Ann Thorac Surg 2007;84:1786-1792. doi:10.1016/j.athoracsur.2007.05.040
© 2007 The Society of Thoracic Surgeons
Review
Choice of Surgical Lesion Set: Answers From the Data
A. Marc Gillinov, MD*
Department of Thoracic and Cardiovascular Surgery, The Atrial Fibrillation Innovation Center, The Cleveland Clinic, Cleveland, Ohio
* Address correspondence to Dr Gillinov, Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic/F24, 9500 Euclid Ave, Cleveland, OH 44195 (Email: gillinom{at}ccf.org).
| Dr Gillinov discloses that he has financial relationships with Edwards Lifesciences, AtriCure, Medtronic, Boston Scientific, and St. Jude Medical.
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Abstract
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Surgical ablation of atrial fibrillation has gained widespread acceptance, particularly in patients having concomitant cardiac surgery. Today, surgeons can choose from a variety of ablation technologies to facilitate operations intended to treat atrial fibrillation. Evidence suggests that virtually all of the available energy sources are effective at creating lines of conduction block on the arrested heart. However, there is controversy surrounding the choice of lesion set when these new devices are used. The purpose of this review is to address the critical question of lesion set by detailed consideration of contemporary data focusing on the (1) pathogenesis of atrial fibrillation, (2) results of catheter ablation, and (3) results of surgical ablation.
The ideal algorithm for development of medical therapy for an illness or condition includes four key steps: (1) identification of the condition, (2) characterization of the pathophysiology of the illness, (3) design and implementation of targeted therapies based on pathophysiology, and (4) assessment of results of therapy. The interventional treatment of atrial fibrillation (AF), whether catheter-based or surgical, is in large part empiric and has not yet incorporated all elements of this algorithm. As regard to surgical AF ablation, many important questions remain unanswered; one of the key points of contention being the choice of lesion set [1–5]. With more than 2 decades of experience with surgical ablation of AF, surgeons have conducted a few randomized trials addressing this question. Several recent studies and editorials focus on application of alternate energy sources and document short-term and intermediate-term results of a small series of patients having surgical ablation of AF [1–7]. It seems that new ablation technologies can be used to replace traditional cut-and-sew lesions at surgical ablation [1–7]. However, there is no conclusive data to guide choice of surgical lesion set at this time, particularly in patients having concomitant ablation. Several lines of evidence provide important information to guide the surgical treatment of AF in the concomitant surgical setting. The purpose of this article is to search for clues to the choice of surgical lesion set, focusing on (1) the pathogenesis of AF, (2) the results of catheter ablation, and (3) the results of surgical ablation.
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Methods
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Relevant published data was identified by a Medline search using the keywords "maze procedure," "surgical ablation," "catheter ablation," "atrial fibrillation ablation," "ablation failure," and "atrial fibrillation and pathogenesis." All large clinical series published in the year 2000 or beyond were reviewed. Studies including particularly relevant material that informs choice of lesion set were cited.
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The Pathogenesis of AF
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The pathogenesis of AF is incompletely understood, and this, of course, creates an immediate difficulty for the development and implementation of new therapies. The mechanism(s) of AF vary among affected individuals and are probably more complex than the discrete, well-characterized causes of most other arrhythmias (eg, Wolff-Parkinson-White Syndrome, typical right atrial flutter). Commonly proposed mechanisms of AF include rapid local activity from pulmonary vein and nonpulmonary vein triggers, single-circuit re-entry, and multiple circuit re-entry [8, 9]. It has also been demonstrated that substrate modification and perturbations of the autonomic nervous system contribute to the initiation or maintenance of AF, or both, in some individuals [9]. Of these mechanisms, the concept of initiation of AF by pulmonary vein triggers has gained the greatest attention and has influenced most modern techniques of catheter ablation and many current surgical approaches.
In Haissaguerre and colleagues [10] landmark 1998 article, he used endocardial mapping to identify triggers of AF in 45 patients with paroxysmal AF; 94% of triggers were in the pulmonary veins. These foci were observed to trigger AF with bursts of rapid discharges. Of note, 16 patients had more than one point of origin of atrial ectopic beats, emphasizing the complex nature of the initiation of paroxysmal AF. These findings provided key support for the concept that an anatomically-based ablation strategy could be used to treat patients with paroxysmal AF. Although subsequent intracardiac mapping studies [11, 12] confirmed a role for the pulmonary veins in the genesis of paroxysmal AF, they identified a higher preponderance of nonpulmonary vein triggers than reported by Haissaguerre and colleagues [10]. For example, a recent report documented that 47% of ectopic foci triggering AF were located outside the pulmonary veins, with 18% in the right atrium and multifocal triggers in 27% [11]. Common sites of nonpulmonary vein triggers of AF are the superior vena cava and the left atrial posterior free wall; these sources of ectopic activity are more prevalent in women and in those with left atrial enlargement [12].
Clue No. 1: The pathogenesis of paroxysmal AF frequently involves nonpulmonary vein triggers.
Mapping studies have demonstrated that persistent and permanent AF have different features from paroxysmal AF [13, 14]. This is believed to be related in part to more extensive modification of the atrial substrate in patients with persistent and permanent AF [8]. In patients with mitral valve disease, atrial enlargement and fibrosis and deranged atrial electrophysiology are likely to contribute to the pathogenesis of AF [15]. These changes may affect both the right and left atria. Paroxysmal AF is associated with higher frequency pulmonary vein activity than is permanent AF, supporting the notion that focal triggers in the pulmonary veins are less important in those with permanent AF [14]. In cardiac surgical patients with permanent AF, localized sites of high frequency activity that may represent rotors or macro-re-entrant circuits that initiate or maintain AF, or both, have been identified in both atria [16]. Corroborating this data, Nitta and colleagues [17] used sophisticated mapping techniques to identify both right and left atrial mechanisms of permanent AF.
Clue No. 2: Persistent and permanent AF frequently have different pathogenesis from paroxysmal AF and therefore may require ablation strategies directed more at the substrate than at triggers.
Recently there has been renewed interest in the role of the intrinsic cardiac nervous system in the pathogenesis of AF [18]. The heart has both extrinsic and intrinsic autonomic innervation. Extrinsic nerves arise from the brain and the thoracic paravertebral ganglia. Current attention has focused on the relationship between the intrinsic nervous system and AF. The intrinsic nerves, which include nerves and ganglia located on the large vessels and heart, can be approached by both endocardial and epicardial ablation [18–22]. Mehall and colleagues [19] have designed a schematic diagram that designates the ganglionated plexi located near the right and left pulmonary veins. Studies of these ganglionated plexi, which are collections of parasympathetic and sympathetic neurons clustered in fat pads at the pulmonary vein–left atrial junctions, suggest that they may be important in the initiation or maintenance, or the initiation and combination of both paroxysmal and permanent AF. Specifically, Scherlag and colleagues [23] have suggested that neurotransmitter release by the ganglionated plexi results in changes in autonomic tone that cause activation of pulmonary vein triggers and induce AF when such triggers fire. Experimental evidence demonstrates that activation of these nerves can indeed induce rapid firing from the pulmonary veins [24].
It is likely that many of the ganglionated plexi are ablated as a byproduct of epicardial pulmonary vein isolation. Procedurally, the ganglionated plexi are located by high frequency stimulation of fat pads at the pulmonary vein–left atrial junctions. Bradycardia during high frequency stimulation is presumptive evidence of the presence of ganglionated plexi; inability to induce such bradycardia after ablation is taken as confirmation that the ganglionated plexi have been destroyed. A small number of clinical studies have suggested that the addition of ganglionated plexus ablation to pulmonary vein isolation improves results when compared with pulmonary vein isolation alone [19, 22–25]. In addition, ganglionated plexus ablation alone has been used to treat AF [26]. However, it is likely that endocardial-based ablation of the ganglionated plexi damages a large volume of adjacent myocardium, and this effect on the atrial substrate makes it difficult to discern the precise impact of ablation of the nerve tissue. Furthermore, the long-term impact of ablation of the ganglionated plexi has been questioned, as experimental evidence suggests that re-innervation may occur with time [27]. Finally, the relative importance of the ganglionated plexi in paroxysmal versus permanent AF is unknown.
Clue No. 3: Ablation of the ganglionated plexi is a potentially useful, but unproven, strategy for AF ablation.
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Catheter Ablation
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Both randomized and nonrandomized studies have demonstrated that extensive catheter ablation is more effective than medical therapy at treating paroxysmal, persistent, and permanent AF [22, 28–31]. Recognizing these data, recent guidelines support a role for ablation in the management of AF [32]. Mechanisms of success of catheter ablation may include isolation of pulmonary vein and nonpulmonary vein triggers, interruption of drivers, substrate modification that makes re-entrant pathways unsuitable, promotion of electro-anatomic remodeling, denervation, atrial mass reduction, or some combination of these factors. Lesion sets used by different electrophysiology groups vary widely, but generally they incorporate extensive left atrial ablation that includes pulmonary vein isolation; many laboratories also use right atrial lesions. However, there is even controversy concerning the necessity for pulmonary vein isolation at the time of catheter ablation. Reported mid-term "success" ranges from 50% to 90%, with most series in the 70% to 80% range after one or more ablation procedures [22, 28–32]. Of note, similar results with catheter ablation have been reported in patients with and without mitral valve disease, raising the possibility that mechanisms of AF may not be substantially different in surgical and nonsurgical patients [33, 34].
As with surgical ablation, there is controversy concerning choice of lesion set at catheter ablation [35, 36]. Recent results in patients with paroxysmal AF support the notion that a more extensive lesion set improves outcomes in such patients; specifically, in patients with paroxysmal AF, addition of the mitral isthmus lesion seems to confer an extra 10% to 20% post-ablation freedom from AF or other atrial tachyarrhythmias [37, 38]. It is generally agreed that patients with permanent AF, who have more pronounced changes in the atrial substrate, should receive left atrial connecting lesions in addition to pulmonary vein isolation [36, 39, 40]. Right atrial lesions also enhance success; incorporation of extensive right atrial ablation, including cavo-tricuspid isthmus ablation, increased success by 24% in a prospective, randomized study of patients with persistent or permanent AF [39].
Clue No. 4: More extensive lesion sets, including right atrial lesions and a mitral isthmus lesion, improve results of catheter ablation when compared with pulmonary vein isolation alone.
Consideration of the mechanisms of failure of catheter ablation is instructive. Failures are usually caused by gaps in ablation lines. Although there is controversy concerning the necessity for transmural lines of conduction block, experimental evidence clearly demonstrates that small discontinuities in linear lesions conduct have the potential to participate in re-entrant arrhythmias or to allow propagation of abnormal impulses [41, 42]. At the time of catheter ablation, most electrophysiologists routinely assess the pulmonary veins for acute isolation [36, 37]. However, in patients with recurrent AF after catheter ablation, the most common finding is incomplete pulmonary vein isolation; correspondingly, repeat isolation of the pulmonary veins is associated with success [43, 44]. In addition, atrial tachycardias that are distinct from AF after catheter ablation develop in some patients. These are frequently macro-re-entrant tachycardias that depend on the mitral isthmus or gaps in previous ablation lines [45].
Clue No. 5: Ablation lines should be transmural and continuous.
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Surgical Ablation: The Cox-Maze III Procedure
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The Cox-maze III operation, or maze procedure, is the gold standard for the surgical treatment of AF. In fact, it is the most effective curative therapy for AF yet devised, and this must be considered when new surgical approaches to AF are developed. Cox and colleagues [46] designed the procedure empirically on the basis of early experimental and clinical evidence concerning the pathophysiology of AF; however, subsequent study has demonstrated that this understanding of the pathophysiology of AF was incomplete. To improve results and simplify the operation, they modified the procedure twice, culminating in the Cox-maze III procedure [46].
In the maze procedure, right and left atrial incisions and cryolesions are constructed to interrupt the multiple, disorganized re-entrant circuits that characterize AF (Fig 1). In addition, these lesions direct the sinus impulse from the sinoatrial node to the atrioventricular node along a specified route. Multiple "blind alleys" off this main conduction pathway (the maze analogy) allow coordinated electrical activation of the atrial myocardium. Key components of the maze procedure include en-bloc isolation of the pulmonary veins and posterior left atrium, a connecting lesion to the mitral annulus, extensive right atrial lesions, and excision of the left atrial appendage. The incision in the atrial septum, which was incorporated to enhance surgical exposure, may be omitted if exposure is adequate without it. Aside from management of the left atrial appendage, lesion sets created with catheter ablation increasingly resemble that of the maze procedure.

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Fig 1. (A) Left atrial lesion set of the Cox-maze III procedure. The pulmonary vein encircling lesion is depicted. The left atrial appendage has been excised. Cryolesions are created at the mitral annulus and coronary sinus (inset). (B) Right atrial lesion set of the Cox-maze III procedure. The intercaval incision extends from the superior vena cava to the inferior vena cava. Incisions in the right atrial appendage and in the body of the right atrium extend to the tricuspid annulus, where cryolesions are created. The incision in the atrial septum, which was included primarily to facilitate exposure of the posterior left atrium, is not depicted.
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Cox and colleagues [46] have reported the largest series of patients undergoing the maze procedure. Among 346 patients, the reported cure rate was 99%, and only 2% required long-term postoperative anti-arrhythmic medication. However, this historical study used recurrence of symptomatic AF as an endpoint, which almost certainly overestimates the cure rate. In addition, the maze procedure virtually eliminated the risk of late stroke [47]. Applying more intense post-ablation rhythm monitoring techniques, other centers have documented excellent results with the maze procedure, with restoration of sinus rhythm in 75% to 95% of patients, low risk of late stroke, and very low operative morbidity and mortality [48–50]. Recent studies demonstrate similar success in patients undergoing lone and concomitant maze procedures [50, 51]. Pattern of AF (ie, paroxysmal, persistent, or permanent) has no impact on the results of the maze procedure, suggesting that the extensive bi-atrial lesion set addresses the multiple and varied mechanisms of AF in these different groups [48].
Clue No. 6: The extensive bi-atrial lesion set of the maze procedure is associated with high rates of success, regardless of AF type.
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Surgical Ablation: Alternate Energy Sources
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The development of new surgical approaches to AF has been predicated on two factors: (1) focus on the role of the pulmonary veins and left atrium in the initiation and maintenance of AF, and (2) development of new ablation technologies that use alternate energy sources to facilitate rapid and safe creation of lines of conduction block under direct vision [1–7, 52]. A variety of ablation tools have been developed to replace cut-and-sew lesions and thereby facilitate surgical ablation of AF. These probes and catheters are designed to create long, continuous, linear lesions that block conduction. Energy sources that have been used include radiofrequency, laser, ultrasound, microwave, and cryothermy [1–7, 52–56]. Formal dose-response curves have not been published for many of these devices, and transmurality is not guaranteed, particularly when ablation is performed from the epicardium of the beating heart. However, there is a wealth of data documenting clinical results with new ablation technologies. As with the Cox-maze III procedure, most series focus on patients having concomitant surgical ablation. With these modalities, treatment success ranges from 40% to 98% [1–7, 52–56]. Replacing selected lesions of the maze procedure with bipolar radiofrequency, Melby and colleagues [53] have achieved success rates equal to those documented with the cut-and-sew technique. Similarly, comparing unipolar radiofrequency to the cut-and-sew technique, Chiappini and colleagues [57] observed no difference in success between the two groups. In a recent review of nearly 4,000 patients having surgical ablation, the cut-and-sew technique and alternate energy sources produced similar rates of conversion to sinus rhythm [52]. At this point, there is little controversy concerning replacement of cut-and-sew lesions with those created using new energy sources.
Clue No. 7: Alternate energy sources can be used to replace selected cut-and-sew lesions.
The central question concerns choice of lesion set when alternate energy sources are used at surgical ablation. Virtually all surgical lesion sets include pulmonary vein isolation. However, a few series document acute electrical isolation of the pulmonary veins, a desirable procedural endpoint [53]. Some reports suggest that simple pulmonary vein isolation, either en bloc as a box lesion or with separate, wide lesions around the right and left pulmonary veins, suffice to treat AF in patients having concomitant surgical procedures [58, 59]. However, these findings are easily misinterpreted and may not be applicable to most patients with AF. In one study claiming success with this strategy, "en bloc isolation of the pulmonary veins" included a connecting lesion to the mitral annulus [58]. In a report focusing on patients with short duration paroxysmal AF, pulmonary vein isolation seemed equal to the cut-and-sew maze procedure in treatment of AF [59]. However, other studies of small numbers of patients suggest that recent onset paroxysmal AF in mitral valve patients frequently disappears with correction of mitral valve pathology alone [60, 61]. Thus, it seems that pulmonary vein isolation alone should have a limited role in the management of surgical patients with paroxysmal AF unless the AF is of recent onset and is not the key indication for surgery.
It is well-documented that pulmonary vein isolation is associated with poor results in patients with permanent or continuous AF [62, 63]. Such patients require a more extensive lesion set, and the lesion connecting the pulmonary veins to the mitral annulus should be included in patients with permanent AF [62, 64]. Failure to create this lesion, termed the "mitral isthmus" lesion, seems to leave patients at increased risk for both AF and atypical left atrial flutter [62, 64]. When performed, this lesion must be transmural and include the coronary sinus. However, care must be taken to avoid injury to branches of the circumflex coronary artery when constructing this lesion. We currently favor cryothermy for creation of this lesion.
Clue No. 8: Pulmonary vein isolation alone is usually not the optimum strategy for concomitant ablation in cardiac surgical patients.
There is considerable controversy concerning the need for right atrial lesions in AF patients having concomitant surgery. Many reports document good results with left atrial lesions alone [52, 56, 62, 63]. In a prospective analysis of 70 patients with permanent AF, Deneke and colleagues [65] found no benefit to the addition of right atrial lesions. However, a subsequent meta-analysis of 5,885 patients demonstrated superior freedom from post-ablation AF in patients receiving lesions in both atria [66]. Addition of the right atrial lesions of the maze procedure reduces the occurrence of both atrial fibrillation and typical right atrial flutter [67]. These findings are concordant with those reported for catheter ablation.
Clue No. 9: A bi-atrial lesion set optimizes results in cardiac surgical patients.
As with catheter ablation, examination of surgical ablation failures provides an insight into choice of the lesion set. Selected interactions between patient and procedural factors have been associated with ablation failure; these have implications for treatment. Among patients having concomitant surgical ablation, increased left atrial size has been consistently identified as a risk factor for recurrent AF [62]. Two clinical studies postulate that left (and possibly right) atrial reduction at the time of ablation improves results [68, 69]. It has been suggested that such a strategy should be used when maximum left atrial dimension exceeds 5.5 cm [69]. Possible mechanisms of increased efficacy with this approach include excision of tissue that houses triggers or rotors, interruption of drivers, and substrate modification with reduction in volume of contiguous tissue below the threshold required to sustain AF.
Clue No. 10: Atrial size reduction in those with atrial enlargement may improve results.
There is controversy concerning the necessity for transmural lesions at the time of surgical ablation. Although it has been demonstrated that transmurality is not always necessary to achieve conduction block and successful ablation, transmurality does ensure conduction block. Therefore, we believe that transmurality is integral to surgical ablation. Experimental data suggest that heat-based energy sources create transmural lesions when applied to the endocardium of the arrested heart [7, 70, 71]. However, clinical data demonstrate that such energy sources can not be assumed to result in transmural lesions when applied to the epicardium of the beating heart [72]. Clinical experience confirms that lesion integrity influences results. Relying on post-ablation electrophysiologic study, Gaita and colleagues [63] demonstrated that cryothermy produced the intended lines of posterior left atrial conduction block only 59% to 71% of the time. Restoration of sinus rhythm was much more common in patients with complete lesions as demonstrated by electro-anatomic mapping than in those with gaps [63].
Other studies that include post-surgical electrophysiologic assessment support the importance of gaps in lesions. Performing an electrophysiologic study in 23 patients with recurrent AF after surgical ablation, Wazni and colleagues [73] found that one third of the patients had pulmonary vein–left atrium conduction recovery and 28% had tachyarrhythmias involving the coronary sinus or mitral isthmus. In a similar study of 20 patients having electrophysiologic examination after failed surgical ablation, Magnano and colleagues [74] documented left atrial flutter in 45% and typical right atrial flutter in 30%; macro-re-entrant tachycardias frequently resulted from breaks in ablation lines around the pulmonary veins, again emphasizing the importance of continuous, transmural lesions.
Clue No. 11: Ablation lines should be continuous and transmural.
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Surgical Ablation: The Left Atrial Appendage
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Stroke is the most feared complication of AF. When stroke occurs in AF patients, it is usually attributed to left atrial thrombi, the majority of which arise from the trabeculated portion of the left atrial appendage [75]. The Cox-maze III procedure, which includes excision or exclusion of the left atrial appendage, virtually eliminates the risk of late stroke [47]. Whether this is attributable to restoration of sinus rhythm, management of the appendage, or both, has not yet been determined. Other studies suggest that excision or exclusion of the appendage at the time of mitral valve surgery reduces the risk of late stroke [76]. However, the appendage must be completely excluded or excised to realize this potential benefit [77]. Although it has not yet been conclusively demonstrated that management of the left atrial appendage reduces the risk of thromboembolic events, adverse clinical sequelae related to appendage exclusion or excision are rare.
Clue No. 12: Surgical ablation should include management of the left atrial appendage.
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Conclusions
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At this time, it is not possible to define the precise mechanism(s) of AF in patients undergoing concomitant surgical procedures. Therefore, the ablation approach chosen incorporates a certain amount of empiricism. However, the data presented concerning the pathogenesis of AF and the results of catheter and surgical ablation may be used to guide surgeons in their choice of lesion set (Table 1). Although Cox and colleagues [46] had far less information than we do today when they formulated the Cox-maze III procedure, available data suggest that this bi-atrial lesion set optimizes results of surgical ablation. In the electrophysiology laboratory and in the operating room, best results are achieved with this extensive bi-atrial lesion set. Using current surgical ablation technology, these lesions can be performed in 15 to 20 minutes on the arrested heart. Until it becomes possible to identify the cause(s) of AF in individual patients, application of the Cox-maze III lesion set is the best means of ensuring successful ablation in cardiac surgical patients.
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