Volume 14, Issue 3 , Pages 224-242, Autumn 2009
Total Thorascopic Ablation of Atrial Fibrillation Using the Dallas Lesion Set, Partial Autonomic Denervation, and Left Atrial Appendectomy
Article Outline
Minimal access ablation of atrial fibrillation (AF) has undergone a progression. As our experience has grown, the lesion set has progressed from simple pulmonary vein (PV) isolation to a more comprehensive lesion set, which can be placed epicardially, and more closely replicates the left atrial lesions of the Cox maze III. Access has progressed from bilateral mini thoracotomies initially described by Wolf and coworkers,1 to a totally thorascopic approach highly modified from that initially described by Puskas and coworkers2 and Yilmaz and coworkers.3
In our initial approach, 74 patients (46 paroxysmal, 14 persistent, 14 longstanding persistent) underwent bilateral PV antral electrical isolation using a bipolar radiofrequency clamp. (Groups were defined as follows: paroxysmal was defined as recurrent AF that terminates spontaneously within 7 days; persistent AF was defined as AF sustained beyond 7 days, or lasting less than 7 days but requiring either pharmacologic or electrical cardioversion; longstanding persistent AF was continuous AF of greater than 1-year duration.) Of the 74 patients, 13 had undergone one prior ablation, six had two prior ablations, and one patient had three prior ablations. Fifteen of the 74 had permanent pacemakers in place. All patients underwent transesophageal echocardiograms on the table before the procedure, and those who had undergone a prior catheter ablation had a left atrial magnetic resonance imaging or left atrial computed tomographic scan.
Rhythm was monitored by office electrocardiography (ECG) at 1, 3, and 6 months. At 6 months, the burden of AF was assessed by a 14- to 21-day auto-triggered event monitor. When patient circumstances dictated, a 24-hour Holter monitor was substituted for the 21-day event monitor. The long-term monitors used sampled the rhythm at 15-second intervals. When AF was detected by irregular rhythm, a single 15-second rhythm strip was recorded. Another rhythm strip was not recorded during that episode. Accordingly, we counted the number of episodes of AF but were unable to determine the duration of episodes over 15 seconds or the true burden of AF. Patients with pacemakers underwent pacemaker interrogation for episodes of AF (Table 1).
Table 1. Outcomes of Ablation in Initial Series of 74 Patients
| Follow-Up | Paroxysmal Atrial Fibrillation Patients (N = 46) | Persistent/Longstanding Persistent Atrial Fibrillation Patients (N = 28) | ||
|---|---|---|---|---|
| EKG (N = 43) | Holter/PM Interrogation/Event Monitor (N = 43) | EKG (N = 27) | Holter/PM Interrogation/Event Monitor (N = 23) | |
| NSR | NSR | NSR | NSR | |
| 6 Months | 43 (100.0%) | 36(83.7%) | 22(81.5%) | 13(56.5%) |
| 6 Months off AAD | 33(76.7%) | 30(69.8%) | 13(48.1%) | 8(34.8%) |
One might expect that PV antral isolation and partial autonomic denervation would not be adequate treatment for patients in persistent and longstanding persistent AF because of the associated changes in the left atrial substrate, which occur in these conditions.4 This electrical remodeling of the left atrium results in a fixed shortened refractory period and a shortened fibrillatory interval.5 Passive mechanical stretch of the left atrium that occurs in this chronic condition can in itself be arrythmogenic.6, 7 Atrial fibrosis has also been associated with AF.8, 9 Therefore, it is likely that isolating the PV triggers alone is insufficient treatment for persistent and longstanding persistent AF. Hence, a more extensive lesion set similar to the left-sided Cox maze III is necessary.
To accomplish a lesion set replicating the left-sided Cox maze III lesion set, a connecting lesion would need to be added between the left- and right-sided PVs, a connecting lesion to the base of the atrial appendage, and a connecting lesion to the mitral valve annulus. Traditionally, these connecting lesions are placed endocardially between the left and right inferior PVs, and from the right inferior PV down to the mitral valve annulus crossing the left atrial isthmus. However, when the epicardium is approached in a minimally invasive fashion, there are three inhibitors to placing the lesions in these locations. First, with currently available techniques, there is little to no visualization affordable posteriorly behind the left atrium. Second, as the circumflex coronary artery frequently overlies the mitral valve annulus, there is significant risk for collateral damage to this vital structure. Finally, the epicardial landmark for the mitral annulus is the coronary sinus. However, it has been shown10 that the coronary sinus can be up to 13 mm away from the mitral valve annulus, thus risking an incomplete connection which may result in left atrial flutter.
However, in the minimally invasive approach, we can obtain excellent visualization through the transverse sinus behind the aorta and the pulmonary artery. Therefore, we have conceived of and developed a lesion set (the Dallas Lesion Set) that places all of the connecting lesions on the dome of the atrium (Fig. 1). By working behind the superior vena cava and through the transverse sinus, we can place a transverse connecting lesion across the dome of the left atrium connecting the right superior PV with the left superior PV. It is then only a short extension of this line on the left side that connects it to the base of the left atrial appendage. The connecting lesion to the mitral valve annulus can also be accomplished on the dome of the left atrium within the transverse sinus. The left fibrous trigone touches the mitral valve annulus and connects it to the aorta at the aortic root. The left fibrous trigone meets the aortic valve at a point where the left coronary cusp and the noncoronary cusp join. Therefore, with good visualization, we can place this connecting lesion from the left fibrous trigone at the anterior mitral valve annulus, across the anterior dome of the atrium, and touching transverse dome line. This then replicates all of the left atrial lesions of the classic Cox maze III operation. Another short linear lesion connecting the left superior pulmonary vein to the left fibrous trigone then constructs a closed triangle on the dome of the atrium. By sensing and pacing within this triangle, one can test for entrance and exit block, thus demonstrating acute conduction block of all the dome lesions. Figure 2 shows the surgical approach to the transverse sinus, which is further detailed in the diagrams that follow.
Figure 1.
The Dallas Lesion Set. SVC = superior vena cava; v. = vein.
Figure 2.
Plane of access for left and right ablation on atrial dome in transverse sinus.
Twenty-nine patients (10 persistent, 19 longstanding persistent) were operated on using the Dallas Extended Lesion Set with intraoperative mapping for confirmation of block. The median left atrial size was 5.4 cm. Follow-up at 6 months was with 2-week event monitor (20/29), pacemaker interrogation (8/29), or ECG (1/29). At 6 months 23/29 (79.3%) were free of atrial fibrillation. The patient who had only ECG follow-up was in AF on ECG and refused a longer term monitor.
Only one of the patients failed as persistent AF. The others who failed, all failed as paroxysmal with a low residual burden of AF and were asymptomatic. Of the 6 failures, two patients had 1 episode, one patient had 2 episodes, one patient had 4 episodes, one patient had 6 episodes, and one had ECG alone for an undetermined number of episodes. All of these were “symptomatic successes.” The other failure had >50 episodes of continuous AF.
Early results with a minimally invasive extended linear lesion set suggest increased efficacy over pulmonary vein isolation for patients with persistent and longstanding persistent atrial fibrillation.
Operative Technique
Figure 3.
(A) Proper positioning of the patient in the operating room is critical to obtaining a successful surgical result. The surgeon must have free access to the posterior axillary line bilaterally. Additionally, the use of long thorascopic instrumentation means that the arm must be out of the way so that the instruments can be maneuvered in multiple different planes. Initially, we tried positioning the arm up over the forehead; however, we found that the upper arm was continually in the way, inhibiting movement of the long instruments.
To gain access to the posterolateral thorax and have the arms out of the way of instrumentation, we elevate the thorax of the patient on three to five bath blankets. The arms are then placed on slightly padded arm boards on each side of the operating table. The patient is prepped and draped so that the surgeon has access to the entire lateral thorax bilaterally, the sternum, and both groin areas in case they should be needed for urgent access.
External defibrillator pads are placed behind the right shoulder and on the left flank. If sterile defibrillator pads are available, one can be placed over the sternum and one directly posterior on the back of the patient.
(B, C) We perform the operation with three ports. Starting on the right side, a 5-mm port is introduced in the mid-axillary line in the third intercostal space. CO2 insufflation expands the field and depresses the diaphragm. Using a 30-degree scope, one can obtain good visualization throughout the thorax once absorptive atelectasis of the lung has taken place.
The two other ports placed are both 10-mm ports. One is placed in the mid-clavicular line in approximately the second intercostal space and the other in the mid-axillary line in approximately the seventh intercostal space. Both of these ports are placed so that instruments passed through them can access the transverse sinus, behind the superior vena cava and immediately cephalad to the right atrial appendage. This spot can actually be seen “through the pericardium” with a 5-mm scope. To determine the exact placement of the 10-mm port sites, a spinal needle is passed through the chest wall with the tip targeting the transverse sinus. Its position on the chest wall is changed until the site of best access is determined. Once the optimal site for these ports is determined, a 15-mm incision is placed and the 10-mm ports are advanced. Because multiple instrument changes will be made through these port sites, and because insufflation of CO2 in the chest is critical to maintain proper visualization, 0-silk sutures with a Red Rubber Robinson tourniquet are placed around each of these port sites. Then when the ports are later removed to allow introduction of other various sized instruments, the tourniquet can be run down to maintain the insufflation pressure within the thorax. (C) Left side where all ports are placed more posteriorly.
Figure 4.
(A) Working through these port sites, the right pericardium is open from the diaphragm to the level of the aorta approximately 2 cm anterior to the phrenic nerve. Great care is taken at all times to not stretch the phrenic nerve. Pericardial retraction sutures are placed utilizing an automatic suturing device and brought out through the posterolateral chest wall. Then using two blunt instruments, the fibroareolar tissue between the inferior vena cava and the right inferior pulmonary vein is dissected away until there is a wide opening into the posterior pericardium.
(B) Attention is then directed to the space between the right superior pulmonary vein, the right pulmonary artery, and the superior vena cava. The pericardium is bluntly and sharply dissected away until a portion of the superior vena cava is converted to intrapericardial. Then using a suction irrigator for retraction in the left hand and an L cautery device in the right hand, the tissue between the superior vena cava and the right pulmonary artery are divided along the entire course of the superior vena cava. Having thus surrounded the superior vena cava, one should be able to elevate it and see through the transverse sinus with a 5-mm scope.
The visceral pericardium surrounds the superior vena cava and behind it inserts onto the muscular dome of the left atrium. Behind the superior vena cava, between the two leafs of investing pericardium as they insert on the dome of the left atrium, there is always a very well-established fat pad behind the superior vena cava and in front of the left atrial muscular dome. This fat pad must be dissected away so that the ablation devices can get down to the muscular dome of the atrium. Fat is a relative insulator to radiofrequency energy. If one tries to burn through this fat, this is a common site of a gap in the ablation line leading to a failure of the procedure. Accordingly, it is critical that this fat pad be dissected until the operator can see the muscular dome of the left atrium. a. = artery; IVC = inferior vena cava; n. = nerve; SVC = superior vena cava; v. = vein.
Figure 5.
At this point, the 10-mm port that is in the most caudad site is removed. The lighted dissector (AtriCure, Cincinnati, OH) will not fit through the 10-mm port but will easily slide through the port site. Once it is introduced into the chest, the skin tourniquet is run down to reestablish the CO2 pressure within the chest and ensure ongoing exposure and visualization. This lighted dissector is advanced through the space between the right inferior pulmonary vein and the inferior vena cava into the posterior pericardium. Then by slowly and carefully articulating the clamp, the lighted blunt tip is dissected through the space between the right pulmonary artery and the right superior pulmonary vein. The clear plastic sheath is pulled off of the dissector and the lighted dissector is withdrawn. RIPV = right inferior pulmonary vein; RPA = right pulmonary artery; RSPV = right superior pulmonary vein.
Figure 6.
This clear plastic tape is merely a leader, the other end of which attaches to the posterior jaw of a bipolar radiofrequency ablation clamp (AtriCure).
At this point, a sensing pen is passed through the most cephalad port site and used to obtain a baseline electrogram on multiple sites on both the superior and the inferior pulmonary veins. These baseline electrograms should show transmitted electrical activity from the atrium. After the ablation lines have been placed, the electrograms in the pulmonary veins are again obtained and this time the absence of transmitted electrical activity from the atrium indicates acute entrance block has been obtained. Alternatively, if the patient is in sinus rhythm, one can pace in the pulmonary veins and look for exit block.
The pen is also utilized to deliver high-frequency stimulation to locate the presence of active ganglionated plexi. These are located by uncovering the bradycardic response (greater than 50% increase in R-to-R interval in response that occurs when one stimulates right over a ganglionated plexi).11
The closed bipolar clamp is then introduced through the most-caudad port site and the tourniquet is again snuggled around the shaft of the clamp to reestablish the pneumothorax. By pulling the clear plastic tape up and out through the second intercostal space port site, the posterior jaw of the clamp is then delivered behind the right-sided pulmonary veins. It is manipulated until the jaws are well up on the antrum of the pulmonary vein and well away from the bifurcation of the pulmonary veins. Three to five firings of the clamp are then done to produce an ablation line on the right pulmonary vein antrum.
After the ablation lines are completed with the clamp, the pen is again utilized to test in areas that were previously positive. If they are still positive, indicating they were not ablated with the clamp, this same sensing pen is utilized to deliver radiofrequency energy performing further ablation until all the areas that were positive for ganglionated plexi are now negative. RIPV = right inferior pulmonary vein; RSPV = right superior pulmonary vein.
Figure 7.
The internally cooled, linear bipolar radiofrequency device is now introduced through the most caudad port site. This device (Cooled Rails; AtriCure) has a deflectable tip and a malleable shaft. Now that the fat pad behind the superior vena cava has been divided, one can clearly see the muscular dome of the left atrium when the superior vena cava is elevated. The linear bipolar ablation device is positioned behind the superior vena cava. It is utilized to make a linear burn from the right superior pulmonary vein across the dome of the left atrium pointing toward the left superior pulmonary vein. In most cases when looking through the transverse sinus, the left superior pulmonary vein and even left atrial appendage can easily be visualized through this approach. This ablation line from the right superior pulmonary vein toward the left superior pulmonary vein is placed as posteriorly on the dome of the atrium as possible. Sometimes fibroareolar connective tissue between the atrial dome and the right pulmonary artery must be divided to allow this posterior placement of this ablation line. LSPV = left superior pulmonary vein; RPA = right pulmonary artery; RSPV = right superior pulmonary vein; SVC = superior vena cava.
Figure 8.
The tip of this same ablation device is now articulated to the right and further bending of the malleable shaft is done if possible. The tip is positioned at the junction of the noncoronary cusp and the left coronary cusp of the aorta. This juncture as well as the left main coronary can usually be easily visualized by placing the 30-degree 5-mm scope behind the superior vena cava and into the transverse sinus. The operator will see that the left main coronary artery is 2 to 3 cm away from the site of this ablation. Confirmation of the location of the tip of the ablation device can be done by looking at the transesophageal echo. Utilizing the mid-esophageal, long access, 140-degree view, the left fibrous trigone where the aortic annulus touches the mitral annulus can easily be visualized. Slight wiggling of the ablation device produces movement that is readily apparent on the echo view when the device is in the proper position. A lesion is then burned from the fibrous trigone obliquely on the dome so that it connects the left fibrous trigone to the transverse ablation line across the dome of the atrium. This linear ablation line can be touched up by using the bipolar pen to also deliver radiofrequency ablation lesions in a “stamping” fashion.
This completes the lesions that are placed from the right thorascopic approach. The pericardium is then closed, and a long catheter (I-Flow Corporation, Lake Forest, CA) to continuously infuse Marcaine is tunneled beneath the pleura to bathe all the intercostal nerves. A 19-French silastic chest tube is placed. The ports are withdrawn; the lung is inflated, and all the wounds closed. a. = artery; RPA = right pulmonary artery.
Figure 9.
Next the left side is approached. The approach is similar to the right side but somewhat more posterior. The 5-mm camera port is placed in the third intercostal space between the mid axillary line and the posterior axillary line and CO2 is insufflated. Again, spinal needles are advanced through the chest to determine the exact positioning of the other two ports so that their site will afford access to the left atrial appendage and the transverse sinus. Usually, the cephalad port is in the midclavicular line at approximately the second intercostal space and the caudad port is in the sixth or seventh intercostal space at the posterior axillary line.
Figure 10.
Working through these ports, the pericardium is opened. However, on the left side, the opening to the pericardium is done posterior to the phrenic nerve. Great care must be taken to avoid injury to the phrenic nerve. When extending the incision cephalad, care must also be taken not to injure the recurrent laryngeal nerve as it courses beneath the aorta. To protect the phrenic nerve, a single suture is placed in the anterior leaf of the pericardium, just posterior to the phrenic nerve, and this is brought out through the anterior chest wall. This lifts the phrenic nerve out of the field and also helps to expose the atrial appendage. LIPV = left inferior pulmonary vein; LPA = left pulmonary artery; LSPV = left superior pulmonary vein; n. = nerve.
Figure 11.
Working through these ports, one should be able to visualize into the transverse sinus and see the lesions that were placed from the right side. The sensing pen is placed and baseline electrograms in the pulmonary veins are recorded. Then high-frequency stimulation is performed to locate any active ganglionated plexi and their positions are noted. Following this, the ligament of Marshall is divided all the way posterior.
Thereafter, the lighted dissector is introduced from the most caudad port site and directed around the pulmonary veins with the tip coming up at the point of the divided ligament of Marshall. LIPV = left inferior pulmonary vein; LPA = left pulmonary artery; LSPV = left superior pulmonary vein.
Figure 12.
The bipolar radiofrequency clamp is then introduced through the most caudad port site. Using the guide that was attached to the lighted dissector, the posterior jaw is introduced behind the pulmonary vein and the clamp is closed well up on the pulmonary vein antrum where three separate firings are performed, changing the position of the clamp each time. The clamp is withdrawn and the pen is again introduced. Sensing in the pulmonary veins should now show electrical silence, indicating entrance block so that no atrial electrical activity is transmitted into the veins. Alternatively, if the patient is in sinus rhythm, one can pace in the pulmonary veins and look for exit block. Finally, the pen is used to stimulate in any areas where active ganglionated plexi were previously located. If these sites have not been ablated by the application of the radiofrequency clamp, they are now ablated by applying radiofrequency energy through the pen device. LIPV = left inferior pulmonary vein; LPA = left pulmonary artery; LSPV = left superior pulmonary vein.
Figure 13.
The clamp is withdrawn and the linear radiofrequency ablation device is introduced through the most caudad port site. The atrial appendage and the pulmonary artery are retracted to open up visualization into the transverse sinus. One can readily see the dome line coming across from the right side as it is aimed toward the left superior pulmonary vein. The linear ablation device is now used to complete this dome line so that it connects the right superior pulmonary vein over to the left superior pulmonary vein as far posteriorly as can be done in a transverse sinus.
The malleable linear ablation device is now articulated to the left and bent to the left. Another ablation line is placed from the left fibrous trigone to the right superior pulmonary vein. LOM = Ligament of Marshall; LPA = left pulmonary artery; LSPV = left superior pulmonary vein.
Figure 14.
With the ablations that have been done on the dome, an inverted triangle has now been constructed. The sensing pen is placed into the triangle. If each of these ablation lines is transmural, then there will be no conducted atrial activity into this triangle and the recorded electrogram will be flat. Alternatively, if the patient is in sinus rhythm, one can pace in this triangle and look for exit block to confirm that acute block has been obtained.
Figure 15.
Finally, a stapling device is introduced through the most caudad port site and carefully positioned around the base of the atrial appendage. Using the transesophageal echo to help guide the placement, the stapler is closed on the base of the atrial appendage and it is amputated. The amputated atrial appendage is withdrawn with the stapler. An infusion catheter is then threaded subpleural from caudad to cephalad to allow continuous infusion of Marcaine along all the intercostal nerve roots. The pericardium is reapproximated with a single stitch; a chest tube is placed, and all of the wounds are closed in layers. Sterile dressings are applied; the patient is awakened, extubated in the operating room, and transferred to the postoperative care ward.
Conclusions
The multiple burns that have been done usually result in producing an effusive pericarditis. To limit this and allow early removal of the pleural catheters, all patients are started on steroids in the operating room and continued on an oral form for 3 to 5 days postoperatively. All preoperative medications, including antiarrhythmics, are reinstated. Unless contraindicated, coumadin is started on all patients and the dosing is refined as an outpatient. Most patients are discharged on the third postoperative day. Patients are seen at 1, 3, and 6 months postoperatively. The 1-month visit is for wound checks. At the 3-month visit a 24-hour Holter is done. If the Holter shows no atrial fibrillation, atrial tachycardia, and no atrial flutter, and the patient reports no episodes of the same, the antiarrhythmic medications are discontinued. At the 6-month visit, a 2-week monitor is done. If the 2-week monitor shows no atrial fibrillation, atrial tachycardia, and no atrial flutter, the coumadin is discontinued unless it is specifically indicated for another reason. A 2-week monitor is done at 1 year postoperatively and at 12-month intervals thereafter for life. If the patient has any recurrence of atrial dysrhythmia, he is referred for full electrophysiological study in the electrophysiologic laboratory.
References
- Video assisted bilateral pulmonary vein isolation and left atrial appendage exclusion for atrial fibrillation. J Thorac Cardiovasc Surg. 2005;130:797–802
- Thorascopic radiofrequency pulmonary vein isolation and left atrial appendage exclusion. Ann Thorac Surg. 2007;83:1870–1872
- . Completely thorascopic bilateral pulmonary vein isolation and left atrial appendage exclusion for atrial fibrillation. J Thorac Cardiovasc Surg. 2008;136:521–522
- Surgery for permanent atrial fibrillation: Impact of patient factors and lesion set. Ann Thorac Surg. 2006;82:502–513discussion 513-514
- Electrical remodeling due to atrial fibrillation in chronically instrumented conscious goats: Roles of neurohumoral changes, ischemia, atrial stretch, and high rate of electrical activation. Circulation. 1997;96:3710–3720
- . Stretch-activated ion channels in the heart. J Mol Cell Cardiol. 1997;29:1511–1523
- Chloride conductance in human atrial cells. J Mol Cell Cardiol. 1995;27:2403–2408
- Dynamic nature of atrial fibrillation substrate during development and reversal of heart failure in dogs. Circulation. 2002;105:2672–2678
- Mechanisms of atrial remodeling and clinical relevance. Curr Opin Cardiol. 2005;20:21–25
- Anatomic and electrophysiologic relation between the coronary sinus and mitral annulus: Implication for ablation of left-side accessory pathways. Am Heart J. 1998;136:93–98
- . Release of autonomic mediators in cardiac tissue by direct subthreshold electrical stimulation. J Pharmacol Exp Ther. 1963;141:185–194
James R. Edgerton reports receiving speaker and consultant fees from Atricure.
PII: S1522-2942(09)00060-9
doi:10.1053/j.optechstcvs.2009.05.003
© 2009 Elsevier Inc. All rights reserved.
Volume 14, Issue 3 , Pages 224-242, Autumn 2009
