Substrate-Based Ablation for Atrial Fibrillation




Abstract


Atrial substrate modification is required for a successful outcome in a minority of patients with paroxysmal atrial fibrillation (AF), and in most patients with persistent AF. Substrate modification is considered when AF persists despite effective elimination of pulmonary vein (PV) arrhythmogenicity by extraostial PV isolation (PVI), antral PVI, or wide area circumferential ablation. Substrate modification strategies are linear ablation, ablation guided by complex fractionated atrial electrograms, and ablation of ganglionic plexi. Termination of AF to sinus rhythm or to an atrial tachycardia is considered the most favorable procedural end point for substrate modification. Complete bidirectional conduction block should be confirmed when linear ablation is performed.




Keywords

arrhythmogenic substrate, atrial fibrillation, catheter ablation

 




Key Points





  • Atrial substrate modification is required for a successful outcome in a minority of patients with paroxysmal atrial fibrillation (AF) and in most patients with persistent AF.



  • Substrate modification is considered when AF persists despite effective elimination of pulmonary vein (PV) arrhythmogenicity by extraostial PV isolation (PVI), antral PVI, or wide area circumferential ablation.



  • Substrate modification strategies are linear ablation, ablation guided by complex fractionated atrial electrograms, and ablation of ganglionic plexi.



  • Termination of AF to sinus rhythm or to an atrial tachycardia is considered the most favorable procedural end point for substrate modification.



  • Complete bidirectional conduction block should be confirmed when linear ablation is performed.





Mechanisms of Atrial Fibrillation and Rationale for Substrate Ablation


The pathogenesis of atrial fibrillation (AF) is complex and multifactorial. Pulmonary vein (PV) tachycardias have demonstrated that they play a critical role in both initiation and perpetuation of AF.


Although elimination of PV arrhythmogenicity has been highly effective for paroxysmal AF, it has modest efficacy for persistent AF, suggesting that mechanisms beyond the PVs also contribute to perpetuation of AF in these patients.


AF promotes diffuse electroanatomic remodeling. AF results in a nonhomogeneous decrease in atrial refractoriness and slowing of intraatrial conduction. Histologic examinations of atrial tissue in patients with AF show patchy fibrosis, which may contribute to the nonhomogeneity of conduction. Atrial biopsies from patients undergoing cardiac surgery show an increase in cell size, loss of sarcoplasmic reticulum and atrial myofibrils, changes in mitochondrial shape, accumulation of glycogen granules, alteration in connexin expression, and increase in extracellular matrix. Structural changes in response to AF may be a consequence of a physiologic adaptation to chronic Ca 2+ overload and metabolic stress. Reduction of atrial compliance and contractility during AF may enhance atrial dilation, which may add to the persistence of AF.


In the multiple-wavelet hypothesis proposed by Moe and Abildskov, multiple randomly propagating and self-perpetuating daughter wavelets act as a mechanism for perpetuation of AF. Critical to the multiple-wavelet hypothesis is a minimal left atrial size that can accommodate the wavelength as determined by the product of the conduction velocity and the effective refractory period (ERP). More recently, high-frequency sources (i.e., rotors), as a result of anisotropic reentry, have demonstrated the ability to perpetuate AF in experimental and simulation models. A novel mapping approach targeting focal sources and rotors has been developed and in some studies was shown to improve AF ablation outcomes in patients undergoing PV isolation (PVI); focal impulse and rotor modulation (FIRM) ablation is discussed in Chapter 18 .


Modulation of the autonomic innervation of the atria through ganglionic plexi (GP) has also been suggested to play a role in AF because an increase in vagal tone is associated with a decrease in the ERP and an increase in spontaneous depolarizations from the PVs and elsewhere in the atria. A number of ablation strategies have been proposed, alone or in combination, to target substrate-related mechanisms beyond the PV arrhythmogenicity, particularly in patients with persistent AF ( Table 17.1 ).



TABLE 17.1

Strategies for Substrate Ablation


































Ablation Strategy Targets Mapping Substrate Altered End Point
PV isolation PV antrum and encircling tissue Anatomic with or without 3D mapping PV arrhythmogenicity
CFAE
Autonomics
Microreentry
Rotors
Debulking
Complete PV and antral electrical isolation
Linear ablation LA roof
Mitral isthmus
Posterior wall isolation
Anatomic with or without 3D mapping Macroreentry
CFAEs with or without autonomics
Rotors
Conduction block across lines
Electrogram-guided ablation CFAEs
Frequency gradient
Activation gradient
Electrogram features with or without computerized analysis Slow conduction
Rotors, high-frequency sources
Autonomics
AF termination
Elimination of CFAE
Autonomics Parasympathetic ganglionic plexi
LOM
High-frequency pacing (plexi)
Angiography (LOM)
Autonomics with or without CFAE Absence of vagal response

3D, 3-Dimensional; AF, atrial fibrillation; CFAE, complex fractionated atrial electrograms; LA, left atrium; LOM, ligament of Marshall; PV, pulmonary vein.




Antral Pvi


Pathophysiology


The pathophysiologic basis for PVI is covered in detail in Chapter 14 . The PVs may serve as critical sources of rapid repetitive depolarizations, referred to as intermittent PV tachycardias , as a result of triggered activity, automaticity, or reentry that both initiate and sustain AF. In addition to a direct role of the PVs, the atrial tissue around the PVs may harbor complex myofibril arrays, GP, and areas of slow conduction and fractionated electrical activity, which also contribute to AF. In addition to eliminating PV arrhythmogenicity, PVI may also result in ablation of anchor points for rotors, which are more prevalent in the antral regions of the PVs; debulking of the left atrium (LA); ablation of GP; and ablation of arrhythmogenic foci other than the PVs, such as the ligament of Marshall (LOM) and posterior LA.


Mapping and Ablation


Antral PV isolation involves electrical isolation of the PVs and their respective antra, which often includes most of the posterior left atrial wall, at the anterior aspect of the left-sided PVs, where ablation is performed along the ostial aspect of the ridge between the left atrial appendage and the PVs ( Figs. 17.1 and 17.2 ). By extending the encircling lesions outside the PV into the antral or atrial tissue, residual arrhythmogenic foci and GP may simultaneously be eliminated. Thus PVI is generally considered a cornerstone of current catheter ablative therapy for AF. The end point of ablation is complete electrical isolation of the PV, confirmed preferably with a circular mapping catheter.




Fig. 17.1


A 3-dimensional electroanatomic depiction of the left atrium and the pulmonary veins (PVs) is shown in a right posterior oblique projection with cranial angulation. Two encircling PV lesions were created. A roofline was added. LI, Left inferior; LS, left superior; RI, right inferior; RS, right superior.

From Oral H, Pappone C, Chugh A, et al. Circumferential pulmonary-vein ablation for chronic atrial fibrillation. N Engl J Med . 2006;354:934-941. With permission.



Fig. 17.2


A, Possible atrial substrates responsible for the initiation and maintenance of atrial fibrillation (posteroanterior atrial view shown). Note the concentrated distribution of important substrates near the pulmonary veins (PVs) and posterior left atrial wall. B, Potential effects of PV isolation and linear ablation on left atrial substrate for atrial fibrillation. Ostial PV isolation may eliminate PV arrhythmogenicity but little else. Antral (orange highlight) and wide area PV isolation may also eliminate arrhythmia mechanisms near the PV. Linear ablation (roofline shown) may interrupt macroreentry circuits with variable collateral effects on fractionated electrograms and autonomics. CFAE, Complex fractionated atrial electrogram; GP, ganglionic plexi.


Outcomes


The clinical outcomes after PVI are reviewed in Chapter 14 , Chapter 15 . PVI is generally considered an appropriate stand-alone procedure for patients with paroxysmal AF. Patients with nonparoxysmal forms of AF typically require additional ablation, specifically for substrate modification, to achieve maximal benefit from ablation procedures.


Problems and Limitations


PVI is a complex and technically demanding procedure. However advances in catheter technology and energy sources have improved efficacy, efficiency, and safety of the ablation procedure.


An important safety consideration during ablation along the posterior left atrial wall is the risk of inadvertent collateral injury to the esophagus. Atrioesophageal fistula is a rare but often fatal complication. Ingestion of barium paste and esophageal temperature monitoring have both been used to prevent injury to the esophagus during ablation. However, esophageal luminal temperature measurement may underestimate the true esophageal tissue temperature. There are also attempts to move the esophagus away from the target sites by using specially designed steerable probes.




Linear Ablation


Pathophysiology


Catheter ablation for AF initially consisted of linear ablation to emulate the Cox surgical maze procedure. Linear catheter ablation was first limited to the right atrium and had low efficacy. Later linear ablation was performed in the LA. Linear ablation has been performed both as a stand-alone strategy and as an adjunctive strategy to other ablation techniques targeting the PV antrum and complex electrograms. Several studies demonstrated that additional linear ablation improves the clinical efficacy of catheter ablation in patients with paroxysmal and persistent AF. The original intent of linear ablation for AF was to interrupt macroreentrant circuits. Other possible mechanisms by which linear ablation may improve outcomes of AF ablation are interruption of microreentrant circuits, elimination of anchor points for high-frequency sources, and atrial debulking. Complex fractionated atrial electrograms (CFAEs) may also be prevalent along the course of linear lesions such as the septum or the roof. Finally, autonomic ganglia may be eliminated during linear ablation at certain sites.


Linear lesions may be a necessary step in the conversion of AF to sinus rhythm, often through an intermediate step of atrial tachycardia. In a study that used a stepwise ablation strategy including isolation of thoracic veins, ablation of CFAEs, and linear ablation until AF terminated, linear ablation was necessary in more than 80% of the patients with persistent AF for termination.


Mapping and Ablation


Linear ablation has been performed along the roof of the LA between the contralateral superior PVs, along the lateral mitral isthmus between the ostium of the left inferior PV and the lateral mitral annulus, along the left atrial septum, from the anterior aspect of the right PV antrum to the septal mitral annulus, along the posterior mitral annulus parallel to the coronary sinus, anteriorly between a roofline and anterior mitral annulus, and along the right atrial aspect of the interatrial septum from the superior vena cava (SVC) to the inferior vena cava (IVC; Fig. 17.3 ). In addition, a box set of lesions to isolate the posterior LA has been performed with an improvement in efficacy in some studies. At present, the left atrial roof and the mitral isthmus are the most commonly targeted sites. Although completeness of conduction block along a linear lesion has not been uniformly assessed, it is always desirable to confirm complete bidirectional conduction block. Incomplete block with slow conduction promotes reentry and may facilitate proarrhythmia, often in the form of persistent or recurrent atrial flutters. Previous studies have suggested that macroreentrant circuits may be present during AF. Elimination of high-frequency drivers that lead to fibrillatory conduction often results in termination of AF to a macroreentrant tachycardia. Therefore linear ablation may interrupt these macroreentrant circuits that coexist with AF.




Fig. 17.3


Linear ablation lesions for the left and right atria. The view perspective is anteroposterior. Pulmonary vein (PV) encircling lesions are shown in blue broken lines and linear lesions in solid red lines . The posterior box set is shown in blue, and the single-ring lesion set is shown in red . CVT, Cavotricuspid isthmus; LA, left atrium; LI, left inferior; LS, left superior; RI, right inferior; RS, right superior.


Left Atrial Roof Line


The goal of the roof line is to produce a line of block between the left and right superior PVs ( Fig. 17.4 ; also see Figs. 17.2 and 17.3 ). The line should be directed as cranially as possible avoiding the posterior wall where esophageal injury may result. It is efficient to perform this ablation after encircling PVI such that the roofline connects the gap between the PVI lines. A long fixed curve (Daig SL0) or steerable sheath can greatly improve catheter contact and stability. Two techniques for creation of this line have been described. In the first method, the catheter is positioned at the margin of the left superior PV and dragged to the right superior PV. The catheter tip is maintained in a perpendicular orientation to the atrial wall ( Fig. 17.5 ). The sheath extends almost to the distal electrode to support and steer the catheter. Energy is delivered for 30 to 60 seconds at each site, moving the catheter by approximately 5-mm increments between locations. Catheter temperature and impedance should be closely monitored because of the perpendicular electrode orientation that may predispose to tissue overheating, steam pops, and perforation. Introduction of contact force sensing ablation catheters have been extremely helpful to create effective lesions safely. (Please see chapter 3 .)




Fig. 17.4


A 3-dimensional anteroposterior electroanatomic map of the left atrium showing nonencircling ablation lesions. Anterior, septal, and rooflines were created in this patient. LAA, Left atrial appendage; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; MA, mitral annulus; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein.

From Oral H, Chugh A, Good E, et al. Randomized comparison of encircling and nonencircling left atrial ablation for chronic atrial fibrillation. Heart Rhythm . 2005;2:1165-1172. With permission.



Fig. 17.5


Anteroposterior views of ablation catheter position during ablation at the left atrial roof. (1) The right superior (RS) and left superior (LS) pulmonary veins (PVs) are opacified by contrast injection, showing a concave orientation of the roof. Ablation is started at the ostium of the LSPV (2) and progressively moved to the ostium of the RSPV (6) . Note that the ablation catheter is almost entirely in the long sheath, ensuring good control and tissue contact. Extra care is needed because any sudden push may result in perforation.

From Jais P, Hocini M, O’Neill MD, et al. How to perform linear lesions. Heart Rhythm. 2007;4:803-809. With permission.


The second approach positions the catheter at the right superior PV with the catheter retroflexed over the sheath ( Fig. 17.6 ). The electrode is parallel to the tissue with this technique. The sheath and catheter are then advanced, driving the electrode toward the left superior PV. Releasing the catheter deflection will also advance the catheter toward the left vein.




Fig. 17.6


Alternative approach to creation of the roofline. The ablation catheter placed in the right superior pulmonary vein (RSPV) is deflected, and the sheath and catheter assembly are progressively pushed toward the left superior pulmonary vein (LSPV; 2–5 ).

From Jais P, Hocini M, O’Neill MD, et al. How to perform linear lesions. Heart Rhythm . 2007;4:803-809. With permission.


Assessment of Conduction Block


A complete linear lesion should result in widely separated double potentials along the length of the line ( Table 17.2 ). A delay of more than 100 ms is usually indicative of complete block, but reliance on conduction time alone can be misleading. During left atrial appendage pacing, posterior left atrial activation should proceed in a caudal-to-cranial direction. Differential pacing maneuvers are also useful to detect slow residual conduction through the line. As the pacing site moves away from the edge of the line, the conduction time from the stimulus to the electrogram on the opposite side of the line will shorten with complete block, but will prolong in the presence of residual slow conduction through the line ( Fig. 17.7 ).



TABLE 17.2

Assessing Conduction Block Across Linear Ablation Lines




















Finding/Maneuver Finding Indicative of Complete Block Comment
Widely split electrograms >100 ms generally indicates block Absolute time between electrogram components depends on local conduction velocities
Block may be present with shorter times and conduction persistent with longer times
Differential pacing Pacing site close to edge line produces longer conduction times from stimulus to opposite side of line than pacing at site away from line Must pace from immediate edge of line
Propagation from pacing adjacent to line Pacing on either side of line produces two wave fronts, each propagating toward the ablation line from opposite directions Roofline: pace LAA and confirm that posterior wall is activated from caudal to cranial direction
Mitral isthmus line: pacing CS lateral to line produces proximal to distal CS activation and pacing CS medial to the line produces distal-to-proximal CS activation
Anterior mitral isthmus line: pacing lateral to line produces atrial septal activation from the posterior and lateral directions
Posterior wall isolation: entrance and exit block within box

CS, Coronary sinus; LAA, left atrial appendage.



Fig. 17.7


Roofline and encircling lesion around the right pulmonary veins (RPVs, dashed line, 1 and 3 ). The encircling lesion around the left pulmonary veins is not shown. The roofline is assessed during pacing from the anterior left atrium from a decapolar catheter across the anterior–superior left atrium. The distal decapolar bipole is located in the left atrial appendage; the proximal bipole is located at the septum. The ablation catheter is used to map the low posterior left atrium (1) , where a 144-ms delay is recorded (2) . In the high posterior left atrium, closer to the roofline (3) , a 172-ms delay (4) is recorded, demonstrating an activation front from the caudal to cranial direction.

From Jais P, Hocini M, O’Neill MD, et al. How to perform linear lesions. Heart Rhythm . 2007;4:803-809. With permission.


Mitral Isthmus Line


The goal is to produce a continuous line of block from the lateral mitral isthmus to the left inferior PV. It is recommended that a multipolar catheter be placed in the coronary sinus spanning the linear lesion to serve as an anatomic reference and to monitor the effects of ablation. Up to 70% of patients require ablation within the distal coronary sinus to achieve conduction block. If ablation within the coronary sinus is not possible or unacceptable to the operator due to high impedance or concern for left circumflex artery injury, the creation of this line should be carefully considered. As with any linear ablation, the creation of incomplete linear lesions is often counterproductive by prolonging procedure time, increasing the risk of complications, and possibly creating a proarrhythmic substrate. Using a long sheath, the ablation electrode is positioned at the lateral mitral annulus to record an atrial-to-ventricular ratio of 1:1 or 1:2 ( Fig. 17.8 ). The electrode can be perpendicular or parallel to the tissue (see Fig. 17.8 ). The site on the annulus can be selected to result in the shortest distance to the left inferior vein and its previously created encircling lesion. Lesions are delivered at each site for 30 to 60 seconds with a power limit of 30 to 35 W. Starting at the mitral annulus, the catheter and sheath are rotated with clockwise torque to move the electrode toward the PV in 5-mm steps. Care should be taken to detect inadvertent catheter displacement abruptly into the left inferior PV or appendage. Progress during ablation is gauged by splitting of the ablation electrogram and by delay in conduction across the lesion on the coronary sinus catheter during pacing proximal or distal to the line. Conduction times longer than 100 ms from the stimulus to the electrogram on the opposite side of the line are often associated with conduction block across the line. A more lateral line from the base of the appendage to the annulus may produce block when the initial line fails. Ablation within the coronary sinus can be required to achieve complete block. Ablation in the coronary sinus should be limited to use of irrigated catheters with maximal power of 20 to 25 W. The catheter should be deflected toward the endocardium to avoid the left circumflex artery. An average of 5 ± 4 minutes of radiofrequency (RF) delivered in the coronary sinus usually completes isthmus block in 84% of patients. Ethanol ablation of the vein of Marshall has been considered to achieve complete mitral isthmus block in patients refractory to RF catheter ablation.




Fig. 17.8


Mitral isthmus ablation line. Anteroposterior views are shown. A, (1) Ablation of the mitral isthmus starts at the lateral mitral isthmus. (1–6) The sheath and catheter are rotated clockwise to extend the lesion posteriorly to the ostium of the left inferior pulmonary vein. During this movement, the ablation catheter is progressively pulled back in the sheath. B, (1 and 2) The sheath and catheter are used to increase tissue contact at the mitral isthmus, with an almost 180-degree curve of the ablation catheter. Despite good contact, the resulting lesion is insufficient in some patients. Moreover, the tip of the catheter may abruptly dislodge into the left atrial appendage and perforate. Therefore although this approach is useful in some patients, it should not be used in the first instance because it carries a greater risk than the method described in A. (3) Ablation catheter tip at the ostium of the left atrial appendage. This is the only position where the orientation is truly perpendicular to the tissue. In some patients, this is the only method for achieving complete isthmus block.

From Jais P, Hocini M, O’Neill MD, et al. How to perform linear lesions. Heart Rhythm . 2007;4:803-809. With permission.


Assessing Conduction Block


Achieving complete conduction block along the mitral isthmus can be challenging. With complete isthmus block, widely separated electrograms, usually by more than 100 ms, should be recorded along the length of the ablation line. Pacing the coronary sinus or appendage distal to the ablation line results in proximal-to-distal coronary sinus activation on the septal side of the line ( Fig. 17.9 ). Likewise, coronary sinus pacing proximal to the line results in distal-to-proximal coronary sinus activation lateral to the line. As the pacing site is moved away from the edge of the ablation line, the conduction time from the stimulus to the electrograms recorded on the opposite side of the line decreases in the setting of conduction block, but increases in the setting of slow conduction across the line ( Fig. 17.10 ). To assess conduction block accurately, it is important to position the catheters as close as possible to the mitral isthmus line.




Fig. 17.9


Mitral isthmus line (dashed) connecting the mitral annulus (MA) to the left inferior pulmonary vein (continuous white lines). (1) Pacing from bipole 3–4 of the coronary sinus (CS) catheter, immediately septal to the linear lesion, is associated with a 170-ms delay recorded with the ablation catheter at the lateral edge of the line. (2) When pacing is performed more proximally from bipole 5–6, the activation route in the presence of complete block is shortened; accordingly, the delay at the ablation catheter is shorter (160 ms). (3) Bidirectional block is demonstrated because pacing lateral to the line of the ablation catheter is associated with proximal-to-distal CS activation. The double potentials observed at the CS ostium are the result of previous CS ablation required to convert this patient with persistent atrial fibrillation.

From Jais P, Hocini M, O’Neill MD, et al. How to perform linear lesions. Heart Rhythm . 2007;4:803-809. With permission.



Fig. 17.10


Mitral isthmus block. A, Differential pacing to assess counterclockwise block across an ablation line in the mitral isthmus. The ablation catheter is positioned medial to the ablation line in the left atrium. Pacing was performed in the coronary sinus, and as the pacing site was switched from the distal electrodes (CS 1–2) to a more proximal pair of electrodes (CS 3–4), the interval between the pacing stimulus and the local electrogram recorded from the ablation catheter shortened from 230 to 210 ms. B, Clockwise conduction block along the mitral isthmus. Note that atrial activation progresses from the proximal (CS 9–10) to distal (CS 1–2) electrodes during left atrial pacing medial to the ablation line. Abl d, Distal bipole of the ablation catheter; Abl p, proximal bipole of the ablation catheter; CS, coronary sinus; Stim, stimulus.

Morady F, Oral H, Chugh A. Diagnosis and ablation of atypical atrial tachycardia and flutter complicating atrial fibrillation ablation. Heart Rhythm . 2009;6:S29-S32. With permission.


Anterior Left Atrial Line


The goal of this procedure is to create a line of block from either the right superior PV or roofline to the anterior mitral annulus (see Fig. 17.2 ). This line serves as an alternative to the mitral isthmus line and also interrupts more localized reentry circuits in this area. It is recommended that the line start at the anterior mitral isthmus ( Fig. 17.11 ). The ablation catheter is withdrawn with counterclockwise torque to maintain contact with the anterior or anteroseptal left atrial wall. When the ablation electrode reaches the level of the transseptal puncture, clockwise torque is begun and the catheter advanced to reach the right superior PV or roofline. The anterior line may lead to a significant delay in atrial conduction and left atrial appendage activation and may adversely affect left atrial transport function.




Fig. 17.11


Position of the ablation catheter during anterior line ablation. An anteroposterior view is shown. The lesion is started at the superior–medial mitral annulus (1) . The ablation catheter and long sheath are progressively withdrawn (2) with counterclockwise torque to reach the level of the fossa ovalis. At this point (3) , the catheter torque should be clockwise, and the catheter is advanced to connect the line either to the lesion encircling the right pulmonary veins or to the roofline (4 and 5) . Abl, Ablation; CS, coronary sinus.

From Jais P, Hocini M, O’Neill MD, et al. How to perform linear lesions. Heart Rhythm. 2007;4:803-809. With permission.


Assessing Conduction Block


With complete conduction block, widely separated electrograms should be recorded along the entire length of the line. In addition, pacing the anterior LA just lateral to the line results in left atrial activation proceeding from lateral and posterior directions to activate the left atrial septum. As the pacing site is moved away from the edge of the ablation line, the conduction time from the stimulus to the electrograms recorded on the opposite side of the line decreases in the setting of conduction block, but increases in the setting of slow conduction across the line.


Inferior Mitral Annulus Line


Ablation along the inferior mitral isthmus parallel to the coronary sinus may be performed to interrupt muscular connections between the atrium and coronary sinus and other foci that may perpetuate AF. This line is generally used within the strategy of ablation of complex atrial electrograms. This line is begun with the catheter forming a loop in the LA and directed back toward the atrial septum ( Fig. 17.12 ). The electrode is then withdrawn from the 7- to 4-o’clock position as viewed in the left anterior oblique projection. Opening the catheter curvature as the tip moves laterally will improve tissue contact. Ablation within the coronary sinus is needed to eliminate all complex atrial activity and to produce maximal slowing of the AF rate (see Fig. 17.12 ). The end point for this ablation line is the elimination and organization of complex atrial electrograms within the coronary sinus or significant slowing of the atrial cycle length.




Fig. 17.12


Anteroposterior fluoroscopic visualization of the catheter positions during ablation of the inferior left atrium (top) and coronary sinus (bottom) . Top, After looping the catheter into the atrium facing the coronary sinus ostium (left) , the catheter is gradually withdrawn parallel to the coronary sinus along the posterior mitral annulus toward the lateral left atrium (middle and right images) to ablate the left atrial endocardium. Bottom, Corresponding catheter position at the ostial, middle, and distal segments within the coronary sinus to ablate the epicardial aspects of the left atrial to coronary sinus connections.

From O’Neill MD, Kim KT, Jais P, et al. Ablation strategies in chronic atrial fibrillation. In: Aliot E, Haïssaguerre M, Jackman WM, eds. Catheter Ablation of Atrial Fibrillation . Malden, MA: Blackwell Futura; 2008:163-189. With permission.


Posterior Left Atrial Isolation


The goal of this lesion set is complete electrical isolation of the left atrial posterior wall. Two techniques are described (see Fig. 17.3 ). In the left atrial box set, the PVs are isolated by antral encircling ablations, and a roofline is created as described previously. A linear lesion is then created between the left and right inferior PV to complete the set. Alternatively, the continuous single-ring linear lesion extends up the ridge between the left PV and the atrial appendage, across the roof, inferiorly along the interatrial septum between the foramen ovale and right PVs, then inferior to the right PV, and lateral across the atrium to meet the start of the line by ascending lateral to the left inferior PVs. Completion of this line isolates the PV and posterior left atrial wall en bloc ( Fig. 17.13 ).




Fig. 17.13


Isolation of left atrial posterior wall and all four pulmonary veins using a single ring of ablation. The radiofrequency lesions are shown as red dots on the volume-rendered computed tomographic image. A, Left posterior oblique view. B, Right anterior oblique cranial view. C, Posterior–anterior view. D, Anterior–posterior caudal view with clipping plane to display posterior left atrium shows the ring of ablation encircling the posterior left atrial wall. LAA , Left atrial appendage; LIPV , left inferior pulmonary vein (light green dots); LSPV , left superior pulmonary vein (dark green dots); RIPV , right inferior pulmonary vein (light blue dots); and RSPV , right superior pulmonary vein (dark blue dots) .

From Lim TW, Koay CH, McCall R, et al. Atrial arrhythmias after single-ring isolation of the posterior left atrium and pulmonary veins for atrial fibrillation. Circ Arrhythmia Electrophysiol . 2008;1:120-126. With permission.


Assessing Conduction Block


The end point for both approaches is the absence or dissociation of electrograms within the lesion box and exit block during pacing from the posterior wall. The PV should also be isolated with the single-ring approach.


Outcomes


Mitral and left atrial rooflines increase AF cycle length to an extent similar to PVI, and AF cycle length prolongation is associated with improved outcome in some studies. Linear lesions may be a necessary step in conversion of AF to sinus rhythm, often through an intermediate step of atrial tachycardia. In a study that used a stepwise ablation strategy, including isolation of thoracic veins, ablation of CFAEs, and linear ablation until AF was terminated, linear ablation was necessary in more than 80% of the patients for termination of persistent AF. For patients with persistent AF, the addition of linear lesions to PVI at the initial procedure reduces the incidence of subsequent macroreentrant arrhythmias. In patients with paroxysmal AF, the addition of confirmed mitral isthmus ablation reduces the recurrence rate of AF to 13% at 1 year, compared with 31% for those undergoing PVI alone. The addition of mitral isthmus ablation also improves outcomes in patients with persistent AF.


After the single-ring lesion, macroreentrant atrial arrhythmias may occur in 34% of patients after the procedure, and recurrent AF may be noted in 35% of patients. Gaps in the ring lesion were found in all patients undergoing repeat ablation for AF after the single-ring approach. Gaps in the ring lesion and mitral annular flutter are responsible for most atrial flutters. The most frequent site of ring gaps is along the left atrial appendage ridge. In a randomized trial, the completion of the box set did not improve outcomes compared with antral PVI and roofline alone.


Recent randomized trial, however, demonstrated that linear ablation after PV isolation (with or without CFAE ablation) did not improve clinical efficacy in patients with persistent and long-standing persistent AF. In another recent study, linear ablation was not incremental after circumferential PV isolation. A meta analysis also suggested that linear ablation after PV isolation is not incremental and may increase the risk of proarrhythmia because of atrial flutter and tachycardias.


Problems and Limitations


The optimal indications and sites for placement of linear lesions are not known. The greatest difficulty with linear ablation is achieving and confirming complete block across the lesions. This is particularly difficult for the mitral isthmus line, which may require extensive ablation within the coronary sinus to accomplish. Incomplete linear lesions may be proarrhythmic and may lead to refractory atrial flutters that are often highly symptomatic. The additional catheter manipulation and ablation may also increase the risk of procedural complications.




Electrogram-Guided Atrial Ablation


Pathophysiology


An intraoperative epicardial mapping study in humans suggested that areas of CFAEs may indicate sites of slow conduction, conduction block, wave front collision, or anchor points for reentrant circuits that can perpetuate AF. CFAEs may also indicate sites of high-frequency sources (rotors), fibrillatory conduction, and sites of autonomic innervation. CFAEs have been targeted for ablation to eliminate both paroxysmal and persistent AF. CFAEs are quite prevalent and can be found at many sites in both atria. The sites that most commonly harbor CFAEs are the interatrial septum, left atrial roof, left atrial appendage, near the PVs, and along the crista terminalis in the right atrium. Clustering of CFAE sites near the PVs appears to be more pronounced in patients with paroxysmal compared with nonparoxysmal forms of AF. CFAEs may be recorded over 38% to 56% of the left atrial endocardium.


Mapping and Ablation


CFAEs are identified during AF by visual assessment or by automated computerized algorithms ( Fig. 17.14 ). In the original description by Nademanee and coworkers, CFAEs were defined as (1) atrial electrograms that are fractionated and composed of two or more deflections, and/or have perturbation of the baseline with continuous deflections of a prolonged activation complex over a 10-second recording period; or (2) atrial electrograms with a very short cycle length (≤120 ms) averaged over a 10-second period. In addition, these electrograms are usually considered to be of low voltage (<0.15 mV). Other electrogram characteristics that have been targeted for ablation are sites with a large (>70 ms) temporal gradient between activation of the proximal and distal ablation bipoles, sites with continuous electrical activity without isoelectric intervals, sites with a cycle length less than the mean left atrial cycle length, and sites demonstrating centrifugal activation ( Fig. 17.15 ; Table 17.3 ).


Feb 21, 2019 | Posted by in CARDIOLOGY | Comments Off on Substrate-Based Ablation for Atrial Fibrillation

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