachycardia in 9.2 sec.

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