Vt Related To Regions Of Scar

The Reentry Substrate

The most common cause of VT is reentry through regions of scar, most commonly an old MI (Fig. 4). Other scar-related VTs occur because of arrhythmogenic right ventricular dysplasia, sarcoidosis, Chagas' disease, and other nonischemic cardiomyopathies. Two features of ventricular scarring lead to reentrant VT (40-42). First, dense scarring creates regions of anatomic conduction block. Second, the "scar" is not comprised completely of dense fibrotic tissue, but also contains surviving myocyte bundles (43,44). Fibrosis between myocytes and myocyte bundles decreases cell-to-cell connections. The excitation wavefront propagates in a zig-zag manner from myocyte bundle to myocyte bundle, increasing the time for depolarization to procede through the region and thereby causing slow conduction (44). Circulation of an excitation wavefront around an area of block leads to reentry. With slow conduction, each cell in the circuit has sufficient time to recover after each depolarization.

Most scar-related reentry circuits that allow catheter mapping can be modeled as shown in Fig. 4 (45-48). Depolarization of myocytes in or near the scar or infarct generates only low-amplitude electrical signals that are not detectable from the body surface. The QRS complex occurs after the circulating wavefront reaches the border of the infarct and propagates across the ventricles. The site where the wavefront leaves the tachycardia focus is known as the exit. The location of the exit around the border of the scar is a major determinant of the QRS morphology. Often, the region of the scar that contains the exit can be inferred from the QRS morphology. The region proximal to the exit often forms a relatively narrow isthmus, which is a good target for catheter ablation. After the circulating wavefront leaves the exit, the wavefront travels through a broad outer loop along the margin of the scar or a loop within the scar (inner loop) to return to the isthmus. Circuits can consist of multiple loops or single loops. In some cases reentry results from circulation of a single broad reentry path around a region of block; i.e. a single outer loop. Radiofrequency catheter ablation lesions are usually small in relation to the entire circuit and outer loops (3). Thus, the approach to ablation is to identify a narrow isthmus or channel in the circuit where a small number of radiofrequency lesions can interrupt reentry. Once a single channel is interrupted, there may be other channels that cause other tachycardias (49) (Fig. 4, panels B and C). Multiple morphologies of sustained monomorphic tachycardia, indicating multiple potential reentry circuits, are common (Fig. 4, panels B and C). Multiple morphologies of tachycardia make mapping and ablation more difficult, but do not preclude success. Often multiple morphologies of tachycardia originate from one general region of abnormal conduction (50).

Reentry circuits can occur in any region around the scar. In most cases, a portion of the reentry circuit is located in the subendocardium, where it can be ablated. However, portions of the circuit are often deep within the endocardium and cannot be identified

Scar Related Reentry

Fig. 4. Mechanism of reentry associated with ventricular scar is illustrated. The schematics show a view of the left ventricle from the apex looking into the ventricle toward the mitral and aortic valves. A region of heterogeneous scar is present in the inferior wall. In (A), the reentry wavefront circulates counterclockwise around and through the scar. Regions of dense scar create an isthmus in the circuit. The QRS onset occurs when the wavefront emerges from the isthmus at the Exit. It then circulates around the border of the scar, returning to the isthmus. Slow conduction through some regions in the scar is caused by discontinuities between myocyte bundles, as illustrated in the magnified image at the right. A wavefront that enters the bottom left myocyte bundles takes a circuitous course to emerge at the superior left bundle. In (B), an ablation catheter has been introduced through the aortic valve and positioned in the reentry circuit isthmus. In (C), following ablation of the isthmus for VT-1, a second VT is still possible because of reentry through an isthmus beneath the mitral valve. This circuit revolves in the opposite direction from the first circuit; the resulting VT has a different QRS morphology. (See color plate 5 appearing in the insert following p. 208.)

Fig. 4. Mechanism of reentry associated with ventricular scar is illustrated. The schematics show a view of the left ventricle from the apex looking into the ventricle toward the mitral and aortic valves. A region of heterogeneous scar is present in the inferior wall. In (A), the reentry wavefront circulates counterclockwise around and through the scar. Regions of dense scar create an isthmus in the circuit. The QRS onset occurs when the wavefront emerges from the isthmus at the Exit. It then circulates around the border of the scar, returning to the isthmus. Slow conduction through some regions in the scar is caused by discontinuities between myocyte bundles, as illustrated in the magnified image at the right. A wavefront that enters the bottom left myocyte bundles takes a circuitous course to emerge at the superior left bundle. In (B), an ablation catheter has been introduced through the aortic valve and positioned in the reentry circuit isthmus. In (C), following ablation of the isthmus for VT-1, a second VT is still possible because of reentry through an isthmus beneath the mitral valve. This circuit revolves in the opposite direction from the first circuit; the resulting VT has a different QRS morphology. (See color plate 5 appearing in the insert following p. 208.)

or ablated using a catheter at the endocardium (51). In some cases, the reentry circuit is epicardial in location. Some regions appear to give rise to endocardial portions of reentry circuit with disproportional frequency (50,52). In patients with prior inferiorwall infarction, the mitral annulus forms a barrier to conduction that often delineates a portion of the reentry circuit. In some cases, a surviving rim of myocardium beneath the mitral annulus creates a long isthmus for reentry. The resulting VT has a RBBB configuration when reentry occurs with the circulating wavefront propagating from septal to lateral in the isthmus, and a LBB configuration when the circuit revolves in the opposite direction (50).

Mapping Scar-Related Tachycardias

The first step in mapping is to identify the abnormal region. The region of scar is usually evident from an assessment of the ventricular-wall motion as an area of akinesis or dyskinesis. Regions of scar are also be identified during catheter-mapping as areas with low-amplitude electrograms (53,54). Fig. 5 shows a voltage map of the left ventricle in a patient with an old anterior-wall MI. The scar can thereby be identified during stable sinus rhythm. In addition, the region that contains the reentry-circuit exit can often be located by pace-mapping, although this is less reliable than for the idiopathic tachycardias discussed previously (1). Pacing from the mapping catheter during sinus rhythm can also identify regions of slow conduction in the scar, indicated by long conduction delays between the stimulus and the QRS onset (55). Thus, during stable sinus rhythm, it is often possible to locate the scar, the likely quadrant of the scar that contains the reentry circuit exit, and the regions of slow conduction. To determine whether these areas are in the reentry circuit rather than a bystander region, further evaluation is performed during tachycardia.

By plotting the local activation at each site in the ventricle during VT, the entire reentry circuit can occasionally be delineated (Fig. 5, panel C). In most patients, portions of the reentry circuit are deep within the endocardium, and are inaccessible to endocardial electrode catheters. In addition, VT is often not tolerated sufficiently to allow enough time to move a mapping catheter to all regions of the ventricle. Therefore the approach is focused on rapidly identifying a critical isthmus, which is often proximal to the exit (45). At these sites, depolarization precedes the QRS onset; the electrogram timing is referred to as "presystolic" or diastolic (Fig. 5), often with short-duration, low-amplitude signals referred to as "isolated diastolic potentials" (56-59). To confirm that such a site is in the circuit and is not a bystander, the effect of pacing at the site is evaluated. Pacing stimuli that capture have a predictable effect on the tachycardia, depending on whether the pacing site is in the reentry circuit at a narrow isthmus or is at a bystander region. This is known as entrainment mapping (45,57,59). Entrainment is continuous resetting of the reentry circuit by pacing at a rate faster than the circuit. At sites in a reentry circuit isthmus, the circuit can be reset without altering the QRS morphology (known as entrainment with concealed fusion or concealed entrainment) (Fig. 5, panel D), indicating that excitation wavefronts are capturing a relatively small region before interacting with the reentry circuit. This finding, in conjunction with other features of entrainment, allows a circuit isthmus to be identified without sampling sites throughout the ventricle. Radiofrequency current can then be applied during tachycardia; tachycardia termination provides further evidence that the site is critical to the reentry circuit. Additional radiofrequency lesions may be applied to enlarge the ablation lesion. Programmed stimulation is then repeated to attempt to reinitiate VT.

Entrainment Mapping

Fig. 5. Findings during catheter mapping in a patient with recurrent VT late after anterior-wall MI are shown. Left ventricular mapping was performed with an electroanatomic mapping system that records and displays catheter position along with the electrograms recorded. In (A) and (B) are shown the right anterior oblique (RAO) and left lateral views, respectively. Electrogram voltage is designated by colors with the lowest voltage shown in red, progressing to greater voltage regions of yellow, green, blue, and purple. The large anteroapical infarction is indicated by the extensive red region. In (C), the activation sequence of induced VT is shown in the RAO view of the left ventricle. The colors now indicate the activation sequence, with red being the earliest activation (identifying the re-entry circuit exit), progressing to yellow, green, blue, and purple. The reentry circuit has a figure-eight configuration, consisting of two reentrant loops (marked by the red arrows) circulating clockwise and counterclockwise and sharing a common central path. A bystander region of abnormal conduction that is outside of the reentry circuit is marked by the pink arrow. (D) Shows the effect of pacing during tachycardia (entrainment) in the central common pathway ischmus. From the top are surface ECG leads I, II, III, V1, and V6 and an intracardiac recording from the ablation catheter. Pacing accelerates the QRS complexes to the pacing rate, but without changing the QRS morphology compared to that of tachycardia. Furthermore, there is a delay of 160 ms from the

stimulus to the following QRS onset, indicating slow conduction from the pacing site, through the common path to the exit (red area in C). These findings indicate that the pacing site is in an isthmus in the reentry circuit. Radiofrequency ablation at this site abolished tachycardia. (See color plate 6 appearing in the insert following p. 208.)

stimulus to the following QRS onset, indicating slow conduction from the pacing site, through the common path to the exit (red area in C). These findings indicate that the pacing site is in an isthmus in the reentry circuit. Radiofrequency ablation at this site abolished tachycardia. (See color plate 6 appearing in the insert following p. 208.)

Ablation of Ventricular Tachycardia After MI

The common occurrence of multiple tachycardias in an individual patient, and the various approaches to ablation, makes the interpretation of catheter ablation results somewhat confusing. When VT is observed to occur spontaneously, this tachycardia is often referred to as a "clinical tachycardia." Tachycardias induced in the electrophysi-ology laboratory that have not been previously documented to occur spontaneously are sometimes referred to as "nonclinical tachycardias." This situation is complicated because the 12-lead ECG is often not recorded when VT is terminated by an implantable cardioverter defibrillator or by emergency medical technicians. Some centers select patients who exhibit only one predominant morphology of "clinical" VT documented with an ECG. If other tachycardias are induced at the time of study, these may be ignored if they have not been observed to occur spontaneously. This approach reduces the number of radiofrequency lesions required, but is more likely to leave potentially important reentry circuits intact. A second approach targets all tachycardias that can be induced and mapped. Some patients who have a "clinical tachycardia" that is no longer inducible at the end of the procedure may be referred to as "not inducible" despite the fact that other tachycardias are inducible. If tachycardias that were inducible at the beginning of the procedure have been eliminated, but other tachycardias are inducible, we designate this result as "modified." The reentry substrate has been altered, but some reentry circuits remain. These issues also confuse the interpretation of reported long-term outcomes. If a single tachycardia is targeted and ablated, but other tachycardias that were not targeted occur during follow-up, this may be reported as a successful outcome. In some cases, episodes of recurrent tachycardia are markedly reduced but not abolished—a result designated as a "clinical success."

Radiofrequency catheter ablation that targets a single "clinical" morphology of VT in selected patients was reported by Gonska and colleagues in 72 patients (60). The targeted tachycardia was no longer inducible at the end of the procedure in 74% of patients. During a follow-up, 60% of the group were free from recurrent tachycardia. Stevenson, Rothman, Strickberger, and colleagues targeted multiple tachycardias for ablation in 108 patients with recurrent episodes of sustained monomorphic tachycardia (61-63) (Fig. 6). Average left ventricular ejection fraction (LVEF) in these series ranged from 0.22-0.33; amiodarone therapy had been ineffective in 14-76% of patients. During the ablation procedure, an average of 3.6-4.7 different VTs were inducible per

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