Ann Thorac Surg 2008;86:1960-1964. doi:10.1016/j.athoracsur.2008.07.066
© 2008 The Society of Thoracic Surgeons
New Technology
Toward a Definitive, Totally Thoracoscopic Procedure for Atrial Fibrillation
John Sirak, MD*,
Danielle Jones, RN,
Benjamin Sun, MD,
Chittoor Sai-Sudhakar, MD,
Juan Crestanello, MD,
Michael Firstenberg, MD
Ohio State University Department of Surgery, Division of Cardiothoracic Surgery, Columbus, Ohio
Accepted for publication July 14, 2008.
* Address correspondence to Dr Sirak, Ohio State University Division of Cardiothoracic Surgery, Doan N-820, 410 W. 10th Ave, Columbus, OH 43210 (Email: john.sirak{at}osumc.edu).
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Abstract
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Purpose: Evolution of anti-arrhythmia surgery beyond the Cox maze III has been hampered by the difficulty in implementing a complete lesion set in a truly minimally invasive approach. In this study, we introduce a true port-access procedure that addresses both autonomic and anatomic sources of atrial fibrillation, with real-time verification of all technical endpoints.
Description: A total of 32 patients with persistent or longstanding persistent atrial fibrillation underwent the totally thoracoscopic anti-arrhythmia procedure incorporating pulmonary vein isolation, mapping of epicardial autonomics, extended linear ablations across critical segments of atrial substrate, and ligation of the left atrial appendage. All aspects of the procedure were confirmed with intraoperative electrophysiologic testing.
Evaluation: With 1 week of continuous rhythm surveillance at 3, 6, and 13 months postoperatively in all patients, 21 of 24 patients with 6-month follow-up are in sinus rhythm with no anti-arrhythmia medications.
Conclusions: An anti-arrhythmia operation that is highly effective in patients with advanced forms of atrial fibrillation can be safely performed through a totally port-access approach.
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Introduction
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In the aftermath of the Cox maze III procedure, anti-arrhythmia surgery has suffered from the sacrifices of efficacy for procedural simplicity, and of verifiability of technical endpoints for decreased invasiveness. At the same time, the Cox maze III is still recognized as the gold standard for surgical therapy of atrial fibrillation, because the operation addresses the anatomic substrate conducive to the macro re-entrant circuits characteristic of atrial fibrillation [1]. However, increasing evidence points to the role of epicardial autonomics in lowering the fibrillation threshold in patients with atrial fibrillation [2]. Recent innovations in anti-arrhythmia operations have resulted in techniques to map and ablate epicardial autonomics systematically. However, recent reports detailing minimally invasive anti-arrhythmia procedures suffer from two limitations. First, an extended ablation set to address macro re-entry is omitted, resulting in impaired efficacy against advanced atrial fibrillation [3]. Second, a mini-thoracotomy, involving a muscle-splitting incision (typically 8 cm or larger) is used for instrumentation access, resulting in significantly increased patient morbidity and discomfort [4]. Therefore, we present a totally thoracoscopic procedure that systemically verifies the technical endpoints in treating both the autonomic and the substrate-based causes of atrial fibrillation [5].
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Technology
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Patient Selection
This retrospective analysis was completed in compliance with institutional review board guidelines. The need for patient consent was waived. During a 13-month period, a total of 32 patients underwent the total thoracoscopic anti-arrhythmia procedure. Twenty-nine of these patients had longstanding persistent atrial fibrillation and 3 had persistent atrial fibrillation; none had paroxysmal atrial fibrillation. Four patients had previously undergone at least one percutaneous left atrial ablation. Routine preoperative testing consisted of a 12-lead electrocardiogram, a chest roentgenogram, transthoracic echocardiography, and a nuclear myocardial stress evaluation.
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Technique
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The patient is positioned supine with a large padded roll underneath the spine. The arms are placed at a 90° angle relative to the torso. Right-sided access consists of a 10-mm port in the sixth interspace at the anterior axillary line, a 5-mm port in the fourth interspace at the mid axillary line, a 5-mm port in the third interspace at the anterior axillary line, and a 5-mm port in the third interspace at the mid-clavicular line. CO2 is insufflated into the chest to a pressure of 8 mm Hg. The pericardium is divided 2 cm anterior to the right phrenic nerve. The pericardiotomy extends caudally to the diaphragm, with clear visualization of the oblique sinus and inferior vena cava. The pericardiotomy is continued cephalad up to the reflection onto the superior vena cava, and then medially to the aorta. Retraction sutures are placed (Endo Stitch; AutoSuture, Norwalk, CT) on the posterior leaf of the pericardium at the levels of the transverse and oblique sinuses, and anteriorly at the level of the sinotubular junction of the aorta.
The entire oblique and transverse sinuses are opened with blunt and sharp dissection. In particular, it is vitally important to remove all areolar tissue overlying the inferior pulmonary vein at the superior border of the oblique sinus to expose all autonomic-bearing surfaces in the subjacent atrial tissue. Similarly, dissection of the entire transverse sinus is extended across the entire dome of the left atrium to the base of the left atrial appendage, resulting in complete separation of the left atrium from the branch pulmonary arteries. This maneuver is facilitated by medial retraction of the superior vena cava with an endoscopic Kittner inserted in the medial third interspace port.
The first ablations comprise an extended lesion set designed to interrupt left atrial macro re-entrant circuits. Using a bipolar radiofrequency ablation pen, a series of ablations is performed across the dome of the left atrium linearly from the base of the left atrial appendage to the introitus of the right superior pulmonary vein (Fig 1). A second, perpendicularly oriented series of ablations is connected from the line across the dome to the anterior trigone of the mitral valve, located at the aorto-mitral confluence at the base of the noncoronary root of the aorta. Exposure for this maneuver is facilitated by simultaneous gentle retraction of the aorta medially and of the right atrial appendage laterally (Fig 2). Lesion placement at the mitral trigone is confirmed by transesophageal echocardiography. While the ablation pen is gently balloted on the left atrium at the noncoronary root of the aorta, corresponding movement is demonstrated at the aorto-mitral confluence by transesophageal echocardiography (Fig 3). The continuity of both ablation lines is verified by at least 90% attenuation of the electrocardiogram amplitude, as measured by dragging a diagnostic electrophysiology catheter along the length of the ablation lines. Repeat ablations are performed as necessary to achieve continuity.
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Fig 1. An endoscopic Kittner retracts the superior vena cava anteromedially, exposing the transverse sinus from the right superior pulmonary vein to the left atrial appendage. In the left panel, the right atrial appendage is retracted laterally, thereby exposing the noncoronary root of the aorta.
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Fig 2. Access to the noncoronary root of the aorta is facilitated by lateral retraction of the right atrial appendage. A vertical line of ablations was performed extending from the anterior trigone of the mitral valve to the connecting ablations across the dome of the left atrium. (IVC = inferior vena cava; RIPV = right inferior pulmonary vein; RSPV = right superior pulmonary vein; SVC = superior vena cava.)
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Fig 3. Ablation of the anterior mitral trigone is verified by demonstration on transesophageal echocardiography of compression of the noncoronary sinus of aorta.
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High-frequency testing of the epicardial autonomics is performed in a manner similar to the technique described by Mehall and colleagues [6]. Each of the testing sites is stimulated at a rate of 1,000 Hz and an amplitude of 18 volts (Oscor Pace 203H; Oscor, Palm Harbor, FL) with at least a doubling of the R-R interval qualifying as a positive response. The positive sites are noted for repeat testing subsequent to the pulmonary vein isolation. Isolation of the pulmonary veins is performed with a dry bipolar radiofrequency clamp (Atricure EMR, Cincinnati, OH). Inclusion of the autonomic-bearing interatrial groove tissue into the clamp is facilitated with use of an endoscopic Kittner. Bidirectional block of both pacing and sensing across the ablation line is confirmed separately for each pulmonary vein. Finally, repeat autonomic testing is performed; all remaining responsive sites are re-ablated as necessary, with the bipolar radiofrequency pen until all autonomic reactivity is extinguished.
The remainder of the right-sided extended lesions consists of a line of ablations connecting the inferior pulmonary veins, extending from the right through the oblique sinus across the posterior left atrium. Exposure is facilitated by an endoscopic Kittner retracting the interatrial groove medially, thereby opening up the oblique sinus. In addition, ablations are performed to connect the right inferior pulmonary vein to the coronary sinus, and to the inferior vena cava. These linear ablations are applied with sufficient redundancy to assure lesion continuity as verified by electrocardiographic signal attenuation.
A similar array of port incisions is made in the left chest, with the exception of the sixth interspace port, which is placed in the posterior axillary line. The pericardium is divided posterior to the phrenic nerve, cephalad from the reflection onto the left pulmonary artery, caudad to the inferior pulmonary vein. Below the inferior pulmonary vein, the pericardiotomy is scalloped directly posteriorly toward the spine. Retraction sutures are placed on the medial leaf of the pericardium at the level of the left atrial appendage, and on the lateral leaf just caudal to the inferior pulmonary vein.
A 5-mm endoscopic fan retractor, placed in the third interspace port in the mid-clavicular line, is used to retract the left atrial appendage gently, medially and caudally. With simultaneous retraction cephalad on the left pulmonary artery, the ligament of Marshall is divided sharply. Meticulous division of all fibers of the ligament allows for complete cardiac autonomic denervation and facilitates subsequent encirclement of the pulmonary veins (Fig 4). Medial to the stump of the ligament of Marshall, the line of ablations previously placed across the dome of the left atrium is visualized. Additional ablations are performed to extend this line onto the os of the left superior pulmonary vein and to the base of the left atrial appendage. In addition, the line of ablations originating from the right inferior pulmonary vein across the posterior left atrium is extended to the OS of the left inferior pulmonary vein. Again, lesion continuity is verified by electrocardiographic signal attenuation throughout its length. Note that the exposure of the transverse and oblique sinuses allows re-verification of lesions placed during the right-sided portion of the operation, thereby minimizing any effect of tissue desiccation on testing results. In summary, the three extended connecting ablations consist of a line between the superior pulmonary veins across the dome of the left atrium, a perpendicular connection from the dome line to the anterior trigone of the mitral valve, and a line across the posterior left atrium between the inferior pulmonary veins.
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Fig 4. Meticulous division of the ligament of Marshall is essential for reasons of both complete autonomic denervation and optimizing exposure for the left-sided ablations. (LIPV = left inferior pulmonary vein; LSPV = left superior pulmonary vein.)
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The left-sided autonomic testing and isolation of the pulmonary veins is conducted as previously described. Ligation of the left atrial appendage is performed with the EZ-45 No-Knife endoscopic stapler (Ethicon Endosurgery, Cincinnati, OH) under transesophageal echocardiography guidance, allowing verification that the appendage is completely obliterated.
Postoperative Management and Follow-Up
Patients routinely receive only beta-blocker therapy postoperatively. Anti-arrhythmia medications are not used routinely, because all patients leave the operating room in sinus rhythm. In the event of a relapse of atrial fibrillation, amiodarone is administered, followed by synchronized cardioversion as needed. After hospital discharge, in addition to routine office electrocardiograms, patients undergo 1 week of continuous event monitoring with a self-actuated telemetry device (CardioNet, San Diego, CA) at 3, 6, and 13 months after their operation. Treatment failure is defined as any episode of atrial fibrillation or flutter lasting 30 seconds after an initial 3-month blanking period.
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Clinical Experience
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Patient characteristics are detailed in Table 1. The operation was completed in all patients. Average operative time was 217 minutes. One patient underwent conversion to a median sternotomy due to an intraoperative retraction injury at the base of the left atrial appendage. This injury occurred due to overly aggressive retraction using an endoscopic Kittner. Since that time, only an endoscopic fan retractor is used on the left atrial appendage. There were no other complications. The mean length of inpatient stay was 2.1 days.
Of the 24 patients 6 months out from their operation, follow-up per protocol is available in all. Twenty-one of these 24 patients (87.5 %) are in sinus rhythm; none of these 21 patients are on any anti-arrhythmic therapy, other than a low-dose beta-blocker. All 3 patients who failed to maintain sinus rhythm had longstanding persistent atrial fibrillation of at least 3 years' duration. The relapse into atrial fibrillation in these patients occurred on withdrawal of anti-arrhythmia therapy 3 months after their operations. Five patients, including the three failures, underwent cardioversion within the first 3 months postoperatively. None of the entire cohort of patients required a pacemaker or experienced atrial flutter.
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Comment
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Recent advances in minimal access surgery for atrial fibrillation have effectively addressed the need to treat the autonomic macro-environment conducive to atrial fibrillation in patients with otherwise structurally normal hearts. However, clearly pulmonary vein isolation and autonomic ablation alone are an insufficient treatment of the diseased left atrial substrate characteristic of longstanding persistent atrial fibrillation. In more advanced atrial fibrillation, electrical remodeling of the left atrial myocardium results in the ability of macro re-entry circuits to become self-sustaining, thereby resulting in an autonomous source of atrial fibrillation [7]. Omitted in previous reports of minimally invasive anti-arrhythmia procedures is a directed therapy to the left atrial substrate, thereby significantly compromising the efficacy of any anti-arrhythmia procedure in the large nonparoxysmal subset. The inclusion of the three critical connecting ablations in this procedure is designed to systematically treat the arrythmogenic left atrium characteristic of advanced atrial fibrillation. However, without real-time assessment of their completeness, these ablations would be of little value, and even worse, potentially arrythmogenic. Verification of all technical endpoints is the minimum acceptable standard for any definitive procedure for atrial fibrillation. Fortunately, improved technologies for delivering and verifying extended lesions have been incorporated into a newer iteration of this procedure, with commensurate advances in patient outcomes expected.
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Disclosures and Freedom of Investigation
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All equipment was purchased at cost by the host institution. Patient selection, operative technique, and study design were determined solely at the discretion of the authors.
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Footnotes
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Disclaimer The Society of Thoracic Surgeons, the Southern Thoracic Surgical Association, and The Annals of Thoracic Surgery neither endorse nor discourage use of the new technology described in this article.
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References
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- Harada A, Konishi T, Fukata M, Higuchi K, Sugimoto T, Sasaki K. Intraoperative map guided operation for atrial fibrillation due to mitral valve disease Ann Thorac Surg 2000;69:446-450.[Abstract/Free Full Text]
- Scherlag B, Yamanashi W, Patel U, Lazzara R, Jackman W. Autonomically induced conversion of pulmonary vein focal firing into atrial fibrillation J Am Coll Cardiol 2005;45:1878-1886.[Abstract/Free Full Text]
- Puskas J, Lin E, Bailey D, Guyton R. Thoracoscopic radiofrequency pulmonary vein isolation and atrial appendage exclusion Ann Thorac Surg 2007;83:1870-1872.[Abstract/Free Full Text]
- Wudel J, Chaudhuri P, Hiller J. Video-assisted epicardial ablation and left atrial appendage exclusion for atrial fibrillation: extended follow-up Ann Thorac Surg 2008;85:34-38.[Abstract/Free Full Text]
- Calkins H, Brugada J, Packer D, et al. HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation Heart Rhythm 2007;6:1-46.
- Mehall J, Kohut R, Schneeberger E, Taketani T, Merrill W, Wolf R. Intraoperative epicardial electrophysiologic mapping and isolation of autonomic ganglionic plexi Ann Thorac Surg 2007;83:538-541.[Abstract/Free Full Text]
- Allessie MA. Atrial fibrillation-induced electrical remodeling in humans: what is the next step? Cardiovasc Res 1999;44:10-12.[Free Full Text]
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Abstract
Introduction
