Am J Physiol Heart Circ Physiol 286: H2072-H2077, 2004.
First published January 29, 2004; doi:10.1152/ajpheart.00595.2003
0363-6135/04 $5.00
Thoracic vein ablation terminates chronic atrial fibrillation in dogs
Angela M. Park,1
Chung-Chuan Chou,1
Paul C. Drury,1
Yuji Okuyama,1
Anish Peter,1
Akira Hamabe,1
Yasushi Miyauchi,1
Robert M. Kass,2
Hrayr S. Karagueuzian,1
Michael C. Fishbein,3
Shien-Fong Lin,1 and
Peng-Sheng Chen1
1Division of Cardiology, Department of Medicine, and 2Division of Cardiothoracic Surgery, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles 90048-1865; and 3Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095-1679
Submitted 2 July 2003
; accepted in final form 4 January 2004
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ABSTRACT
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The thoracic vein hypothesis of chronic atrial fibrillation (AF) posits that rapid, repetitive activations from muscle sleeves within thoracic veins underlie the mechanism of sustained AF. If this is so, thoracic vein ablation should terminate sustained AF and prevent its reinduction. Six female mongrel dogs underwent chronic pulmonary vein (PV) pacing at 20 Hz to induce sustained (>48 h) AF. Bipolar electrodes were used to record from the atria and thoracic veins, including the vein of Marshall, four PVs, and the superior vena cava. Radio frequency (RF) application was applied around the PVs and superior vena cava and along the vein of Marshall until electrical activity was eliminated. Computerized mapping (1,792 electrodes, 1 mm resolution) was also performed. Sustained AF was induced in 30.6 ± 6.5 days, and ablation was done 17.3 ± 8.5 days afterward. Before ablation, the PVs had shorter activation cycle lengths than the atria, and rapid, repetitive activations were observed in the PVs. All dogs converted to sinus rhythm during (n = 4 dogs) or within 90 min of completion of RF ablation. Rapid atrial pacing afterward induced only nonsustained (<60 s) AF in all dogs. Average AF cycle lengths after reinduction were significantly (P = 0.01) longer (183 ± 31.5 ms) than baseline (106 ± 16.2 ms). There were no activation cycle length gradients after RF application. We conclude that thoracic vein ablation converts canine sustained AF into sinus rhythm and prevents the reinduction of sustained AF. These findings suggest that thoracic veins are important in the maintenance of AF in dogs.
electrical stimulation; electrophysiology; mapping; pacing
IT IS WELL KNOWN THAT ATRIAL fibrillation (AF), a common arrhythmia, carries a significant morbidity (11). Recently the mechanisms underlying this arrhythmia, particularly the paroxysmal (<48 h) form of AF, have been extensively studied. Work to date has identified focal sources of rapid, repetitive activation from various thoracic veins, including the superior vena cava (SVC; Ref. 23), vein of Marshall (VOM; Ref. 9), and, most commonly, the pulmonary veins (PVs; Ref. 21). These rapid activations are often spontaneous and irregular and characteristically have very high frequencies of activation that can serve as triggers in the genesis of AF. Furthermore, these studies have demonstrated that thoracic veins have arrhythmogenic capability and that, with radio frequency (RF) ablation of these signals from within the veins, paroxysmal AF can be terminated. Whether the same mechanism and therapy are also applicable to cases of sustained AF has not yet been addressed.
Earlier work from this laboratory (26) demonstrated that during sustained AF (>48 h) induced by rapid electrical stimulation of the left atrium (LA), the VOM and PVs activate at significantly shorter cycle lengths than the LA, which in turn activates at shorter cycle lengths than the right atrium (RA). Computerized mapping of the thoracic veins in that model (27) revealed rapid repetitive activation in the PVs during AF. These findings suggested to us that the thoracic veins might also play a role in the maintenance of AF. However, because we did not perform thoracic vein ablation in these earlier studies, a causal relationship between PV rapid, repetitive activity and the maintenance of AF could not be ascertained. In the present study, we used RF energy to isolate the thoracic veins from the atria in a canine model of sustained AF to determine the role of the thoracic veins in maintaining AF. We then performed rapid pacing after ablation to determine whether AF could be reinduced and sustained. These results are used to test the hypotheses that thoracic vein activities underlie the mechanism of sustained AF and that atria alone cannot support sustained AF without the continuous input of rapid activation from thoracic veins.
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METHODS
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Six female mongrel dogs (body wt, 21–28 kg) underwent a two-stage surgical procedure that was approved by the Institutional Animal Care and Use Committee. The procedures conformed to American Heart Association guidelines.
First surgery and pacing protocol.
All dogs received isoflurane general anesthesia via an endotracheal tube. A left lateral thoracotomy was then performed in the 4th intercostal space for optimal visualization of the left superior PV (LSPV). A bipolar screw-in lead was affixed to the LSPV, and the distal end was connected to a Medtronic Itrel neurostimulator. The pericardium was not disrupted. After a 24-h recovery period, the stimulator was programmed to burst pace at a pacing interval of 50 ms for 5 s followed by a 2-s period of no pacing (26). In the first two dogs, a Guidant active-fixation electrode was advanced under fluoroscopic guidance via the right internal jugular vein into the RA to monitor rhythm and verify atrial response to LSPV pacing. The remaining four dogs had only LSPV electrode placement, and rhythm monitoring was recorded intermittently via electrodes placed on the skin. The dogs were checked on a weekly basis for AF induction. The stimulator was turned off to verify underlying rhythms. If AF was documented, the stimulator was kept off for 48 h to document the maintenance of AF. If AF was sustained for >48 h, the pacemaker was turned back on and the dogs were scheduled for a second surgical procedure for mapping and ablation. If sinus rhythm recurred within 48 h, the stimulator was programmed back on to the same protocol and the rhythm was reexamined 1 wk later.
Second surgery for mapping and ablation.
While under isoflurane anesthesia via endotracheal tubes, the dogs were placed in the supine position. The chests were opened via a median sternotomy, and the pericardium was incised and reflected back for exposure of the atrial-PV junction. Bipolar hook electrodes were inserted into the RA, LA, VOM, LSPV, left inferior PV (LIPV), right superior PV (RSPV), and right inferior PV (RIPV) for continuous recording of activity throughout the procedure. Simultaneous computerized mapping of one or more PVs and both atria was also recorded (27). The ablation catheter consisted of seven electrodes at 2-mm spacing with a malleable shaft that could encircle the PVs and apply RF energy to the anterior and posterior aspects. In two dogs, the catheter was hooked to the Cobra RF ablation system (Boston Scientific; Ref. 12) for delivery of RF energy (an average of 60 s per lesion). The temperature was set at 65°C, and the power was set at 50 W. In the other dogs, a 4-mm-tip quadripolar ablation catheter was employed as a roving probe using a Radionics RF generator to create lesions encircling the PVs and on the VOM. RF energy was applied to the epicardial surface along the VOM and each PV within 5 mm of the atrial junction for 1 min at 10 W and 60°C for each application. Electrical recordings were made to ensure that the PVs were electrically isolated. The heart was then fixed with 4% formalin for 1 h and stored in 70% alcohol. The PVs and the tissues overlying the VOM were excised and paraffin embedded. Sections (5 µm) were stained with hematoxylin and eosin for light-microscopic examinations.
Computerized mapping and bipolar electrograms.
Computerized mapping was performed with four electrode patches that were connected to a Unemap 1,792-channel mapping system (Auckland, New Zealand; Ref. 27). Up to four electrode patches were used in the study. Each patch had 448 electrodes, and the interelectrode distance was 1 mm; the patch therefore covered a 1.5 x 2.7-cm area. A patch covering the area between the left atrial appendage and the left PVs was used to map VOM activity. The electrode overlying the anterior aspect of the PV-LA junction was used to map the electrical activity in that area. Electrodes were spaced 1 mm apart in 16 columns and 28 rows; 3 channels from 1 electrode patch recorded the surface ECG. Simultaneous computerized mapping was performed of the RA, LA, VOM, and one or more PVs (LSPV, LIPV, RSPV, RIPV) at baseline and after ablation. Each recording consisted of 8 s of data, which was then analyzed offline according to previously published methods (26). The AF cycle length was calculated based on data obtained from the bipolar electrodes of the mapping system and not from the bipolar hook electrodes. The bipolar electrode used in the mapping system has a small (1 mm) interpolar distance that can register discrete activations even during AF. Therefore, we used bipolar electrograms from the mapping system for cycle length calculations (26). The cycle length is the mean of all AF cycle lengths within a specified area. This method has been used in the past to extract periodicity in noisy time-series signals (4). Activation cycle lengths were determined after each RF ablation. Data are presented as means ± SD. Student's two-tailed t-tests were used to compare the means. Correlation coefficients were calculated between the activation cycle lengths and the numbers of ablations performed. A P value of 
0.05 was considered significant.
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RESULTS
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RF ablation of sustained AF.
Rapid pacing from the LSPV induced sustained AF within 30.6 ± 6.5 days (Fig. 1). There was no clinical evidence of heart failure in any dog. The dogs underwent RF ablation 17.3 ± 8.5 days (7–30 days) after documentation of sustained AF. Successful electrical isolation was documented by the elimination of electrical activity in the SVC and PV (Fig. 2). The ligament of Marshall is located on the epicardium. Successful ablation results in obvious discoloration and charring of this epicardial structure. Four dogs converted to sinus rhythm during RF ablation, whereas two dogs converted within 90 min of completion of RF application (Fig. 3A). In one of the latter two dogs, AF spontaneously converted to atrial tachycardia 78 min later and then to sinus rhythm in 9 min. In the remaining dog, sustained AF converted to atrial tachycardia after thoracic vein isolation. Burst pacing from the RA resulted in tachycardia termination and conversion to sinus rhythm.
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Fig. 1. Induction of sustained atrial fibrillation (AF) by pacing the extrapericardial portion of the pulmonary vein (PV). A: intracardiac electrogram recorded by the pacemaker lead implanted at the right atrial appendage. Pacing lead was connected to a Guidant Discovery II pacemaker. When interrogated, the pacemaker programmer can print out real-time electrograms from the right atrial apex. Atrial (A) and far-field ventricular (V) electrograms are indicated. This electrogram was recorded at the beginning of the pacing protocol within 2 days after surgery. Times when the Medtronic Itrel pacemaker started (on) and ended (off) a cycle of pacing are shown by arrows. Sinus rhythm was present between off and on markers. B: electrogram recorded 4 wk later when the Itrel pacemaker was turned off. Electrogram from the right atrial appendage shows AF. Itrel pacemaker was left in the off mode. C: the dog was still in AF when we returned 48 h later.
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Fig. 2. Effects of radio frequency (RF) ablation on activation patterns recorded by bipolar hook electrodes. A: recordings during baseline AF. Note that the left superior PV (LSPV) has the most complicated and fragmented activation signals. B: recordings during RF application at the orifice of the right superior PV (RSPV). Activation amplitude in RSPV abruptly decreased during RF application (arrow), which indicates successful electrical isolation. There were no activations in the right inferior PV (RIPV), because it had already been isolated. C: only far-field recordings were observed in the four PVs at the end of RF isolation procedures. D: spontaneous conversion of AF to atrial tachycardia 5 min after the last RF application. LAA, left atrial appendage.
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Fig. 3. AF termination recorded by the electrodes of the computerized mapping system. A: a bipolar electrogram recorded from the left atrium (LA) shows AF termination after the completion of RF ablation procedures. B: a bipolar electrogram recorded from the LA shows that burst pacing induces only nonsustained AF after RF ablation procedures.
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Rapid right atrial pacing was successful in reinducing AF in all dogs. However, all induced AF episodes either terminated spontaneously within 60 s (Fig. 3B) or converted to atrial tachycardia before termination (Fig. 4). The average cycle length of reinduced AF was significantly (P < 0.01) slower (183 ± 31.5 ms) than at baseline (106 ± 16.2 ms).
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Fig. 4. Reinduction of AF after spontaneous termination. Electrograms in A and C and the fourth electrogram in B are from the same electrode recording in the left atrial appendage posterior wall. A: AF induced by rapid right atrial pacing (20 Hz, 10 mA). This AF episode spontaneously converted to atrial tachycardia. B: patterns of activation during atrial tachycardia. C: spontaneous conversion from atrial tachycardia to sinus rhythm. Location of the ligament of Marshall, which was ablated, is indicated (dashed line). CS, coronary sinus; LV, left ventricle.
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Effects of RF ablation on AF activation patterns.
Multiple RF applications (n = 15 ± 4 applications/dog) resulted in progressive lengthening of the activation cycle from 95 ± 8.5 ms at baseline to 126 ± 24.6 ms after ablation in RA and from 83 ± 11.4 ms at baseline to 99.4 ± 15.1 ms after ablation in LA. There was a significant positive correlation between the number of ablations and the activation cycle length (RA: r = 0.90, P < 0.01; LA: r = 0.95, P < 0.01).
Computerized mapping demonstrated multiple reentrant wave fronts within the atria. The RA predominantly demonstrated large and fairly organized wave front activity and at times was passively activated from the LA. The SVC was consistently activated passively from the RA. The LA demonstrated multiple small, wandering wavelets with predominantly two identifiable activation patterns: focal activity that 1) propagated from the area of the VOM outward, and 2) originated from PVs and propagated toward the LA and VOM. These findings are consistent with our previous reports (5, 27). After RF ablation, electrical activity within the PV was no longer present (Fig. 2D). Furthermore, when post-RF left atrial activity was analyzed, no wave front activity was noted that extended from the region of the PVs.
Effects of RF ablation on bipolar hook-electrode recordings.
In total, 64 bipolar hook-electrode recordings were analyzed (6 SVC, 8 LSPV, 8 RSPV, 6 LIPV, 6 RIPV, 10 VOM, 10 LA, and 10 RA). Activation patterns from the PVs and the VOM were complex and highly fractionated and were defined as frequent deflections that occurred within <40 ms of one another. PV and VOM (84.7 ± 11.8 ms) activations were consistently faster than the atria. SVC (130.1 ± 19.2 ms) activation appeared slower and more organized compared with the atria and PVs (LSPV, 81.1 ± 9.3; LIPV, 78.8 ± 12.5; RSPV, 80.7 ± 8.2; RIPV, 83.5 ± 16.1 ms). As in previous studies, mean cycle lengths confirmed an activation rate gradient between PVs and the atria. At the end of ablation, activation cycle lengths between the atria and between the LA-PVs (LSPV, RSPV, RIPV, LIPV, and VOM) were not significantly different.
Histopathology of RF lesions.
Transmural lesions were observed in all specimens of the PVs. The Marshall bundles in the ligament of Marshall were also successfully ablated. Typical examples of transmural RF lesions in the PV (Fig. 5A) and the destruction of the Marshall bundle (Fig. 5B) are shown. RF application resulted in hypereosinophilia, basophilia, and loss of cellular details.
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Fig. 5. Transmural lesion induced by RF ablation. A: muscle sleeves of PV. There is full-thickness coagulation necrosis of myocardial cells characterized by increased basophilia, loss of nuclei, and loss of cellular details (hematoxylin and eosin stain, x80 magnification). B: effects of ablation on the atrial wall. There is basophilia of the atrial myocardium (AM) and nerves (N), dilatation of veins (V), and hypereosinophilia of the Marshall bundle (MB) after RF ablation. Whether the tissue appears hypereosinophilic or basophilic depends on the magnitude of the thermal damage (hematoxylin and eosin stain, x16 magnification).
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DISCUSSION
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In this study, we show that rapid electrical stimulation from the LSPV could induce sustained AF. Therefore, pericardial disruption and pericarditis (14) are not the cause of AF in this model. Using this new model, we demonstrated that thoracic vein isolation converted canine sustained AF into sinus rhythm and prevented the reinduction of AF. These findings suggest that thoracic veins are important in the maintenance of AF in this model.
Electrical remodeling and sustained AF.
Traditionally, the mechanisms and maintenance of AF are thought to result from electrical and morphological remodeling within the atria. However, it has become increasingly evident that muscle sleeves within the thoracic veins generate rapid, repetitive activities that serve as triggers in the generation of AF. These rapid activations propagate to the atria and initiate reentry. In normal atria, reentry may self-terminate and result in paroxysmal episodes of AF. Various studies (6, 9, 23) have demonstrated that elimination of these triggers (rapid activations) with RF application results in elimination of paroxysmal AF. For chronic AF, it is generally thought (24) that atrial remodeling provides the necessary substrate for reentry that sustains AF (AF begets AF).
Wijffels et al. (24) reported that sustained (>24 h) AF can be induced in goats with 7 days of rapid pacing. However, the most apparent shortening of the AF cycle length and atrial effective refractory periods occurred within the first 24 h of pacing. Lee et al. (15) reported that atrial effective refractory periods shortened significantly after 1 day of rapid atrial pacing in dogs. These studies show that electrical remodeling occurs within 24 h after rapid atrial pacing in both animal models.
Because atrial remodeling is thought to underlie the mechanism of chronic AF, abolition of triggers within the thoracic veins would not be sufficient to terminate AF. A maze procedure is needed to prevent sustained AF (3). Kress et al. (13) were able to simplify the maze procedure by focusing on PV isolation to terminate chronic AF in a canine model. In the latter study, endocardial ablation was used to isolate the PV and the left atrial appendage. In addition, the authors placed connecting lines between PVs and between the left PV and left atrial appendage. The latter line might have included a portion of the VOM. They were able to terminate chronic canine AF and render it noninducible. In our study, we were able to terminate AF by thoracic vein isolation alone without isolating the left atrial appendage or placing connecting lines between the PVs. Because it was not possible to reinduce AF in these animals, electrical remodeling of the atria alone does not appear to be sufficient to sustain AF in this model.
Importance of thoracic veins in maintenance of sustained AF.
During sustained AF in humans (7) and dogs (10, 17, 26), the LA activates faster than the RA. Small areas of particularly rapid activations can be identified in the PV orifice in humans (7) and in the posterior LA in dogs (17). Williams et al. (25) reported that PV isolation without extensive atrial ablation converted AF to sinus rhythm in 34 of 42 patients (81%) with chronic AF. It was also possible to achieve electrical isolation of the PVs and terminate chronic sustained AF (16, 19, 22). However, not all patients had successful termination with PV isolation. One possible reason for a high rate of failure in some series is that the substrates of sustained AF in many patients are not limited to PVs. Other thoracic veins such as the VOM are also responsible for the maintenance of AF. Complete ablation of these thoracic veins might result in a higher rate of cure. This possibility remains to be proven by studies of VOM isolation in humans. Furthermore, complete isolation of the PVs might be a difficult task if catheter-ablation techniques are used. In this study using animal models, we were able to perform complete thoracic vein isolation via an epicardial approach, which resulted in termination of AF in all dogs studied. Multiple episodes of nonsustained AF were induced after RF ablation to document the absence of substrates for sustaining the AF. Our results strongly support the idea that thoracic veins are important not only as triggers of paroxysmal AF but also in the maintenance of sustained AF (1). These results also suggest that complete thoracic vein isolation might be necessary to cure chronic sustained AF.
How does thoracic vein isolation prevent AF?
We previously demonstrated (27) that there are focal discharges from the PVs during chronic sustained canine AF. Focal discharges are also present in the PVs and VOMs during AF in dogs with congestive heart failure (18). Rapid and fractionated activity is also present within the VOM during permanent AF in humans (8). Because the muscle sleeves of the VOM and PV are insufficiently thick to maintain a transmural reentrant wave front, these focal discharges are most likely due to automaticity and triggered activity, which are known to develop in the PV myocytes as a result of pacing-induced remodeling (2). RF ablation might have destroyed most of the cells in the VOM and near the PV-LA junction, where the majority of the focal discharges originate (27), resulting in quiescent PV and VOM activity after ablation. AF was not able to continue without the focal discharges from the PV and VOM. These data support the idea that in addition to proarrhythmic remodeling in the atria (24), remodeling of the PV cardiomyocytes also plays an important role in chronic pacing-induced AF. RF isolation of thoracic veins stops these focal discharges from reaching the LA and thereby prevents AF.
Limitations.
It is possible that other models of chronic pacing-induced AF (right and left atrial pacing) may also be terminated by PV isolation as was the case in the present model of sustained AF induced by chronic PV pacing. However, we do not have data from this study to test that hypothesis. Our dogs have only been in AF for <30 days. It is possible that dogs with longer or shorter AF duration might respond differently to the thoracic vein isolation than these dogs. Schauerte et al. (20) previously demonstrated that transvascular RF catheter ablation of the parasympathetic pathways can abolish vagally mediated AF. It is possible that some of the results of this study were due to disruption of the fat pads that contain the parasympathetic nerves. Because we did not perform vagal stimulation in this study, we do not have data to prove or disprove this hypothesis.
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GRANTS
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This study was supported by a North American Society of Pacing and Electrophysiology Leonard N. Horowitz Fellowship Award (to A. M. Park); Irvine Biomedical, Inc. and Bayer Yakuhin, Ltd. (to Y. Okuyama); the Cardiac Arrhythmia Research Enhancement Support Group (to Y. Miyauchi); a Cedars-Sinai Electrocardiographic Heartbeat Organization Award (to H. S. Karagueuzian); American Heart Association, Western States Affiliates Grant 0255937Y; a Piansky Endowment (to M. C. Fishbein); a Pauline and Harold Price Endowment (to P.-S. Chen); National Institutes of Health Grants R01 HL-71140, R01 HL-66389, R01 HL-58533, and P50 HL-52319; the University of California Tobacco-Related Diseases Research Program Grant 11RT-0058, and the Ralph M. Parsons Foundation, Los Angeles, CA.
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ACKNOWLEDGMENTS
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The authors thank Rahul Mehra, Bruce Long, and Medtronic Inc. for donating the Itrel pacemaker, and Adam Cates of Guidant Inc. for donating the Discovery pacemaker. The authors also thank Nina Wang, Avile McCullen, Katherine Fu, and Elaine Lebowitz for assistance and Drs. C. Thomas Peter and William J. Mandel for support.
The Unemap mapping system was developed by Drs. Peter Hunter, David Bullivant, and David Budgett of Uniservices and the University of Auckland, New Zealand.
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FOOTNOTES
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Address for correspondence: P.-S. Chen, Cedars-Sinai Medical Center, Division of Cardiology, Rm. 5342, 8700 Beverly Blvd., Los Angeles, CA 90048-1865 (E-mail: chenp{at}cshs.org).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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T.-J. Cha, J. R. Ehrlich, L. Zhang, D. Chartier, T. K. Leung, and S. Nattel
Atrial Tachycardia Remodeling of Pulmonary Vein Cardiomyocytes: Comparison With Left Atrium and Potential Relation to Arrhythmogenesis
Circulation,
February 15, 2005;
111(6):
728 - 735.
[Abstract]
[Full Text]
[PDF]
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Copyright © 2004 by the American Physiological Society.
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