Substrate-Based Ablation for Atrial Fibrillation

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.

$Fig. 17.2, A, Possible atrial substrates responsible for the initiation and maintenance of atrial fibrillation (posteroanterior atrial view shown). Note the concentrated distribution of important substrates near the pulmonary veins (PVs) and posterior left atrial wall. B, Potential effects of PV isolation and linear ablation on left atrial substrate for atrial fibrillation. Ostial PV isolation may eliminate PV arrhythmogenicity but little else. Antral (orange highlight) and wide area PV isolation may also eliminate arrhythmia mechanisms near the PV. Linear ablation (roofline shown) may interrupt macroreentry circuits with variable collateral effects on fractionated electrograms and autonomics. CFAE, Complex fractionated atrial electrogram; GP, ganglionic plexi.$

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.

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.

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 ).

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