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Get in Rhythm. Stay in Rhythm.™ View Replays from Atrial Fibrillation Patient Conference Aug 4-6, 2017, in Dallas, TX
Get in Rhythm. Stay in Rhythm.™ View Replays from Atrial Fibrillation Patient Conference Aug 4-6, 2017, in Dallas, TX

Surgeon Discusses Evolution and Future of Atrial Fibrillation Maze Procedure

Video of Presentation by Dr. James Edgerton from Boston Atrial Fibrillation Symposium 2009

Video of Presentation by Dr. James Edgerton from Boston Atrial Fibrillation Symposium 2009

Febuary 17, 2009 8:21 AM CT

Cardiothoracic surgeon Dr. James Edgerton of The Heart Hospital Baylor Plano (Plano, TX) spoke at an evening presentation at the Boston Atrial Fibrillation Symposium 2009 about the evolution and future of surgical procedures for atrial fibrillation.

Notes about the video:

  1. The video begins four minutes into the presentation and does not include the early evolution, but the slide for that is included at the end of the transcript below.
  2. The video involved some compromises—I could either get close enough to capture the audio, or far enough back to video the slides, so I compromised to accomplish both as best I could. You may need to turn your PC speakers way up. You can also follow along using the transcript if the audio is muffled. You can pause the video to catch the slides. Though not ideal, the content is most important, and this is a rare opportunity for afib patients to see this content.
  3. For those who are squeamish, be aware that this presentation includes videos from actual surgeries.

View the video:  Dr. James Edgerton on Atrial Fibrillation Maze Procedure Evolution

About James R. Edgerton, MD:

A board-certified cardiothoracic surgeon, Dr. Edgerton practices at The Heart Hospital Baylor Plano in Plano, TX. He was recently appointed Adjunct Assistant Clinical Professor at the University of Texas at Arlington and serves as Chair of the Education Committee for the non-profit Cardiopulmonary Research Science and Technology Institute (CRSTI).

Dr. Edgerton began his medical journey in 1974 and received his M.D. Degree from the University of Illinois. He then completed a six-year General Surgery Residency at the University of Florida where he took time out to work full time in the Basic Cardiac Research Laboratory. Dr. Edgerton completed his Cardiothoracic Surgery Residency at the Medical University of South Carolina. Prior to moving to Dallas, Dr. Edgerton founded and led the Great Lakes Cardiothoracic Surgery Associates in Southeast Wisconsin. Earlier, he had served as Medical Director of Cardiac Surgery at Saint Mary's Medical Center in Racine and as the Surgical Director of the Debakey Heart Institute of Wisconsin.

A frequent speaker on topics such as beating heart surgery, the surgical treatment of atrial fibrillation and resynchronization therapy, Dr. Edgerton is an invited lecturer and course director to dozens of national and international education symposiums and has performed cardiac operations and taught surgical techniques on four continents.

Dr. Edgerton is a Diplomate of the American Board of Medical Examiners; a member of the American Association of Thoracic Surgeons (AATS), and is a Full Fellow in the American College of Surgeons and the American College of Chest Physicians. He is also an active member of the Society of Thoracic Surgeons (STS), serving as Chair of the STS Workforce of Practice Education and Board Member of the STS Council on Member Education.

Dr. Edgerton's Profile  Contact info

Video Transcript:

Surgical Procedure Evolution – Now & Future

(Note: Video begins about 4 minutes into the presentation. Initial slides are below.)

We call failure any episode that is greater than fifteen seconds of atrial fibrillation, atrial tachycardia, or atrial flutter.

This is what those patients look like [at 6 months] in the paroxysmal group. If we look at ECG alone, it is very successful; if we add longer-term monitoring, we are down to 81% success, which we thought was respectable. If we look at our persistent and long-standing persistent population, it's a 54% success rate and that is not very good, certainly not for a surgical procedure because this isn't the sort of thing that we can repeat very easily.

If we look at the 12 month experience again for the paroxysmals it may be respectable, but if you look at the persistent and long-standing persistent population, it is clearly inadequate therapy that we were accomplishing, so other than getting the left atrial appendage off, half of these patients were left still with significant burden of atrial fibrillation.

We concluded from that that a minimal access maze is effective treatment for paroxysmal atrial fibrillation, that a more extensive lesion set may be necessary for persistent and long-standing persistent afib, and that follow up by screening ECG alone over estimates success by at least 20%. We now know it is higher than that and that longer term monitoring is essential for accurate determination of elimination of atrial fibrillation.

But why didn’t this work for persistent? As you're sitting there saying, "It's the substrate, dummy; we could have told you this wouldn’t work because of the electrical remodeling that is going on."

So our next step was then to try to replicate the lesions of the Cox maze III that we know, we think we know, has a pretty good success rate, although I will caution you that in the paper they published saying that they have a 95% success rate in ten years, the way those patients were surveyed was a telephone call—"Hello, are you having any afib? No. Thank you. Good bye." That was the follow up.

So we tried to undertake a way to add these two lines in the minimal access approach and that is difficult, particularly when you get to the line across the isthmus to the mitral valve, there are three inhibitors to placing that line. Number one, in the beating heart, particularly in the fluoroscopic view, there is no visualization back there and it is a very difficult area to work. Secondly, when working from epicardial to endocardial, you risk damage to the circumflex coronary artery, which of course is overlying the area. And finally, the epicardial landmark to the mitral valve annulus is the coronary sinus, and we know that's an inconstant landmark—it can get to 13 millimeters away, or worse 3 to 4 millimeters away. If I aim for that, I leave you [the EPs in the audience] with the potential for a terrible left atrial tachycardia that I'm asking you to ablate.

Well we thought we came up with a successful approach to this. In 2006, we began working in the transverse sinus when we realized we can connect to the mitral valve, instead of posteriorly across the isthmus back here where we have to encounter the circumflex coronary, if we go up to the anterior annulus all we really have to do is touch the fibrous trigone, which is nonconductive and is in continuity with the mitral valve and I have an epicardial landmark for that, which is the junction of the non coronary cusp, right here, and the left coronary cusp at the base of the aorta.

You saw already that we can see into the transverse sinus beautifully, so now we have an epicardial landmark where we can connect to the mitral valve annulus. What that looks like, in another view, it's right here, we can connect across here, and drop our line down here, take off the appendage, make a little line to the appendage, and we have replicated all the lines of the Cox maze III procedure. That lesion set looks like this.

So we undertook to do that. This is another little diagram of what that looks like. You’re looking at the transverse sinus again. This is the metal-tipped sucker that has the aorta elevated. Here's the left atrial appendage peeking through from the left side. This is the muscular dome of the left atrium. I want you to see the fibrous trigone—it is white. Can you appreciate that there is an indentation here that is the junction of the noncoronary cusp and the left coronary cusp? It is easier to see if I make it move. You can look right down in here and see the junction of the noncoronary cusp and left coronary cusp, and that white is the left fibrous trigone. So all I have to do is burn to there and I've touched the mitral valve. 

For the skeptics, here’s the 2D echo with the ablating probe located in exactly that spot and I am wiggling it. I think that you can appreciate that I’m touching the anterior leaflet of the mitral valve here. We’ll withdraw that probe and it makes it a little easier to appreciate the aortic valve, which is in continuity with the mitral valve there. 

This is just another little view of the anatomy of the transverse sinus. Here we are looking over the superior vena cava into the transverse sinus, the left main, the junction of the noncoronary cusp and the left coronary cusp, the muscular dome of the atrium there, or I could lift up the superior vena cava—I am not sure if we do it in this view or not—look underneath and see the same thing. It is a pretty good view of the atrial musculature dome through the transverse sinus, behind the aorta, and behind the pulmonary artery and the other side, which is bifurcated, sending the right pulmonary artery branch right here. It’s called the muscular dome of the left atrium.

This is the Coolrail device, making that lesion that I just talked about down to the left fibrous trigone. What I’ve done is put some fixed electrodes on either side of this lesion—I think that Sonny [Jackman] is going to talk about that in a little bit, about what we use those electrodes for—to help map to see whether or not we have a complete line. You can see the line, at least epicardially, and it looks pretty good.

Now if we move over to the left side, then we just need to complete these lines. This is a view from the left side, with the left atrial appendage flopping in the breeze. Again this is all through the five millimeter thoracoscope, and when we look into the transverse sinus here, you should be able to see my lesions coming from the other side. Over here is the Ligament of Marshall and right superior pulmonary vein. We just have to connect that over to here, divide the Ligament of Marshall, circle the pulmonary veins, drop a line to the base of the atrial appendage, and we're done. The left side is actually pretty easy once you have completed the right side. Can you appreciate the burn mark coming from the other side?

We undertook to do 10 cases like that. They had a significant burden of atrial fibrillation. The left atria were a little generous in these patients and 3 were persistent and 7 long standing persistent. Again this was the lesion set that they had. This is what the follow up was. We got a little bit better. There was one patient that refused to wear the two week monitor, but we had event monitors on 80%, pacemaker interrogation on one, and 24-hour Holter on one of the screeners at the airport who would not wear the monitor for two weeks. We used again the consensus statement guidelines for definition of success, and this is what the results looked like, with a 50% success rate—not terribly different from the 46% rate we had before. We were pretty disappointed with this.

If we look at the way they failed, one patient had a single episode—these were all persistent and long standing persistent patients—one had two episodes, one had six episodes, and two patients were still in pretty much continuous atrial fibrillation. Three of these patients were pretty happy, but we weren’t happy because that is not the definition of success. So why didn't that work?

It was about this time that I was getting a better appreciation for this anatomy, and was afraid that I had an incomplete line underneath the superior vena cava. I realized at that time that there is a very thick fat pad there and it is very constant on every patient. I also didn’t know how to test for block and we needed Sonny to come to the operating room with us and teach us how to do that.

So here is that fat pad that I am talking about, the superior vena cava, right atrium, right superior pulmonary vein, and look at all this fat that blocks between the superior vena cava and the muscular dome of the left atrium. Fat is a little bit of an insulator for RF energy. If I try to burn through that—again same view in a different patient—superior vena cava, right superior pulmonary vein, I lifted the superior vena cava up, and I was trying to burn through all this fat down to the muscle of the left atrium and I was afraid that I was having an incomplete line there. So I learned to start taking all this fat down thoroscopically and this is a view of dividing all that fat so that you can start to appreciate I'm going to get down to the muscular dome here, as we come across, just how thick and wide this fat pad is, very constant and always there.

What amazes me isn't that I finally appreciated that this fat pad is there, but that I didn’t see it for the last twenty years that I have been operating on hearts. It is there every time so once we get all that cleared off, we're pretty much down to good muscular atrium, and then started adding this additional dissection to the procedure moving forward.

Sonny was kind enough to come teach us a method for determining block across these lines so we added intraoperative testing for block at the same time and I won’t dwell on this. Sonny, you're going to talk about this, correct? I will move on and let him address this topic.

This is what it looked like in the next 23 patients and that's where we are today. Actually we are about five patients beyond this now. In the next 23 patients, we had 10 persistent and 13 long standing persistent, and again generous left atriums. The follow up was the same, event monitors on 73%, pacemaker interrogation on 26%, and we eliminated the Holters finally. That makes my results look a lot better not having Holters on everyone, and this is what it looks like now. At 6 months, 20 of the 23 were free of any episodes of atrial fib, atrial tachycardia, or atrial flutter on at least 2-week monitoring or continuous monitoring by pacemakers—84% of long-standing persistent, and 90% of persistent. Again I am encouraged by the failures because they're not failing as persistent. These are very happy patients and they are failing under fairly low burden of atrial fibrillation. So, this is early and it's a small series, but we're encouraged by the results.

This is where we've brought ourselves to today, taking this totally endoscopic route. I believe that this can be done sub-xiphoid with a little bit more creativity, some use of non-visual imaging, and further development in the enabling technology by working in partnership with industry.

I always include this picture into the workings of my mind—this bridge. I had an extra day when I was over talking in Bangkok. I didn't realize that the Bridge over the River Kwai was just 90 kilometers outside of Bangkok. Nor did I realize there were two bridges—I thought there was just that bamboo one that we all saw in the movie. All the young people in the audience are going, "what movie?" The Allies bombed this and they took down the center two sections. The bamboo bridge is long gone but they have since rebuilt the center section. That just annoys me when that happens in atrial fibrillation—when I bomb something, I want it to stay interrupted. Thanks for your attention.

Presentation Slides:

Evolution of Surgery for Atrial Fibrillation

1980:  Left Atrial Isolation
1982:  Catheter HIS Bundle Ablation
1985:  Guiradon Corridor Procedure
1986:  Atrial Transection
1987:  Cox Maze
1992:  Maze III
1999:  Beating Heart Maze
2004:  Minimal Access Beating Heart Maze

Surgical Procedure Evolution: The Future

2004:  Minimally Invasive Pulmonary Vein Isolation, Wolf
2005:  Targeted Partial Autonomic Denervation, Jackman
2006:  The Trigone Connection, Extended Lesion Set
2007:  Demonstrate Block of Linear Lesions
2007:  Determine Midterm Outcomes with Extended Lesion Set
2008:  Develop Easier Method of Confirmation of Block of Linear Lesions
2008–2009:  Totally Endoscopic Approach
2010:  Sub-Xiphoid Approach

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Last Modified February 17, 2009

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