Re-entry

Histologic changes in the myocardium and the HPS (scar, calcification, patchy fibrosis, surgical incisions) or functional changes without overt structural heart disease may alter myocardial conduction to permit wavefront propagation along a continuously excitable path such that re-entrant activation may produce tachycardia if the time for a single complete revolution is greater than the longest refractory period in the circuit. The normal fibrous skeleton of the heart may also play a role in promoting re-entry by providing anatomic barriers (e.g., valve annuli) that not only create conduction block but, when in proximity to such altered myocardium, also create corridors of conduction that confine the propagating wavefront, slow impulse conduction, and restrict the direction of wavefront propagation, again facilitating re-entry.

Theoretical Basis for Re-entrant Circuits Associated with Myocardial Scarring

The majority of VTs associated with myocardial scarring arise from re-entrant circuits involving the interface between the normal myocardium and the abnormal myocardium. Initial in vivo evidence for re-entry came from epicardial recordings in dogs 3 to 7 days following acute infarction. El-Sherif and colleagues recorded electrical activity over infarcted tissue bridging the diastolic interval between consecutive VT beats, providing compelling evidence for re-entry.¹³ The clinical relevance of re-entry was subsequently confirmed by intraoperative mapping studies of human VT, using high-density endocardial electrode arrays.¹⁴

Stevenson and coworkers proposed a theoretical model that clarified the components of VT re-entrant circuits and provided a useful framework to analyze the appropriateness of ablation targets (Figure 95-2). In their model, re-entrant circuits contain a region of slow conduction, representing activation of a relatively small mass of ventricular tissue, critical to the initiation and propagation of tachycardia.¹⁵ Mapping studies in canine models and in humans have suggested that these slowly conducting components are often localized to narrow isthmi, isolated from the adjacent myocardium by arcs of anatomic or functional block and that during VT, impulse propagation through these regions occurs in diastole.^16,17 In fact, Wilber and associates demonstrated that in 4 of 12 patients with VT and prior inferior wall infarction, the isthmus defined by the mitral valve annulus and infarct served as a region of slow conduction critical to the re-entrant circuit.¹⁸ Because these isthmi of slow conduction are anatomically narrow and physiologically essential to re-entry, they provide attractive targets for ablation.

FIGURE 95-2 Theoretic re-entrant circuits developing in a post-infarction model. The re-entry circuit is indicated by the black arrows, while open arrows indicate excitation wavefronts leaving the circuit and depolarizing tissue not in the circuit or scar (red regions). A, Circuit that contains two outer loops and a central common pathway (CP) or isthmus of slow conduction creating a figure-of-8 re-entry configuration. The QRS is inscribed when the excitation wavefront leaves the common isthmus through the exit and then proceeds along the outer loop. The excitation wavefronts then re-enter the infarct region at the proximal portion of the common isthmus. Regions that are passively activated but do not participate in the tachycardia circuit are labeled as bystanders (Bys). B, The circuit is contained entirely within the chronic infarct. This circuit consists of an exit and central, proximal, and inner loop regions. C, Single outer loop circuit, in which the excitation wavefront circulates around the margins and in the paths within the chronic infarct (bystanders).

(From Stevenson WG, Friedman PL, Sager PT, et al: Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping, J Am Coll Cardiol 29:1180, 1997.)

When the excitation wavefront emerges from a region of slow conduction to depolarize the remainder of the myocardium at a site designated by Stevenson’s model as the “exit,” the QRS complex is inscribed on the surface electrocardiogram (ECG). Subsequently, the re-entrant wavefront may propagate through normal tissue along the border of the scar (outer loop), through the infarct region (inner loop), or through excitable tissue within the infarct not essential to the circuit (bystander), eventually returning to the proximal segment of the central isthmus of slow conduction.

Re-entrant circuits may be complex. Downar and colleagues observed that strands of surviving myocardial fibers within infarct zones comprise the region of slow conduction required for re-entry and may use alternative entry and exit points during tachycardia.^19,20 The multiplicity of potential re-entrant pathways that result may produce spontaneous changes in the tachycardia cycle length and VT morphology. Moreover, the lack of a single defined exit point suggests that exit sites are poor ablation targets.

Triggers

Triggered activity refers to induced ionic flow across myocyte membranes that stimulate action potential formation linked to, or triggered by, a preceding action potential. This nonstimulated response is referred to as “after-depolarization,” which may occur during (phase II or III) or after (phase IV) the action potential, termed early after-depolarization (EAD) and delayed after-depolarization (DAD), respectively. VT may result from a single after-depolarization that initiates re-entry or from repetitive after-depolarizations that maintain the tachycardia.

Repetitive DADs from the ventricular outflow tracts and associated structures manifest as outflow tract VTs and premature ventricular contractions (PVCs). The focal nature of these tachycardias makes them ideal for study and catheter ablation. Programmed stimulation with rapid pacing or administration of catecholamines is often required for induction and provides a suitable endpoint following ablation. Recognition of the susceptibility of triggered activity to menstrual phases facilitates optimal scheduling for EPS and ablation. VT related to digitalis toxicity also occurs because of DADs but is not an indication for catheter ablation.

EADs contribute to the development of polymorphic VT in the setting of increased transmural dispersion of repolarization (e.g., short QT syndrome [SQTS], long QT syndrome [LQTS], Brugada syndrome). These VTs generally do not lend themselves to study because initiation is often related to secondary factors such as bradycardia, electrolyte derangement, or stress; maintenance is not limited to critical structures but rather may involve the entire biventricular myocardium, providing no specific anatomic or physiological targets for ablation. Further, ablation does not address underlying predisposition to VT.

Clinical Assessment of Myocardial Scarring and Other Considerations

As part of the clinical evaluation of VT, an assessment for structural heart disease is a prerequisite. Identifying the sites of healthy and scarred myocardium is paramount, recognizing that islands of scar tissue may reside within viable myocardium, and islands of viable myocardium may reside within areas of scar tissue.²¹ Coronary stenoses should be identified to predict scar distribution, though scarring may not correlate with regions subtended by coronary arteries if the process is, in fact, idiopathic, dysplastic, or infiltrative. Also, true infarcts may vary in severity in relation to collateral circulation, involvement of watersheds, and availability of dual blood supply, impacting the size, distribution, and transmurality of scar tissue as well as the development of Q waves as seen on ECG. Scarring may be related to prior surgery such as repair of congenital heart disease (CHD) or valvular surgery. In addition, bipolar voltage mapping may not accurately delineate the extent of myocardial scarring, not only because of sampling error but also because anatomically scarred myocardium with overlying hypertrophy, for instance, may be identified as electrically normal.²¹

Intracardiac thrombi should be definitively excluded. Antiarrhythmics should be discontinued or converted to short-acting intravenous (IV) preparations to be discontinued before the EPS, unless these agents slow VT to the point of hemodynamic tolerance that facilitates mapping. Finally, it must be kept in mind that the VT may be epicardial in origin, requiring a pericardial approach that may be hindered in the presence of prior cardiac, thoracic, or abdominal surgery with resultant adhesions within the intended approach trajectory and tissue planes.

Electrocardiogram in Sinus Rhythm and in Ventricular Tachycardia

The approach to VT ablation begins with analysis of a 12-lead ECG obtained during sinus rhythm and in tachycardia. The sinus rhythm ECG is useful in identifying the presence of structural heart disease, particularly (1) prior myocardial infarction (MI) suggested by Q waves, (2) scarring suggested by low-voltage and wide “splintered” QRS morphology arising from delayed and meandering cell-to-cell myocardial conduction, (3) HPS disease suggested by fascicular blocks and increased QRS duration, and (4) alteration in structural geometry with aneurysm formation suggested by persistent ST-segment elevation in the region of a prior MI. An entirely normal ECG is also important as it may suggest an idiopathic type of VT, though structural heart disease must still be excluded. All of these observations aid in anticipating the underlying tachycardia mechanism and provide clues to sites of involvement.²²

When telemetry is available, evaluation of VT onset may provide insight into the mode of initiation, especially if PVCs with a particular morphology initiate the VT, making them important targets for ablation. In the absence of a 12-lead ECG rhythm of VT strips are useful in determining the cycle length (CL) and approximate morphology for comparison with tachycardias induced in the electrophysiology suite to confirm clinical relevance. In patients with implanted rhythm monitors, including permanent pacemakers (PPM) and ICDs, if no recordings are available to assess the morphology for localization, the device may be programmed to detect, but not deliver, therapy once in the electrophysiology suite. The electrograms from VTs induced during EPS may be compared with device recordings of spontaneous VTs. Similarities between electrograms and CL suggest induction of clinical tachycardia, which may then be localized on the basis of 12-lead ECG of VTs recorded during the study.

Electrocardiogram Features Suggesting Epicardial Origin of Ventricular Tachycardia

The normal sequence of myocardial depolarization initiates endocardially within the specialized conduction system and rapidly activates a relatively large amount of myocardium, accounting for a steep intrinsicoid deflection. The spread of activation in VT of endocardial origin is related to cell-to-cell transmission with eventual HPS activation, delaying the intrinsicoid deflection. Depolarization that originates in the epicardium must activate the myocardium through cell-to-cell transmission alone without HPS contribution, further slowing QRS inscription and accounting for the “pseudo–δ-wave” pattern often seen. In VT of right bundle branch block (RBBB) morphology that is successfully ablated at the epicardium as well as during LV epicardial pacing, a duration of pseudo–δ-wave 34 ms or longer and intrinsicoid deflection in V2 of 85 ms or greater is highly sensitive (83% and 87%, respectively) and specific (95% and 90%, respectively) for identifying an epicardial origin. Similarly, QRS width is also related to the contribution of the HPS to global LV activation, though QRS width alone may not discriminate epicardial sites from endocardial sites because myriad factors affect ventricular conduction and activation.²³ However, the overall contribution of intrinsicoid deflection to absolute QRS width is greater for the epicardially activated ventricular depolarization than for the endocardially activated ventricular depolarization.²⁴ A delayed precordial maximum deflection index (MDI, intrinsicoid deflection/QRS width) 0.55 or greater identifies epicardial VT with 100% sensitivity and 98.7% specificity, with best discrimination according to MDI in lead V2 (Figure 95-3).²⁴

FIGURE 95-3 Assessment of the precordial maximum deflection index (MDI). A, The MDI is given by the earliest time to maximum deflection (TMD) in any precordial leads (in this example, lead V3) divided by total QRS duration (QRSd). B, Distribution of precordial MDI values in patients with various types of idiopathic ventricular tachycardia (VT). With a cut-point of 0.55, there is excellent discrimination between epicardial (EPI) VT and endocardial (ENDO) and aortic sinus of Valsalva (ASOV) VTs. LV, Left ventricle; RV, right ventricle.

(From Daniels DV, Lu YY, Morton JB, et al: Idiopathic epicardial left ventricular tachycardia originating remote from the sinus of Valsalva: Electrophysiological characteristics, catheter ablation, and identification from the 12-lead electrogram, Circulation 113:1659, 2006.)

It is important to appreciate that the role of ECG in the approach to VT ablation is to estimate sites of involvement and that the ECG may vary with scar burden and distribution, use of antiarrhythmic agents, and the variable position of the heart within the thorax, either as normal variant or because of intrathoracic pathology causing mediastinal shifting.

The Mapping System

The contemporary approach to VT ablation involves three-dimensional electroanatomic mapping for (1) the creation of a virtual ventricular geometry, (2) the evaluation of the presence of scar tissue and macro–re-entrant circuits, (3) activation sequence assessment, (4) facilitation of the return of the catheter tip to specific targets that may be physiologically important (e.g., for entrainment and pacemapping, and assessment of local electrograms), and (5) labeling of the sites of ablation with respect to chamber geometry and delivery of contiguous ablation lesions. Current mapping systems provide nonfluoroscopic navigation capabilities to permit detailed substrate mapping and analysis without excessive radiation exposure. In VTs involving the HPS, mapping systems may not be required as the bundle branch, fascicular, and Purkinje potentials may be mapped directly.

Vascular Catheterization

Vascular access is required for the placement of at least one diagnostic electrode catheter to deliver programmed stimulation, generally from the right ventricle. Additional access may be required for atrial programmed stimulation to entrain fascicular re-entrant VTs, to record the His and bundle branch potentials in idiopathic and bundle branch re-entry VTs, to permit coronary sinus cannulation as a guide to epicardial origin, and to introduce an inferior vena cava (IVC) catheter to serve as a reference for unipolar recordings. Additional femoral venous access may be required for intracardiac echocardiography (ICE), which is useful in guiding trans-septal puncture, identifying aneurysms, demonstrating endocardial catheter contact, and observing for thrombus formation. And, of course, one femoral access is required for the introduction of the mapping or ablation catheter into the presumed chamber of VT origin; this may be venous if the right ventricle is being mapped or if the trans-septal approach is used to map the left ventricle and arterial if a direct retrograde trans-aortic approach is used.

A dedicated arterial line should be placed for close hemodynamic monitoring. If the retrograde aortic approach is employed, the arterial line may be foregone, and the side port of the vascular sheath transduced; however, unless the sheath is 1 Fr size larger than the ablation catheter, the signal may be dampened with insertion of the ablation or mapping catheter, producing spuriously low pressure recordings. After all the vascular access has been obtained, anticoagulation with bolus heparinization, with or without repeat bolus dosing or continuous infusion, should be administered for prophylaxis against thrombus formation, particularly if left intracardiac chambers will be entered.

Approach to the Left Ventricle

No systematic studies have compared the trans-septal approach with the retrograde transaortic approach in VT ablation; however, a few generalizations may be made. The aortic approach, which is simpler and requires no additional hardware, is the preferred first-line method of access to the left ventricle. Aortic catheter advancement should be performed delicately to avoid damaging or engaging and occluding the coronaries and damaging the aortic valve. In patients with severe aortic atherosclerosis, the risk of atheroemboli as well as traumatic intramural hematoma or frank dissection may be increased. The natural curvature of the catheter as it enters the left ventricle facilitates approaching the posterior wall because of the posteromedial relation of the left ventricular outflow tract (LVOT) to the aortic root. The retrograde aortic approach may rarely limit access to the basal anterolateral wall in very tall or large patients, particularly if smaller curve mapping or ablation catheters are used. The decision to use the retrograde trans-aortic approach should be reconsidered in patients with severe peripheral arterial disease and is contraindicated in patients with mechanical aortic valve prostheses and arterial conduits at the femoral puncture site.

In contrast, the trans-septal approach affords access to the left ventricle in these very patients. The orientation of the catheter may facilitate approaching the septal left ventricle, as the catheter tends to follow the natural curve of the trans-septal sheath. Further, it may provide extended catheter availability to reach the anterolateral left ventricle. The trans-septal approach provides additional stability and may be less arrhythmogenic with respect to the mechanical induction or suppression of VT but requires specific expertise, more hardware, and possibly additional personnel, which prolongs and complicates the procedure.²⁵ Finally, the trans-septal approach is contraindicated in patients with mechanical mitral valve prostheses and may be challenging if closure of an atrial septal defect (ASD) or a patent foramen ovale (PFO) has been performed.

In patients with mechanical aortic and mitral prostheses or other contraindications to both vascular approaches to the left ventricle, an epicardial approach may be considered.

Technique of Pericardial Access

Epicardial ablation may be required in specific instances such as with an ECG suggestive of epicardial origin, failed endocardial ablation, or contraindications to endocardial ablation (for example, presence of mechanical aortic and mitral prostheses, or LV thrombus). Further, it should be considered for patients with nonischemic cardiomyopathy or Chagas’ disease, in which epicardial VTs occur with higher frequency.

Pericardial access, as described by Sosa et al, is obtained under fluoroscopic guidance by advancing an epidural needle or pericardiocentesis needle at 30- to 45-degree angulation toward the scapula while maintaining negative pressure with the plunger of a syringe containing x-ray contrast.²⁶ As the needle tip approaches the cardiac silhouette, the contrast medium is repetitively “puffed,” and will be observed to stain the extracardiac space and structures until the pericardium is breached. Contrast instillation within the pericardial space will layer and outline the cardiac silhouette. Myocardial contact may demonstrate ECG evidence of the injury current, and ventricular penetration will yield bloody aspirate. In the case of right ventricular puncture, usually simple withdrawal of the needle will suffice; the myocardial wall at the site of the puncture will generally collapse and occlude the puncture site, though close observation for hemodynamic compromise is always prudent. In the case of LV puncture, more aggressive management and serial echocardiography to exclude growing pericardial effusion may be required, even in the absence of initially compromised hemodynamics.

When the contrast medium layers along the cardiac silhouette, signifying the position of the needle tip within the pericardial space, a guidewire is advanced far in to maintain pericardial access, observing for a course along the cardiac silhouette or over the cardiac surface and contained by the pericardium and its reflections and not an intracavitary course. A retaining sheath is then advanced over the guidewire to permit introduction and manipulation of the mapping/ablation catheter within the pericardial space (Figure 95-4). If open-irrigated ablation is desired, care must be taken to periodically drain the irrigant or permit continuous drainage via the side port. After the procedure, all intrapericardial hardware must be removed; no specific closure devices are required. A short course of oral nonsteroidal anti-inflammatory drugs, colchicine, or steroids may be prescribed to prevent reactive pericardial inflammation in response to the instilled contrast.

FIGURE 95-4 A, Technique utilized to perform sub-xyphoid approach. A regular Tuohy needle (upper left, inset) is used to reach the pericardial space. B, Left anterior oblique (LAO) image position showing the exact moment when the contrast medium is layering the heart silhouette. C, Guidewire around the heart silhouette correctly positioned inside the pericardial space. D and E, LAO images of catheter into the pericardial space. CS, Coronary sinus; RV, right ventricular.

(From Sosa E, Scanavacca M: Epicardial mapping and ablation techniques to control ventricular tachycardia, J Cardiovasc Electrophysiol 16:449, 2005.)

If a history of prior cardiac surgery, myocarditis, or prior pericardial instrumentation for any reason exists, pericardial adhesions may hinder smooth pericardial access. In such instances, surgical dissection in the electrophysiology suite may be required.

Epicardial ablation should not be performed without prior knowledge of the location and distribution of the coronaries. Intraoperative intermittent coronary angiography may be required to visualize ostia or segments that are proximal to the ablation sites; more than 0.5 to 1 cm is considered a safe intervening distance between the closest coronary segment and ablation catheter tip. An alternative is to perform preoperative coronary angiography in the electrophysiology suite using views predetermined to be those used for ablation, which permits comparison of anticipated ablation sites and coronary distribution on stored angiographic views; however, only simultaneous visualization of the coronaries during RF delivery can exclude intraprocedural coronary injury.

Irrigated Radiofrequency Delivery: Clinical Considerations in Ventricular Tachycardia Ablation

While the evolution of ablation catheter technology has seen much progress, a particularly significant advance with respect to VT ablation has been the development of irrigation methods to cool the catheter tip, avoiding excessive heating at the tissue-electrode interface, and preventing coagulum and char formation but improving energy delivery deep within tissue.

Clinical experience with irrigated RF ablation has demonstrated its benefit in VT resistant to ablation with nonirrigated catheters.²⁷ Of relevance is the fact that the lesions are large and may penetrate scar tissue and effectively ablate surviving myocyte bundles deep to the regions of fibrosis.²⁸ However, in patients with structural heart disease, particularly LV or right ventricular dysfunction, congestive failure may develop because of excessive volume overload from mismatch of irrigant volume and urine output. In contrast, inadequate irrigant flow rate may fail to prevent char or coagulum formation, thereby preventing effective ablation because of increased impedance and increasing risk of thromboembolism. In addition, intramural boiling can lead to eruption of steam through the myocardial wall, also known as steam pops, with a potential for cardiac perforation.

In the first report on internally cooled RF ablation in humans with VT related to structural heart disease, cerebrovascular events and cardiac tamponade occurred more frequently than in the Multicenter European Radiofrequency Survey (MERFS) and the North American Society of Pacing and Electrophysiology (NASPE) survey, though differences in study design and study population may have been contributing factors. The mortality rate related to heart failure was no different from the reported procedure-related mortality rate (2.7%). The overall mortality at 1 year in this cohort was 25%, with 73% related to heart failure, and the majority sustaining recurrent VT.²⁹

In a multicenter prospective study of patients with VT associated with prior MI undergoing open-irrigated RF ablation, a similar major complication (10%) and procedure-related mortality rates (3%) were reported. The overall mortality at 1 year in this cohort was 18%, with 79% of those deaths attributed to recurrent VT. Of note, no clinically evident thromboembolism occurred, and better flow and electrode surface cooling afforded by open-irrigation systems were offered as explanations.^30,31

While irrigated RF ablation potentially improves lesion transmurality, this may not be necessary and may increase risk of perforation in patients with structurally normal hearts, requiring ablation of overlying thin myocardial walls (e.g., right ventricular outflow tract [RVOT]).

Ventricular Tachycardia Caused by Myocardial Scarring

The most common pathophysiology underlying VT is re-entry caused by myocardial scarring, with post-MI VT representing the most prevalent and most clinically significant form. As re-entrant arrhythmias lend themselves to study, re-entrant VT in the setting of ischemic heart disease is the most common form of VT targeted with contemporary ablation techniques.

Electrocardiography in Ventricular Tachycardia Associated with Prior Myocardial Infarction

A standard 12-lead ECG recorded during VT provides an important tool to localize the myocardial exit site and aids in procedure planning to limit the amount of the myocardium that is mapped. While VT localization in the setting of prior MI has its limitations, the methods of Miller et al afford some localization based on the region of prior infarction, QRS morphology in V1 (left bundle branch block [LBBB] or RBBB), pattern of R-wave progression (RWP), and QRS axis.³² In patients with inferior infarction, these authors found LBBB VT with left superior axis and progressive RWP mapped in most cases to the inferobasal septum. RBBB VTs with a superior axis generally arose from the inferobasal free wall, whereas a leftward axis suggested a more medial exit. RBBB VTs with a right inferior axis usually originated from the inferolateral free wall. In patients with anterior infarction, LBBB VTs with a left superior axis were associated with an inferoapical septal exit, whereas VTs with an inferior axis mapped to the anteroapical septum, though RBBB VTs with a right inferior axis also exited from the anteroapical septum. In general, the site of myocardial exit in LBBB VTs was largely confined to the interventricular septum, and VTs associated with inferior infarction commonly exited from the inferobasal left ventricle.

Disregarding the site of prior infarction, Segal et al found that all LBBB VTs arose from the mid- and basal-interventricular septum, whereas RBBB VTs arose away from the septum; RBBB VTs with a superior axis arose posteriorly, and RBBB VTs with an inferior axis arose apically, or anteriorly from the mid- and basal-interventricular septum.³³

Overall, the findings from these studies are concordant and generalize VT exit site localization in structural heart disease along the septal-lateral and anterior-inferior axes: LBBB VTs exit septally or rarely from the right ventricle, whereas RBBB VTs may exit septally or away from the septum in the left ventricle. VTs with an inferior axis exit anteriorly, whereas VTs with a superior axis exit inferiorly or posteriorly.

Pacemapping studies also confirmed these findings and further refined VT localization by contributing the third axis—apical-basal—in which dominant precordial R waves (V1-V5) suggest a more basal exit, dominant R in V3 and V4 suggest an exit between apex and base, and dominant precordial S waves suggest an apical exit (Figure 95-5).³⁴

FIGURE 95-5 Depiction of anticipated ventricular tachycardia (VT) exit site based on 12-lead electrocardiogram morphology. Cut planes divide heart schematic into 12 segments: septal versus lateral segments; basal, mid, and apical segments; and anterior versus posterior or inferior segments. Bundle branch block morphology in lead V1 suggests a septal (LBBB or RBBB) versus lateral (RBBB) exit site. Note that the RBBB-type morphology may arise from septal and lateral segments but may be distinguished by morphology in lead I (and aV_L). VT QRS axis as determined by inferior leads indicates anterior (inferior axis) versus inferior (superior axis) exit sites. Precordial R-wave transition or progression can be highly variable but suggests basal-to-apical axis exit site, with more basal sites manifesting predominant R-wave pattern in patients with RBBB VT and progressive R-wave increase in patients with LBBB VT. Apical sites manifest dominant QS or S-wave pattern in patients with LBBB VT, whereas patients with RBBB VT develop dominant S waves and transition pattern intermediate between apical and basal pattern for mid-left ventricular exit sites. ANT, Anterior wall; LBBB, left bundle branch block; POST/INF, posterior/inferior wall; RBBB, right bundle branch block; SEPT, left ventricular septum (lateral wall not labeled).

Remote Inferior Infarction: A Paradigm for Ablation of Scar-Related Ventricular Tachycardia

The basal inferior or posterior wall receives dual circulation from the distal left circumflex (LCX) and from the proximal right posterolateral branch and the atrioventricular (AV) groove branches of the right coronary artery; this often spares this myocardial territory in the setting of inferior infarction, whether from right or left coronary occlusion. This creates an isthmus of viable tissue between the superior border of an inferior wall scar and the posterior mitral annulus.

As described previously, VT in the setting of remote inferior infarction may be associated with both LBBB VTs with a left superior axis and RBBB VTs with a right superior axis, suggesting propagation within the same circuit around the scar but in opposite directions, with an inferobasal septal exit and an inferobasal lateral exit, respectively. From the surgical experience, successful ablation of VT after remote inferior infarction often included cryolesion delivery within this isthmus of surviving myocardium between the mitral valve annulus and the infarct border.³⁵

Wilber et al examined the frequency at which slow conduction within this mitral isthmus was critical to the maintenance of VT associated with remote inferior infarction in patients undergoing catheter ablation.³⁶ Two morphologies of VT were inducible in their patients—LBBB left superior axis and RBBB right superior axis (Figure 95-6). They observed that single RF energy applications across the mitral isthmus eliminated the inducibility of both morphologies of VT without recurrence over 1 to 11 months of follow-up.

FIGURE 95-6 Schema of mitral isthmus ventricular tachycardia (VT) related to remote inferior myocardial infarction. VTs using the band of tissue between the superior border of an inferior scar (red region) and the mitral annulus may have two different QRS morphologies related to the direction of propagation through this isthmus. Both VT morphologies were successfully eliminated with ablation within the mitral isthmus (four patients studied and the location of their ablation delivery shown with numbered blue squares). RBBB-RAD, Right bundle, right-axis deviation; LBBB-LAD, left bundle, left-axis deviation.

(From Wilber DJ, Kopp ED, Glascock DN, et al: Catheter ablation of the mitral isthmus for ventricular tachycardia associated with inferior infarction, Circulation 92:3481, 1995.)

The paradigm of transecting corridors of conducting tissue underlies the approach to ablation of re-entrant scar-mediated VT. Capitalizing on specific features of the substrate, the associated VT morphologies, and regional anatomy facilitates efficient and expeditious ablation.

Scar Mapping

Knowledge of the distribution of scar tissue permits focus of the mapping process and shortens procedure time. Bipolar voltage mapping using a three-dimensional electroanatomic mapping system is now standard for delineating the extent of VT scarring in the diagnostic electrophysiology suite.³⁷ Mapping is usually performed during sinus rhythm and the appropriate electrogram amplitudes that adequately discriminate tissue types, typically healthy tissue and scar tissue. The width of the voltage window defines electrogram amplitudes that are felt to represent specific tissue histology and conduction characteristics. Histologic studies have demonstrated that the VT circuit comprises viable tissue bundles embedded within and bordering the scar. Voltage mapping allows the identification of these tissue types, which can then be visualized as a color-coded map based on the electrogram amplitudes.

The map is created through point-by-point collection of position and local bipolar electrogram amplitude data, until a sufficient number and distribution of locations have been sampled to permit reliable reconstruction of the ventricular geometry. The positional data are used to construct an anatomic shell of the endocardium. The electrogram amplitudes, expressed as a color spectrum across the operator-defined voltage window, color code the shell creating a colorized voltage map. Current mapping systems use similar display spectra: regions with electrogram amplitude below the lower bound of the voltage window are displayed as red or white, whereas regions with electrogram amplitude above the voltage window upper bound are displayed as violet. Regions with intermediate-amplitude electrograms are displayed in the remaining colors spanning the visible spectrum between red and violet. The resultant maps depict islands of dense scar as red or white, surrounded by a multicolored border of viability, in a violet-colored “sea” of normal myocardial tissue.

Based on porcine infarct model bipolar voltage mapping studies from the University of Pennsylvania, borders of akinetic myocardium, defined by intracardiac echocardiography, correlated with 2.0-mV isopotential lines, whereas 1.0 mV isopotential lines were consistently adjacent to the scar border on pathologic analysis.³⁸ The same group used the CARTO system (Biosense Webster Inc., Diamond Bar, CA) to map the LV myocardium in people without structural heart disease and identified that more than 95% of sampled sites had electrograms greater than 1.55 mV. On the basis of their prior work, electrogram voltage less than 0.5 mV was arbitrarily designated as “dense scar.” Though few studies have validated these values against more traditional definitions of scarring, the thresholds continue to be applied, with reasonable clinical success, in contemporary ventricular mapping studies.

Activation Mapping

When VT does not cause hemodynamic instability, the arrhythmia may be allowed to sustain for EPS. Mapping during VT permits observation and study of the activation sequence of the various intracardiac sites at which recording electrode catheters have been positioned; therefore, it is referred to as activation mapping. This affords an opportunity to directly evaluate the regions and structures that participate in the VT circuit, as well as the relationships among the circuit anatomy, associated electrograms, and physiology critical to its maintenance, which may identify potential sites for ablation.

Sites of earliest activation (at least 50 ms presystolic) have been postulated to represent exit routes from the circuit to the ventricles and were assumed to be close to regions necessary for the maintenance of re-entry.^4,39 However, the success rate of ablation at these sites has been modest. The limitations with this approach include difficulty identifying the QRS onset from which to reference sites of diastolic, early activation, as well as diastolic or presystolic activation occurring in bystander sites not critical to the VT circuit.⁴⁰ Subsequently, diagnostic stimulation methods applied at sites of diastolic activity—termed isolated diastolic potentials (IDPs)—have proven useful in identifying the sites that are truly integral parts of the re-entrant circuit.⁴¹

Isolated Diastolic Potentials

Slow conduction through an isthmus bounded by lines of functional or anatomic block during re-entrant VT may produce low-amplitude IDPs preceding the QRS onset by as much as hundreds of milliseconds (Figure 95-7).^42–44 Although “bystander” regions may generate IDPs, potentials that cannot be dissociated from VT despite repeated induction of arrhythmia may signify essential components of the re-entrant circuit and important ablation targets. Fitzgerald and coworkers isolated such potentials in 7 of 14 post-infarct VTs. In each case, ablation at the site of these IDPs was successful.⁴⁵ Subsequently, Bogun and associates observed uniform concordance between sites of IDPs that could not be dissociated from post-infarct VTs and sites of concealed entrainment, providing additional evidence that isolated diastolic potentials originate in critical regions of slow conduction.⁴³

FIGURE 95-7 Catheter mapping during ventricular tachycardia reveals potentials separated from other intervening signals by an isoelectric phase during ventricular diastole—isolated diastolic potentials (IDPs). The relation between the IDPs and intervening ventricular electrograms is fixed, suggesting 1 : 1 activation. Identification of IDPs signifies regions of slow conduction that may participate in the re-entrant circuit.

Entrainment with Concealed Fusion

Entrainment mapping depends on the presence of an “excitable gap” in re-entrant circuits.⁴⁶ During tachycardia, an interval exists when the myocardium within a discrete portion of the re-entrant circuit has recovered from the preceding activation wavefront but has not yet been depolarized by the next orthodromic wavefront. When a train of pacing stimuli is applied to a re-entrant circuit during tachycardia at a CL less than the tachycardia CL such that each stimulus falls within this “excitable gap,” the orthodromic wavefronts initiated by pacing propagate through the circuit, whereas the antidromic wavefronts collide with the returning orthodromic impulses. The resulting acceleration of QRS complexes to the pacing rate during tachycardia constitutes entrainment.

During VT, entrainment from a site outside the tachycardia circuit results in fusion of the paced and tachycardia QRS morphologies, producing a blended intermediate QRS morphology. When pacing from within the circuit, the paced and tachycardia QRS morphologies appear identical, so entrainment results in the fusion of identical QRSs. This absence of apparent fusion is termed concealed fusion and suggests pacing from within the tachycardia circuit (Figure 95-8).

FIGURE 95-8 Concealed entrainment. Ventricular pacing through the mapping catheter at a cycle length just shorter than ventricular tachycardia (VT) cycle length accelerates VT to the pacing cycle length. Cessation of pacing permits continuation of VT at the spontaneous or intrinsic cycle length. Note that the entrained VT morphology is identical to spontaneous VT. Entrainment is achieved without manifest fusion, hence “concealed.”

To verify concealed fusion, it is essential to pace at several CLs during entrainment.¹⁵ Pacing at slower rates outside the re-entrant circuit may produce minimal QRS fusion and masquerade as concealed fusion, as wavefronts propagating away from the pacing site and wavefronts emerging from the tachycardia circuit collide close to the pacing site. Pacing at faster rates in these regions, however, should produce progressive fusion as the point of wavefront collision moves away from the pacing site.

Entrainment with concealed fusion alone, however, does not specifically localize critical regions of slow conduction within re-entrant circuits. Theoretically, pacing adjacent bystander sites may produce entrainment with concealed fusion (Figure 95-9). Supporting this concept, Bogun and colleagues observed that in 14 patients with post-infarct monomorphic VT, the positive predictive value of concealed entrainment for localizing successful RF ablation targets was only 54%.⁴⁷ Therefore, additional criteria have been developed to enhance specificity.

FIGURE 95-9 Schematic contrasting entrainment with concealed fusion at a site within a theoretical re-entrant circuit (site D) and at a bystander site (site E). The circuit contains a protected region bounded by inexcitable tissue from site C to sites D and A. Tachycardia wavefronts exit the protected region at site A. A stimulus at site D or E produces an orthodromic wavefront that propagates toward site A, where it exits the protected isthmus to activate the remainder of the myocardium and propagate through the circuit from site A to sites B and C, resetting the tachycardia. Whether the stimulated wavefront originates at site D or E, the impulse exits the circuit at site A, the tachycardia exit site. Therefore, QRS intervals during pacing and tachycardia are identical, as demonstrated in the tracings below the schematic. The postpacing interval (PPI) and S-QRS intervals may be used to differentiate sites within the tachycardia circuit and bystander regions. Following entrainment at site D, the stimulated wavefront propagates from the pacing site to sites A, B, and C, returning to site D resulting in a PPI equal to the tachycardia cycle length. After stimulating site E, in contrast, the orthodromic wavefront must travel into the tachycardia circuit, traverse the circuit, then return to site E before a local electrogram is recorded at the tip of the pacing catheter. The PPI would, therefore, exceed the tachycardia cycle length. The interval between the stimulus and the onset of the QRS (S-QRS) represents the conduction time from the pacing site to the exit site (site A). When stimulating within the circuit at site D, the time from the local electrogram recorded during tachycardia at the pacing site to the QRS onset (E-QRS) approximates the S-QRS interval. Pacing bystander site E produces an S-QRS interval that exceeds the E-QRS interval.

Postpacing Interval

After demonstration of concealed entrainment, the further demonstration of a postpacing interval (PPI) equal to the tachycardia cycle length suggests that a pacing site represents an essential portion of the re-entrant circuit.⁴² After pacing within a re-entrant circuit, the stimulated orthodromic wavefront makes one revolution through the circuit before returning to the pacing site, where a local electrogram is recorded. The time from the last captured pacing stimulus in a pacing train to the next local electrogram recorded at the pacing site—the PPI—should equal the tachycardia CL. When a site outside the re-entrant circuit is paced, the paced wavefront must propagate into the circuit, around the circuit, and back to the pacing site. This would result in a PPI exceeding the tachycardia CL by the conduction time to and from the VT circuit (see Figure 95-9).

The approximation of the tachycardia CL by the PPI depends on the maintenance of a consistent re-entrant pathway and stable conduction velocities during tachycardia and pacing. Slowing of conduction or the development of functional block will prolong the PPI, irrespective of the pacing site. In canine models of VT, these confounding factors were demonstrated to occur during rapid pacing.^48,49 Therefore, it is critical to use the slowest stimulus trains, usually 10 to 40 ms shorter than the VT cycle length, for analysis of PPI.¹⁵

Errors in the measurement of the PPI may also arise from stimulation and recording techniques.⁵⁰ Unless unipolar stimulation during entrainment is used, the point from which excitation spreads remains uncertain. Although the same distal electrode used for pacing should ideally be used to record the unipolar electrogram for measurement of PPI, the unipolar stimulation artifact often obscures this signal, necessitating the substitution of unipolar or bipolar signals recorded from more proximal poles. When closely spaced electrodes are used for stimulation and recording, minimal error is introduced to the measurement.⁵¹ If the recording and stimulation electrodes are farther apart, particularly in the presence of depressed myocardial conduction velocity, substantial error may result. Finally, the predictive accuracy of the PPI depends heavily on the ability to differentiate near-field from far-field recordings.

Stevenson and coworkers reported that a PPI within 30 ms of the VT cycle length was strongly associated with successful RF ablation–mediated termination of tachycardia.⁴² This finding was not confirmed by Bogun and associates who found that the prevalence of PPI within 30 ms of the VT CL did not differ substantially between effective and ineffective ablation target sites.⁵² These conflicting findings may have been caused by important methodologic differences, and while the statistical correlation with clinical success remains controversial, PPI is broadly applied in evaluating tachycardias and assessing proximity to critical sites within re-entrant circuits.

S-QRS Interval

During entrainment with concealed fusion, the interval between the pacing stimulus and the QRS onset (S-QRS interval) represents the conduction time from pacing site to the exit site for a re-entrant circuit. When pacing within a circuit, the time from the local electrogram recorded at the pacing site to the QRS onset during tachycardia is ordinarily within 20 ms of the S-QRS interval. In contrast, pacing a bystander site does not produce an S-QRS interval that approximates the local electrogram to QRS (E-QRS) interval during tachycardia (see Figure 95-9).^15,42 Also, according to the Stevenson model of entrainment mapping, when S-QRS is 30% to 70% of the VT CL, it suggests a location central or proximal within a slowly conducting isthmus. S-QRS intervals less than 30% of the VT CL suggest distal sites within the isthmus, or exit sites and sites that exceed 70% of the VT CL, represent inner loops (Figure 95-10). Entrainment of VT is shown in Figure 95-11. Application of the Stevenson algorithm suggests that the mapping catheter is located at an exit site.

FIGURE 95-10 Ventricular tachycardia (VT) entrainment response interpretation algorithm. If pacing entrains tachycardia with concealed fusion, the postpacing interval (PPI) or S-QRS interval is assessed to determine whether the site is in the re-entry circuit. If the site is not in the circuit, it is classified as an adjacent bystander. If the site is in the circuit, the S-QRS interval expressed as a percentage of the tachycardia cycle length is used to classify the site relative to the circuit exit. Sites with an S-QRS interval 70% of the VT cycle length (VTCL) have the highest incidence of tachycardia termination and are referred to collectively as isthmus sites. If pacing entrains the tachycardia with QRS fusion and the PPI is consistent with a re-entry circuit site, the site is classified as an outer loop. Sites where pacing entrains the tachycardia with QRS fusion and the PPI exceeds the tachycardia cycle length are remote bystanders. The EG-QRS interval from the electrogram is recorded at the pacing site during VT to QRS onset.

(From Stevenson WG, Friedman PL, Sager PT, et al: Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping, J Am Coll Cardiol 29:1180, 1997.)

FIGURE 95-11 Example applying entrainment mapping criteria (Stevenson algorithm). A, Sustained ventricular tachycardia cycle length (VTCL) 380 ms. B, Overdrive pacing at 30 ms shorter than VTCL accelerates the tachycardia to the pacing CL with paced morphology identical to clinical tachycardia (concealed entrainment), and cessation of pacing results in continuation of tachycardia at clinical CL. C, Measurement of the postpacing interval (PPI)—interval from the last pacing stimulus to the first electrogram on the pacing channel (PPI = 397 ms). D, Measurements of intervals between pacing stimulus and associated paced QRS, and electrogram to associated QRS; difference between these intervals (S-QRS less E-QRS) is 19 ms. All findings thus far suggest that the pacing site is within the tachycardia circuit. Ablation at this location fails to terminate the tachycardia. Note that that the S-QRS interval is only ∼13% of the VTCL, suggesting that the catheter location is actually at an exit location and not within a conducting isthmus of tissue inside the scar.

Recently, El-Shalakany and colleagues evaluated the accuracy of entrainment mapping criteria for predicting the termination of VT by a single RF lesion. In 15 consecutive patients with coronary artery disease, they attempted RF ablation of 20 monomorphic VTs. They looked for the following at each potential ablation site: (1) exact QRS match during entrainment; (2) PPI approximating VT cycle length; and (3) E-QRS interval (during VT) equal to S-QRS interval (during pacing/entrainment), but less than 70% of VT CL. At all of the 19 sites that met all three criteria, tachycardia terminated with a single RF application. In contrast, ablation failed to terminate VT at 24 of 25 sites not meeting all three criteria.⁵³ Bogun and coworkers prospectively evaluated the predictors of effective ablation in the presence of concealed entrainment. Studying 14 patients with coronary artery disease and hemodynamically stable monomorphic VT, they found that concealed entrainment alone carried a positive predictive value (PPV) of 54% for successful ablation. This increased to 72% when the S-QRS/VT CL ratio was less than 70% and increased to 82% when the S-QRS interval matched the E-QRS interval. The finding of mid-diastolic potentials associated with VT further enhanced the PPV to 89%.⁴⁷

Pacemapping

Unipolar pacing from the tip of the mapping catheter (cathode) during sinus rhythm permits comparison between paced QRS complexes and the QRS complexes during clinical VT, referred to as pacemapping.^54–56 This technique is applicable to both stable and unstable VTs, as pacing is performed during SR for brief periods and should not provoke hemodynamic embarrassment. Pacing is performed at a rate similar to that of clinical tachycardia because local myocardial conduction velocities and refractory periods may change with the frequency of activation, altering the surface ECG morphology. The ECGs during pacing and tachycardia are then compared. Optimal pacemaps are those with the closest match between QRS morphologies, including both R wave/S wave ratio and fine notching, in each of the 12 leads (Figure 95-12).

FIGURE 95-12 Pacemapping. Pacemapping, in this case of ventricular tachycardia (VT) (left), is undertaken by pacing through the roving mapping catheter (right) from various candidate myocardial locations in an effort to reproduce the morphology of the clinical arrhythmia. True pacemap matches must reproduce not only the overall polarities of the QRS, but its smaller undulations, notches, and minor details. Note how the paced QRS complexes reproduce not only the primary vectors of the Q, R, and S waves of the clinical VT but also the more subtle features, and that these characteristics are reproduced in all 12 leads of the standard electrocardiogram, that is, a “12 of 12” match.

Pacemapping in structural heart disease is limited primarily because pacing may produce QRS patterns grossly disparate from VT despite their proximity to a VT exit. This occurs because the spread of ventricular activation from a pacing site may be different from the sequence of activation during VT exiting from the same site. In addition, the amount of myocardium initially activated, which determines the QRS morphology, may differ significantly between pacing and VT. Excessive pacing current and use of a bipolar pacing configuration rather than a unipolar pacing configuration, both of which increase the size of the virtual electrode, may also significantly impact the QRS morphology. Such observed QRS differences between pacing and VT would divert the operator away from a potentially important VT exit site. Therefore, pacemapping should be performed at two times the diastolic threshold at the tachycardia CL. If unipolar pacing results in significant stimulus artifact obscuring the QRS itself, closely spaced bipolar pacing, which approximates unipolar pacing with a pacing area small enough to not significantly augment the virtual electrode or obscure the paced complex, can be used.

Complementary Use of Substrate and Pacemapping

The most widely applied approach involves voltage mapping during sinus rhythm and pacemapping around the perimeter of scar tissue to identify paced QRS matches most closely approximating the target VT morphology, thereby identifying exit sites of the scar that could be clinically relevant. Linear ablation lesions are then delivered at these sites, obliquely transecting the edges of the scar, with the expectation of interrupting a critical portion of the re-entrant circuit (Figure 95-13).

FIGURE 95-13 Electroanatomic map (CARTO) of the left ventricle in multiple projections (upper left: anteroposterior [AP]; upper right: right anterior oblique [RAO]; lower left: RAO caudal) demonstrating perimitral annular dense scar (red) involving the basal septum, and healthy myocardium (purple) elsewhere. Pacemapping performed at the blue annotation (lower left) produced a “12 of 12” match (see Figure 95-12). Radiofrequency was delivered in a linear fashion just inside the scar border from the site of pacemap match, believed to represent a scar exit site, to the mitral annulus to prevent reentry. Lower right, A fluoroscopic projection of the ablation catheter positioned at the site of pacemap patch is shown.

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