Barbara J. Deal1 and Constantine Mavroudis2 1Northwestern University Feinberg School of Medicine, Chicago, IL, USA 2Peyton Manning Children’s Hospital, Indianapolis, IN, USA Arrhythmia surgery was originally developed as stand‐alone therapy for medically refractory supraventricular tachycardias (SVTs) in patients with structurally normal hearts in the era prior to availability of more potent anti‐arrhythmic medications such as amiodarone and flecainide, and the development of catheter ablation techniques [1, 2]. Introduction of highly successful catheter ablation procedures for most forms of SVT diminished the role of arrhythmia surgery for refractory arrhythmias for several years [3, 4]. Surgical therapy for refractory ventricular tachycardia (VT) has been minimized with the use of implanted defibrillators and advanced ablation techniques, including epicardial approaches [5]. However, an increasing number of patients require reoperations for congenital heart disease or valvar operations for mitral and aortic disease [6]. Arrhythmia surgery offers the opportunity to integrate therapy for atrial fibrillation and atrial flutter under direct vision, with outstanding freedom from tachycardia recurrence [7–10]. As morbidity from arrhythmias in these patients is a leading cause for hospitalizations [11], the ability to incorporate arrhythmia surgery into concomitant cardiac surgeries is important and necessitates familiarity with the indications and techniques for arrhythmia surgery. The purpose of this chapter is to review the historical development of arrhythmia surgery, and current indications, techniques, and outcomes. Current guidelines for arrhythmia surgery are summarized to facilitate optimal planning of reoperations in patients with congenital heart disease [12–16]. The role for prophylactic arrhythmia surgery in certain populations is included [17]. Historical milestones in arrhythmia surgery and catheter ablation techniques are summarized in Figure 42.1. The successful treatment of Wolff–Parkinson–White (WPW) syndrome by endocardial dissection, and later closed‐heart epicardial dissection along the atrioventricular groove, ushered in the widespread use of this treatment for SVT due to accessory connections between 1968 and 1991 [1, 18, 19]. Ischemic VT surgery beginning in 1971 was less successful, but was the only option for some patients during an era prior to coronary stents, defibrillators, ventricular resynchronization, and heart transplantation [20–22]. VT surgery was then applied to patients with tetralogy of Fallot (TOF), who had undergone intracardiac repair in late childhood and developed VT in addition to pulmonary stenosis or regurgitation and were at high risk for sudden death [23, 24]. Repair of TOF in early childhood and improvements in valve‐sparing surgery have minimized late VT, with atrial reentry tachycardia and atrial fibrillation now a much more common arrhythmia in these patients [25–27]. Ablation of the atrioventricular (AV) node to achieve heart block as therapy for AV nodal reentry tachycardia or rapidly conducting atrial fibrillation was supplanted by slow pathway modification of the AV node using a catheter technique [2, 28, 29]. For atrial flutter, the efficacy of surgical ablation of the isthmus between the tricuspid valve and coronary sinus was a landmark achievement in therapy for this common arrhythmia in adults, and the surgical approach was also supplanted by a transcatheter approach [30, 31]. Perhaps most enduring was the development of surgical therapy for atrial fibrillation, after extensive study in the dog model and refinements to minimize sinus node dysfunction and maintain atrial function [32–36]. Subsequent modifications to minimize the number of lesions, an epicardial approach, and the use of alternate energy sources to replace incisions continue, concurrently with the development of transcatheter ablation for atrial fibrillation [37–39]. Figure 42.1 Historical milestones in arrhythmia surgery and catheter ablation. AF, atrial fibrillation; ASD, atrial septal defect; AV, atrioventricular; CHD, congenital heart disease; LA, left atrium; SVT, supraventricular tachycardia; TOF, tetralogy of Fallot; VT, ventricular tachycardia; WPW, Wolff–Parkinson–White. The arrhythmia surgical procedures described above were initially developed for adult patients without significant structural heart disease, and later applied to adult patients with mitral valve disease and atrial septal defects undergoing concurrent surgery [40]. Arrhythmia surgery for younger patients with WPW was extended to patients with structurally normal hearts in 1985 by Holmes and Danielson, and Crawford, achieving a 95% cure [41]. Ott and Garson from Houston extended arrhythmia surgery beyond accessory connections to include atrial and ventricular focal tachycardia with a large series in 1985, with limited success for VT [42–45]. Application of arrhythmia surgery to patients undergoing concurrent repair of congenital heart disease with accessory connections initially involved AV valve repairs in patients with Ebstein anomaly in 1991, with operative mortality of about 9% due to ventricular failure [46, 47]. Our center expanded the surgical ablation techniques to treat both atrial fibrillation and atrial flutter in patients with congenital heart disease of all ages, including neonates [8, 45, 48]. The development of Fontan conversion surgery with arrhythmia surgery and pacemaker implantation for patients with univentricular physiology and prior atriopulmonary repairs began in 1994 and has extended the life expectancy and quality of life for this particularly challenging group of patients [49–56]. Giamberti and colleagues reported their aggregate experience in 50 adults with congenital heart disease using irrigated radiofrequency ablation [44, 57]. The group from Mayo has extensive experience with performance of right‐sided atrial arrhythmia surgery for adults with congenital heart disease [58–62]. Freedom from recurrent SVT in this surgical population ranges from 5% to 15% during follow‐up [8, 44, 45, 50, 53, 57, 58, 60, 62–65]. In the longest follow‐up of arrhythmia surgery outcomes in congenital heart disease, including modified maze procedures for atrial fibrillation in 48% of patients, freedom from tachycardia recurrence of 77% at 10 years postoperatively was reported in Fontan patients [52]. In an effort to standardize care and expand the use of arrhythmia surgery procedures, recent guidelines from the American Heart Association (AHA)/American College of Cardiology (ACC)/Heart Rhythm Society (HRS), and consensus statements from HRS and the Society of Thoracic Surgeons (STS), have included recommendations for concomitant arrhythmia surgery for adults with congenital heart disease, SVT, atrial fibrillation, and VT (Table 42.1) [12–16]. Surgical ablation for atrial arrhythmias is a class I [13] or IIa recommendation [14] for Fontan patients undergoing intracardiac surgery. For patients with other forms of congenital heart disease with associated atrial tachycardia or atrial fibrillation undergoing planned intracardiac surgical repair, arrhythmia surgery is a class IIa recommendation [13, 14]. The most recent STS clinical practice guidelines have a class I recommendation for surgical ablation of atrial fibrillation in adult patients undergoing isolated valve replacement and/or coronary artery bypass grafting [16]. Atrial arrhythmia or accessory connection surgery is a class IIa recommendation for patients with Ebstein anomaly undergoing planned cardiac surgery [13, 14]. VT surgery is rarely recommended. For adult patients with sustained monomorphic VT and congenital heart disease undergoing planned intracardiac repair, surgical ablation is a class IIa recommendation [13], and for other adults with sustained VT, surgical ablation is a class IIb indication in patients failing anti‐arrhythmic medications and transcatheter ablation [15]. Indications for prophylactic arrhythmia surgery in patients without clinical or inducible arrhythmias are summarized in Table 42.2 and will be discussed in more detail at the end of the chapter. Table 42.1 Consensus statements and guideline recommendations for surgical treatment of clinical arrhythmias. ACC, American College of Cardiology; ACHD, adult congenital heart disease; AF, atrial fibrillation; AHA, American Heart Association; AT, atrial tachycardia; CABG, coronary artery bypass graft; CHD, congenital heart disease; COR, class of recommendation; EO, expert opinion; HRS, Heart Rhythm Society; IART, intra‐atrial reentrant tachycardia; LA, left atrial; LD, limited data; LOE, level of evidence; NR, nonrandomized; PVI, pulmonary vein isolation; SVT, supraventricular tachycardia; VT, ventricular tachycardia. Table 42.2 Consensus statements and guideline recommendations for prophylactic arrhythmia surgery in the absence of clinical arrhythmias. ACC, American College of Cardiology; AHA, American Heart Association; CHD, congenital heart disease; COR, Class of recommendation; HRS, Heart Rhythm Society; LD, limited data; LOE, Level of evidence; PACES, Pediatric and Congenital Electrophysiology Society; VT, ventricular tachycardia. Given these guidelines, it is important to screen patients with congenital heart disease for a history of arrhythmias as part of the planning for elective cardiac surgery. Patients with a known history of SVT should undergo electrophysiology study with catheter ablation as feasible preoperatively, or to guide surgical ablation in the setting of atrial tachycardia [13]. Patients with atrial fibrillation exclusively do not require electrophysiology study to guide arrhythmia surgery. Patients with anatomic features putting them at increased risk for arrhythmia development, including those with conduit repairs of right heart obstructive lesions such as TOF or double‐outlet right ventricle, Ebstein anomaly, atrial septal defects, or markedly dilated atria, should undergo an assessment for arrhythmia surgery, which may include 24‐hour ambulatory monitoring, exercise testing, or electrophysiology study. The absence of sinus rhythm or predominantly junctional rhythm on monitoring, chronotropic incompetence with exertion, episodes of AV block, or patients with congenitally corrected transposition of the great arteries may be evaluated regarding the implantation of epicardial atrial or dual‐chamber pacing leads and pulse generator. Successful arrhythmia surgery is based on a clear understanding of the mechanisms of tachycardia present in an individual patient and the anatomy of the conduction system, as well as the specific operative techniques and variations available for each mechanism and anatomic variant [10, 27, 66–73]. Importantly, an intense degree of cooperation and collaboration between the electrophysiologist and surgeon preoperatively as well as intraoperatively facilitates the flow of surgery and contingency strategies. Roles of the electrophysiologist and surgeon for successful arrhythmia surgery are summarized in Table 42.3. Anatomy as seen and described surgically is articulated in distinctly different terms from those used in the electrophysiology laboratory, and the need to draw out surgical anatomy and proposed lesions and clarify terminology is highly advisable in every situation [74]. Using these arrhythmia techniques, surgical repair of congenital heart disease can be viewed as both an anatomic and electrical intervention, with the combined goals of improving hemodynamic status and minimizing morbidity from the development of later arrhythmias. Table 42.3 Roles of electrophysiologist and surgeon for successful arrhythmia surgery. These can usually be successfully treated with a transcatheter approach prior to surgical repair; surgical procedures for these arrhythmias are infrequently required presently [75–79]. This is characterized by abnormal electrical impulse generation originating from a discrete area of the myocardium, typically the right or left atrium, which may be caused by microreentry or an automatic focus (Figure 42.2) [27]. The operative approach includes resection or cryoablation of the offending atrial tissue. Favorable results have been chronicled with cryoablation and excision of automatic foci, with acute success rates over 95% and recurrence of SVT in less than 5% (Figure 42.3). This is due to a reentrant circuit that is situated between the AV node, coronary sinus, and inferior caval vein (Figure 42.4) [27]. Early attempts at transcatheter ablation targeted complete AV nodal ablation with AV block and pacemaker implantation [80, 81]. Subsequent transcatheter ablation modifies the slow pathway or posterior inputs to the AV node, without producing AV block, and effectively treats AV nodal reentry tachycardia. A linear lesion can be placed from the posterior inferior rim of the coronary sinus os to the inferior caval vein. When a right‐sided atrioventricular valve is present, a linear lesion is placed from the valve annulus to the posterior os of the coronary sinus. These lesions will necessarily be modified in those patients with congenital heart defects where there is no right‐sided AV valve (e.g., tricuspid atresia) or absence of the coronary sinus (e.g., heterotaxy syndrome). The operative procedure, when necessary, mirrors the transcatheter approach, with similar results [78, 80, 82]. Figure 42.2 Right focal atrial tachycardia. Focal atrial tachycardia, a localized area of “impulse initiation” that is most commonly automatic in mechanism, firing repeatedly, rapidly, and independent of normal sinus function, which is inhibited. Impulse conduction is spread in a centripetal fashion across the atria, thence to the atrioventricular (AV) node and ventricles. Ablative therapy is aimed at obliteration or isolation of this localized discrete area (“hot spot”). CS, coronary sinus, SA, sino‐atrial. Source: Mavroudis C et al. 2008 / With permission of Elsevier. Figure 42.3 Gross anatomic findings of dysplastic atrial tissue confined to the right atrial appendage responsible for focal atrial tachycardia. Source: Mavroudis C et al. 2003 / With permission of Elsevier. Figure 42.4 Slow–fast or “typical” form of atrioventricular (AV) nodal reentry tachycardia. Atrioventricular conduction encounters a block in the normal fast pathway fibers superior to the compact AV node. The wave front proceeds towards the atrial isthmus, between the coronary sinus (CS) and tricuspid valve, and encounters slowing through the “slow pathway” fibers of the AV node. Exiting the isthmus, conduction is now able to reenter the fast pathway fibers, located anteriorly and superiorly, and perpetuate a reentrant circuit; simultaneously, conduction proceeds inferiorly to the ventricles. Of note is that conduction to the ventricles is not relevant to the tachycardia circuit. Cryoablation of the inferior isthmus region will interrupt the circuit. SA, sino‐atrial. Source: Mavroudis C et al. 2008 / With permission of Elsevier. This can be associated with either manifest accessory connections during sinus rhythm (delta wave on electrocardiogram, or WPW) or concealed accessory connections, with only retrograde conduction possible [27]. The most common form of associated tachycardia is termed orthodromic reciprocating tachycardia (ORT); the circuit is formed by antegrade conduction through the AV node to ventricular myocardium, and retrograde conduction via the accessory connection at the AV groove back to atrial tissue (Figure 42.5). As accessory connections can be successfully treated using transcatheter ablation, catheter ablation is recommended prior to planned surgical repair [83]. About 20–30% of patients with Ebstein anomaly have associated accessory connections, which may pose technical difficulties for catheter ablation due to the abnormal groove and the likelihood of multiple right‐sided accessory connections [84–87]. It is recommended that preoperative electrophysiology studies be performed in patients with Ebstein anomaly to assess for inducible SVT using an accessory connection, with ablation prior to surgery, even in the absence of clinical SVT or manifest WPW [14, 88]. Surgical ablation of the accessory connections can be performed intraoperatively in patients without successful catheter ablation procedures. The operative techniques for accessory connections, including endocardial and epicardial dissection and additional cryoablation, have been summarized previously [28, 89–93] and are shown in Figures 42.6–42.9 and Table 42.4. Presently an epicardial cryoablation approach would likely be employed, precisely confirming the epicardial location of the accessory connection intraoperatively with a multipolar electrode catheter placed along the atrioventricular groove. As the predominant mechanisms of SVT in congenital heart disease are macroreentrant atrial tachycardia and atrial fibrillation, knowledge of these surgical lesion sets is essential for the contemporary care of patients with congenital heart disease of any age [16, 94–96]. The most common mechanism of SVT associated with congenital heart disease is macroreentrant atrial tachycardia, which accounts for at least 75% of SVT and involves the cavotricuspid isthmus (Figure 42.10) and the right atrial incisional area also known as non‐cavotricuspid isthmus‐dependent tachycardia (Figure 42.11) accounts for over 60% of circuits [97–100]. Ablation lines delivered between the tricuspid valve annulus, coronary sinus, and inferior caval vein (the cavotricuspid isthmus) are the strategy of choice for these arrhythmias [98, 101]. Cryoablation or radiofrequency ablative lesions are placed with the intent of transforming the areas of “slow conduction” to areas of “no conduction,” thereby interrupting the slowed conduction that initiates the reentrant circuit. The ablative therapeutic lesions in normal hearts are shown in Figure 42.12. In patients with congenital heart disease, anatomic barriers may be absent or anomalous [102, 103]. Under these circumstances, creative measures are required. For example, since there is no tricuspid valve in tricuspid atresia, the lesions referring to this valve cannot be placed. The same principles are used for cryoablation lesions as for double‐inlet ventricles and heterotaxy syndrome. A more comprehensive explanation of these lesion sets can be noted in Chapter 28. Figure 42.5 Atrioventricular (AV) reciprocating tachycardia depicting concealed Wolff–Parkinson–White (WPW) syndrome. Orthodromic reciprocating tachycardia, the more common form of tachycardia, utilizing an accessory connection. Conduction is blocked in the accessory connection, thus losing the delta wave (now “concealed”). Conduction proceeds normally through the AV node to the ventricle. The delay encountered in the AV node allows the accessory connection to regain electrical function, and the electrical impulse then enters the atria from the opposite direction, from ventricle to atrium, across the accessory connection. This “playing field” includes the atria, AV node, ventricles, and accessory connection. CS, coronary sinus; SA, sino‐atrial. Source: Mavroudis C, Backer CL et al. 2003 / With permission of Elsevier. Figure 42.6 Endocardial technique for dividing left free‐wall accessory connections in Wolff–Parkinson–White syndrome. Source: Mavroudis C, Backer CL et al. 2003 / Wih permission of Elsevier. Figure 42.7 The epicardial approach to left free‐wall accessory connections. A schematic of the left ventricle, viewed from an operative position. The fat pad is mobilized and the atrioventricular junction exposed. Ao, aorta; CS, coronary sinus; LA, left atrium; LAA, left atrial appendage; LV, left ventricle; PA, pulmonary artery. Source: Reproduced by permission from Deal BJ et al. In: Pediatric Cardiac Surgery, 3rd ed. Philadelphia, PA: Mosby; 2003, pp. 713–738. Macroreentrant atrial tachycardia is a slower form of atrial flutter, with isoelectric periods between successive P waves; atrial flutter is characterized by saw‐tooth flutter waves at more rapid atrial rates, without intervening isoelectric periods. Atrial tachycardia develops most commonly in patients with TOF or right heart conduit repairs, atrial septal defects (ASDs), Ebstein anomaly, atrial baffle repairs for transposition of the great arteries, and in patients with univentricular hearts following Fontan surgery [102]. In addition to isthmus‐dependent atrial tachycardia are other atypical right atrial macroreentrant circuits, commonly referred to as “non‐isthmus”‐dependent tachycardia. The lateral right atrial wall at the inferior aspect of the crista terminalis is frequently an area of unexcitable atrial tissue with low‐voltage electrograms and is categorized as “scar” [104]. Ablation of the isthmus of slow conduction between these incisions, patches, or electrical scars forms the basis of treatment strategies for non‐isthmus‐dependent right atrial tachycardia [105, 106]. Figure 42.8 Endocardial technique for surgical division of posterior septal accessory connections in Wolff–Parkinson–White syndrome. The junction of the posterior medial mitral and tricuspid valve annuli forms an inverted V at the posterior edge of the central fibrous body, and the fat pad comes to a point at the apex of that V. The apex of the V is always posterior to the His bundle, although the distance between the apex of the V and the His bundle may vary. As long as the dissection in this region remains posterior to the central fibrous body, the His bundle will not be damaged. After the anterior point of the fat pad is gently dissected away from the apex of the V (i.e., away from the posterior edge of the central fibrous body), the mitral valve annulus comes into view at the point where it joins the tricuspid valve to form the central fibrous body. Ao, aorta; AV, atrioventricular node; CS, coronary sinus; IVC, inferior caval vein; LA, left atrium; LV, left ventricle; RV, right ventricle; SVC, superior caval vein; TV, tricuspid valve. Source: Reproduced by permission from Deal BJ et al. In: Pediatric Cardiac Surgery, 3rd ed. Philadelphia, PA: Mosby; 2003, pp. 713–738. Atrial fibrillation is predominantly a left atrial arrhythmia characterized by very rapid chaotic atrial activity with variable atrioventricular conduction, with rapid oscillations or fibrillatory P waves that vary in amplitude, shape, and timing. Atrial fibrillation is frequently associated with left‐sided valvar pathology and carries an increased risk of atrial thrombosis formation and stroke, in addition to decreased cardiac output [107]. The mechanism of atrial fibrillation may be due to multiple microreentrant atrial wavelets, focal triggers from sleeves of cardiac muscular tissue often within pulmonary veins, or localized reentrant circuits with fibrillatory conduction [108]. Sympathetic and parasympathetic innervation from autonomic ganglia located on the epicardial surface of the posterior left atrium may contribute to perpetuation of fibrillation. In addition to a trigger, an anatomic substrate is needed for the maintenance of atrial fibrillation, and atrial remodeling occurs rapidly with onset of atrial fibrillation. Figure 42.9 Epicardial approach for right free‐wall accessory connections. A schematic view of the exposure of the right coronary fossa and anterior right ventricular atrioventricular sulcus. Ao, aorta; LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle. Source: Reproduced by permission from Deal BJ et al. In: Pediatric Cardiac Surgery, 3rd ed. Philadelphia, PA: Mosby; 2003, pp. 713–738. Table 42.4 Operative techniques for arrhythmia surgery. ASD, atrial septal defect; AV, atrioventricular; CHD, congenital heart disease; DORV, double‐outlet right ventricle; s/p, status post; TAPVR, total anomalous pulmonary venous return; TGA, transposition of the great arteries; TOF, tetralogy of Fallot; VSD, ventricular septal defect; WPW, Wolff–Parkinson–White. Figure 42.10 Cavotricuspid isthmus‐dependent macroreentrant atrial tachycardia. As depicted, the field of activity is the right atrium, where a premature atrial contraction might encounter block in the atrial septum (broken line) and proceed in an alternate route down the right atrial free wall. The wave front may encounter an area of slow conduction (squiggly arrow), in this case between the inferior caval vein, tricuspid valve, and coronary sinus (CS). The delay encountered as the wave front traverses the area of slow conduction allows the atrial septum to recover conduction. The wave front exits the isthmus and proceeds up the atrial septum. Interruption of this circuit is targeted at the inferior isthmus due to the clearly identified landmarks in proximity. AV, atrioventricular; SA, sino‐atrial. Source: Reproduced by permission from Mavroudis C et al. Ann Thorac Surg. 2008;86:864.
CHAPTER 42
Surgical and Transcatheter Management of Arrhythmias
History of Arrhythmia Surgery
Recommendations for Arrhythmia Surgery
COR
LOE
Recommendation
2014 PACES/HRS consensus statement for arrhythmia management in adult congenital heart disease [13]
I
B
A modified right atrial maze procedure is indicated in adults undergoing Fontan conversion with symptomatic right atrial IART
I
B
A modified right atrial maze procedure in addition to a left atrial Cox maze III procedure is indicated in patients undergoing Fontan conversion with documented AF
IIa
B
Concomitant atrial arrhythmia surgery should be considered in adults with Ebstein anomaly undergoing cardiac surgery
IIa
B
A (modified) right atrial maze procedure can be useful in adults with CHD and clinical episodes of sustained typical or atypical right atrial flutter
IIa
B
A left atrial Cox maze III procedure with right atrial cavotricuspid isthmus ablation can be beneficial in adults with CHD and AF
IIa
B
Surgical ventricular tachycardia ablation guided by electrophysiologic mapping should be considered in adults with CHD and clinical sustained monomorphic ventricular tachycardia
IIa
B
Surgical ventricular tachycardia ablation guided by electrophysiologic mapping should be considered in adults with CHD and clinical sustained monomorphic ventricular tachycardia
IIb
C
Surgical ventricular tachycardia ablation guided by electrophysiologic mapping is reasonable in adults with CHD, no clinical sustained ventricular tachycardia, and inducible sustained monomorphic ventricular tachycardia with an identified critical isthmus
IIb
C
Adults with CHD and rapid ventricular tachycardia not mapped preoperatively but mapped intraoperatively may be considered for ventricular arrhythmia surgery
2014 ACC/AHA guidelines for the management of atrial fibrillation [12]
IIa
C
An AF surgical ablation procedure is reasonable for selected patients with AF undergoing cardiac surgery for other indications
IIb
B
A stand‐alone AF surgical ablation procedure may be reasonable for selected patients with highly symptomatic AF not well managed with other approaches
2017 STS clinical practice guidelines for the surgical treatment of atrial fibrillation [16]
I
B‐NR
Surgical ablation for AF can be performed without additional risk of operative mortality or major morbidity and is recommended at the time of concomitant isolated AVR, isolated CABG, and AVR plus CABG operations to restore sinus rhythm
IIa
B‐NR
Surgical ablation for symptomatic AF in the absence of structural heart disease that is refractory to class I/III anti‐arrhythmic drugs or catheter‐based therapy is reasonable as a primary stand‐alone procedure to restore sinus rhythm
IIa
B‐NR
Surgical ablation for symptomatic persistent or longstanding persistent AF in the absence of structural heart disease is reasonable as a stand‐alone procedure using the Cox maze III/IV lesion set compared with PVI alone
IIa
C‐LD
It is reasonable to perform LA appendage excision or exclusion in conjunction with surgical ablation for AF for longitudinal thromboembolic morbidity prevention
III
C‐EO
Surgical ablation for symptomatic AF in the setting of left atrial enlargement (≥4.5 cm) or more than moderate mitral regurgitation by PVI alone is not recommended
2015 ACC/AHA/HRS guideline for the management of supraventricular tachycardia in adults [14]
I
C‐LD
Assessment of associated hemodynamic abnormalities for potential repair of structural defects is recommended in ACHD patients as part of therapy for SVT
IIa
B‐NR
Preoperative catheter ablation or intraoperative surgical ablation of accessory pathways or AT is reasonable in patients with SVT who are undergoing surgical repair of Ebstein anomaly
IIa
B‐NR
Surgical ablation of AT or atrial flutter can be effective in ACHD patients undergoing planned surgical repair
COR LOE Recommendation
2014 PACES/HRS consensus statement for arrhythmia management in adult congenital heart disease: prophylactic arrhythmia surgery recommendations [13]
IIa
B
A modified right atrial maze procedure should be considered in adults undergoing Fontan conversion or revision surgery without documented atrial arrhythmias
IIa
B
Concomitant atrial arrhythmia surgery should be considered in adults with Ebstein anomaly undergoing cardiac surgery
IIb
C
Adults with CHD undergoing surgery to correct a structural heart defect associated with atrial dilatation may be considered for prophylactic atrial arrhythmia surgery
IIb
B
Adults with CHD and inducible typical or atypical right atrial flutter without documented clinical sustained atrial tachycardia may be considered for (modified) right atrial maze surgery or cavotricuspid isthmus ablation
IIb
C
Adults with CHD and left‐sided valvar heart disease with severe left atrial dilatation or limitations of venous access may be considered for left atrial maze surgery in the absence of documented or inducible atrial tachycardia
IIb
C
Closure of the left atrial appendage may be considered in adults with CHD undergoing atrial arrhythmia surgery
III
C
Prophylactic arrhythmia surgery is not indicated in adults with CHD at increased risk of surgical mortality from ventricular dysfunction or major comorbidities, in whom prolongation of cardiopulmonary bypass or cross‐clamp times owing to arrhythmia surgery might negatively impact outcomes
III
C
Empiric ventricular arrhythmia surgery is not indicated in adults with CHD and no clinical or inducible sustained VT
2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death [15]
IIb
C‐LD
In patients with monomorphic VT refractory to anti‐arrhythmic medications and attempts at catheter ablation, surgical ablation may be reasonable
Arrhythmia Surgery Techniques
Preoperative
Intraoperative
Postoperative
Electrophysiologist
Precision of communication is essential
Review clinical arrhythmia history
Review sinus and atrioventricular (AV) nodal function
Review surgical arrhythmia strategy briefly immediately before surgery commences
Define clear strategy, with contingency plans, including empiric ablation
Use of intravenous anti‐arrhythmic medications as indicated, typically following atrial fibrillation surgery
Review prior surgical reports:
Attention to incisions, excisions, patch placement
Location of coronary sinus: right or left atrium
Lead placement on patient’s chest prior to surgery
Esophageal lead or external pacing setup with cooperation from anesthesiologist
Ancillary support: pacing, resynchronization, defibrillator
Optimize rhythm with atrial pacing rates adjusted as hemodynamics change
Characterize arrhythmia substrates
Define multiple mechanisms if present
Distinguish reentry from focal mechanism
Define role of left atrium
If mapping is needed: Induce arrhythmia, with hemodynamic support ready and planned
Map quickly
Terminate arrhythmia promptly, with pacing preferred to cardioversion
Map arrhythmia during hemodynamic surgery
Evaluate for pro‐arrhythmic effects of surgical lesions
Pacing study prior to discharge may be needed
Define surgical arrhythmia strategy with surgeon prior to surgery
Include anatomic visual aids
Flexibility to adapt to limitations of anatomy, technical concerns
Guide adequacy of lesion numbers and locations
Surgeon
Precision of communication is essential
Clear knowledge of arrhythmia mechanisms
Clarify anatomy, use of sterile drawing pen/paper encouraged
Cooperate with arrhythmia strategies
Knowledge of arrhythmia surgery techniques specific to type of arrhythmia
Patience and cooperation with mapping
Clarify optimal ablation strategy to incorporate identified circuits and relevant anatomic barriers
Familiarity with anatomic variants that may pose technical difficulties
Avoid unnecessary lesions or proximity to AV node
Pacing lead placement optimization
Focal Atrial Tachycardia, Atrioventricular Nodal Reentry Tachycardia, and Supraventricular Tachycardia due to Accessory Connections
Focal or Automatic Atrial Tachycardia
Atrioventricular Nodal Reentry Tachycardia
Accessory Connection‐Mediated Tachycardia
Macroreentrant Atrial Tachycardia
Atrial Fibrillation
Arrhythmia substrate
Surgical techniques
Congenital heart disease
Focal atrial tachycardia
Map‐guided resection; cryoablation
Single ventricle, s/p repair
Unrepaired CHD
Structurally normal heart
AV nodal reentrant tachycardia
Slow pathway modification with cryoablation
TGA, s/p Mustard/Senning
Heterotaxy syndrome
AV septal defect
WPW/accessory connection
Endocardial or epicardial dissection and division along atrioventricular groove; cryoablation
Ebstein anomaly
Congenitally corrected TGA
ASD
Hypertrophic cardiomyopathy
Atrial flutter
Cavotricuspid isthmus ablation
Right atrial macroreentry
Modified right atrial maze
Single ventricle, s/p Fontan
TOF, s/p repair
TGA, s/p atrial baffle repair
ASD, TAPVR
Atrial fibrillation
Left atrial Cox maze III lesions with cavotricuspid isthmus ablation ± right atrial maze ± left atrial appendectomy
Single ventricle, s/p repair
TGA, s/p Mustard/Senning
Left heart obstructive lesions
Mitral valve disease
ASD
Ebstein anomaly
Hypertrophic cardiomyopathy
Left atrial macroreentry
Left atrial Cox maze III lesions
Single ventricle, s/p Fontan
ASD
Mitral valve disease
Ventricular tachycardia
Scar or endocardial fibrosis resection; focal ablation; lines of ablation between anatomic landmarks; map‐guided resection or ablation
s/p repair TOF, DORV, VSD
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