2014 Boston AF Symposium
How ECGI (Non-Invasive Electrocardiographic Imaging) Works
Report by Dr. Steve S. Ryan, PhD
Dr. Michel Haissaguerre of the LIRYC Institute in Bordeaux, France gave a presentation entitled “Mechanistic Insights From Noninvasive Mapping of AF—Implications for Catheter Ablation.”
Dr, Haissaguerre began by discussing the concept of voltage vs. noise in reading an ECG. High accuracy can be obtained with a EGM (electrogram signal) of >0.15mV. Body Filtering (ECGI) can miss small local A-Fib signals, but does not affect global patterns.
He found that when mapping Focal A-Fib signals from both inside and outside the heart, they may differ in location by 3.1mm. (This is a relatively small difference and isn’t enough to affect the overall accuracy of the mapping and ablation.)
How ECGI (Body Mapping) Works
He described how the ECGI system works. A patient lies down on his/her back and a technician places a vest-like device with 256 electrodes over his/her chest and stomach. These electrodes combine with rapid CT (Computed Tomography) scans to produce a very detailed 3D color map of the heart. (For a detailed description and discussion of the ECGI system, see 2013 BAFS: Non-Invasive Electrocardiographic Imaging [ECG])
The system automatically detects rotors and foci and computes them into a “Cumulative Map” or movie. These driver regions are ranked, based on statistical prevalence. Dr. Haissaguerre showed slides of these drivers originating from PVs in Paroxysmal A-Fib.
In persistent A-Fib he found multiple interplaying driver regions (median 4, 1 to 7) found in the Left Atrium, PVs and Right Atrium (“driver regions” include both focal sources and rotors). The rotors were temporally and spatially unstable. They were not sustained. Most had 2-3 rotations with a mean of 448ms. They required a statistical analysis of their core trajectory/density. Patients in Persistent Long-Lasting A-Fib for more than six months had the most driver regions and the least success in A-Fib termination after six months.
…ECGI ablation significantly reduced the amount of burns needed to terminate A-Fib.
Compared to the traditional Bordeaux step-wise ablation for persistent A-Fib, ECGI ablation significantly reduced the amount of burns needed to terminate A-Fib.
Dr. Haissaguerre uses a Multielectrode circular catheter not yet approved for use in the US. This catheter can more easily capture and isolate regional targets like rotors that do move a little.
Dr. Haissaguerre’s Conclusions
- Regional clusters of A-Fib drivers can be mapped non-invasively
- ECGI mapping before a procedure identifies critical regions to ablate. This reduces targeted atrial areas and RF delivery. The optimal timing is in the early months of persistent A-Fib.
- There is a need for appropriate ablation tools (such as circular or multielectrode catheters) as rotor targets are not so limited (they tend to move slightly).
Back in 2013 I predicted that “the ECGI system, barring unforeseen circumstances, will rapidly supersede all other mapping systems and will become the standard of care in the treatment of A-Fib patients.”
Not only does the ECGI system produce a complete, precise, 3D, color video of each spot in a patient’s heart producing A-Fib signals, but also an ECGI can be done by a technician before the procedure rather than by a doctor during an ablation. And the ECGI map is a better, more accurate, more complete map than an EP can produce by using a conventional mapping catheter inside the heart.
From a patient’s perspective, ECGI reduces both the time it takes to do an ablation and the number of burns a patient receives.
The only caveat that Dr. Haissaguerre found (which relate to all mapping strategies, not just to ECGI) is that rotors move slightly and are somewhat unstable. A computer has to be used to statistically analyze their core trajectory. But circular catheters can be used to contain and isolate them.
Addendum: April 2015
Jeffrey Patten asked, “I’ve heard that the new mapping and ablation vest system ECGI (CardioInsight), though very detailed with 256 electrodes, doesn’t directly map the septum area. Is that correct?”
It’s correct to say the ECGI does not directly map the septum area. But, that doesn’t mean the septal activity can’t be mapped with the ECGI.
I posed your question to the world-reknown cardiologist, Dr. Pierre Jais of the Bordeaux group. He explained that “the septal activity projects at the anterior and posterior attachments of the septum on both atria.” He added that mapping the septum with the ECGI system “…requires some experience, but is at the end easy.”
So don’t be reluctant to seek out the new mapping and ablation vest system ECGI (by CardioInsight). Just be sure you have a top-notch, experienced operator.
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Last updated: Wednesday, September 2, 2015
2014 Boston AF Symposium
Cellular Remodeling and Mapping of A-Fib
Report by Dr. Steve S. Ryan, PhD
Dr. Sanjiv Narayan of the University of California, San Diego gave a presentation entitled “Cellular Remodeling and Spatial Mapping of Human AF.” Dr. Narayan is known for inventing the FIRM mapping/ablation system (Topera). (For a discussion of the FIRM system, see BAFS 2013: FIRM [Focal Impulse and Rotor Modulation] for Catheter Ablation of A-Fib by Dr. Narayan of UC San Diego).
Background: Understanding the Firm System. Because the FIRM system uses a proprietary, patented algorithm to identify A-Fib producing spots in the heart, it’s hard to understand and evaluate it. (In a private conversation with someone from Topera, this algorithm is a closely guarded secret like the secret recipe for Coca Cola.) If you’re the type of person who likes to look under the hood of your car and understand the mechanics of how it operates, the FIRM system may be very frustrating. (Continued below)1
SUSTAINING MECHANISMS, SUBSTRATES, CFAES
Dr. Narayan began his presentation by discussing Sustaining Mechanisms (Substrate, CFAEs). (CFAEs are Complex Fractionated Atrial Electrograms [an electrogram is a picture of the electrical activity of the heart as sensed by a pacemaker or catheter in the heart]. They are low voltage electrical signals with very short cycle lengths used to identify areas in the heart that need to be ablated.) (For an in-depth discussion of CAFEs, see BAFS 2011: Using CAFEs in Ablating Persistent A-Fib )
Dr. Narayan identified four different types of non-localized sustaining mechanisms―Collision, Block, Pivot Point and Slow Conduction (see graphic online). But these CFAEs have no discrete target. “Localized ablation can’t work.”
Whereas what Dr. Narayan described as Spatially Localized (”Drivers”) are identifiable A-Fib targets. When one ablates these “(true) sources,” A-Fib is eliminated.
But A-Fib remodeling often leads to ‘substrates’ (CFAEs) that are spatially localized.
ROLE OF PACS
Dr. Narayan discussed the role of PACs (Premature Atrial Contractions) in A-Fib remodeling (‘Substrate’, CFAEs). In describing the findings from his own studies of fibrosis and Stiles’ “Reduced Voltage areas”2, PACs trigger A-Fib. But they don’t in patients without A-Fib.
Advanced or cellular remodeling may be due to APD (Action Potential Duration) Oscillations at slow rates in a rotor pattern, and they enable PACs to trigger A-Fib. In mapping these signals, A-Fib is sustained by spatially reproducible rotors.
DR. NARAYAN’S CONCLUSIONS
• Remodeling is the “rosetta stone” linking basic science with clinical observations of A-Fib.
• Remodeling is spatially non-uniform and regional, that explains clinical observations, A-Fib ‘substrates’.
We still don’t understand how the FIRM system algorithms actually work. We can only speculate that the FIRM mapping system identifies Sustaining Mechanisms (Substrate, CFAEs) that produce rotors and filters out others that don’t. However, unless someone “leaks” the algorithms, we’ll probably never know and be able to compare and evaluate the FIRM system.
Dr. Narayan’s findings about PACs (Premature Atrial Contractions) is most important for A-Fib patients. Doctors tend to dismiss PACs because everyone gets them. But as many people with A-Fib know all too well, PACs often precede an A-Fib attack. Dr. Narayan’s studies show that PACs trigger A-Fib attacks, but they don’t in people without A-Fib. And PACs can be very disturbing, even if they don’t trigger A-Fib, particularly in people who’ve had a successful catheter ablation and are A-Fib free.
Can ablation techniques or meds be developed to eliminate PACs and thereby eliminate going into A-Fib? Should EPs ablate for PACs even without A-Fib? (I know of one EP who does ablate for PACs, even in the absence of A-Fib/Flutter.)
Many EPs map and ablate CAFEs (Sustained Mechanisms, Substrates) when trying to “cure” patients in Persistent A-Fib. But according to Dr. Narayan, ablating these areas is ineffective “Localized ablation can’t work,” because there is no discrete target as there is for areas producing rotors. (The ECGI system also seems to identify foci and rotors as compared to CFAEs.) For patients, Dr. Narayan’s observations may result in much less unnecessary burning and scarring of the heart during an ablation procedure.
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Last updated: Wednesday, September 2, 2015
- But here’s a possible way the FIRM system could possibly be evaluated. Take a standard Lasso mapping catheter or a system like ECGI and meticulously identify every possible A-Fib producing spot in, for example, an animal or human heart in long-term persistent A-Fib. Such a heart usually has many different A-Fib producing spots. Carefully mark the exact location of every foci, rotor, potential, CFAE or any spot producing possible A-Fib signals. Then immediately afterwards, use the FIRM mapping system on the same heart and compare the results. The FIRM system usually finds only one or two A-Fib signal sources in each atria. The FIRM algorithm probably filters out a lot of other A-Fib signal sources as noise. What does the FIRM system filter out? What does it select?
In the live satellite case presented at the 2014 Boston A-Fib Symposium in Orlando, the Bordeaux group using the ECGI system found many different foci and rotors in a patient in persistent A-Fib. But these were clustered in predominantly three areas. Would they show up in the FIRM system as only three foci/rotors?
Patent Law: The algorithms to analyze MRI slices, such as used by Dr. Marrouche, or the algorithms to map electrophysiology, such as used by Topera, have to be kept secret. Dr. Marrouche and Topera really have no choice. According to current US patent law (which I highly disagree with), you can’t enforce a patent on a medical technique. But you can for a surgical technique. For you legal types, the statute reads “35 USC 287(c) (1) With respect to a medical practitioner’s performance of a medical activity that constitutes an infringement under section 271(a) or (b) of this title, the provisions of sections 281 , 283 , 284 , and 285 of this title shall not apply against the medical practitioner or against a related health care entity with respect to such medical activity.” This law effectively makes any patent on a medical technique worthless. (Thanks to David Pressman, Patent Attorney for this important observation.)↵
- Stiles MK, John B, Wong CX, et al. Paroxysmal Lone Atrial Fibrillation Is Associated With an Abnormal Atrial Substrate: Characterizing the “Second Factor”. J Am Coll Cardiol. 2009;53(14):1182-1191. doi:10.1016/j.jacc.2008.11.054.↵
2014 Boston AF Symposium
Fibrotic Atrial Cardiomyopathy (FACM)
By Steve S. Ryan, PhD
Dr. Hans Kottkamp of the Hirslanden Hospital in Zurich, Switzerland presented the concept of “Fibrotic Atrial Cardiomyopathy (FACM)” in his talk entitled “Fibrotic Atrial Cardiomyopathy – Implications for Catheter Ablation of AF.”
TYPES OF A-FIB substrates
Dr. Kottkamp discussed two types of substrates (or genotypes) of how A-Fib develops:
- “Focal” A-Fib with the trigger as the only driver and with no (or very limited) structural atrial remodeling over time (even decades or “forever”).
- A-Fib due to a severe underlying structural heart disease, e.g., mitral stenosis which causes significant structural remodeling.
Then he proposed a third type:
- A-Fib as a manifestation of a pre-existing “Fibrotic Atrial Cardiomyopathy (FACM)” which can be mild (I), moderate (II), or severe (III). FAMC involves structural remodeling in a potentially progressive disease process. FAMC may explain what was characterized as “Lone” A-Fib with no previously identifiable cause in an otherwise healthy patient.
(Cardiomyopathy is a heart condition or disease in which the heart muscle is weakened and the heart’s ability to pump blood is impaired. For example, fibrous tissue may partially replace the heart muscle, disabling the heart so that it no longer functions properly and blood no longer moves efficiently. Cardiomyopathy is often accompanied by atrial fibrillation. Dr. Kottkamp’s concept of “atrial cardiomyopathy” isn’t the same thing as normal cardiomyopathy in which the ventricles are impaired.)
PREVIOUS STUDIES OF FIBROSIS
At last year’s Boston A-Fib Symposium (see BAFS 2013: A-Fib Produces Fibrosis—Experimental and Real-World Data), Dr. Kottkamp cited several studies which indicated that A-Fib doesn’t seem to always produce fibrosis, where there is a great variability in the degree of fibrosis.1 This is in contrast with Dr. Jose Jalife’s experimental studies of sheep where A-Fib clearly produces fibrosis (see BAFS 2013: A-Fib Produces Fibrosis—Experimental and Real-World Data). In the real, messy world it isn’t always as easy and clear how to isolate the mechanisms that produce or limit fibrosis. As Dr. Kottkamp points out, sheep are not humans. Fibrosis may work differently in humans compared to animal models like sheep. (Of course it would be unethical to experimentally produce A-Fib and fibrosis in humans as one can in animal models.)
Dr. Kottkamp cited his and other researchers’ histological data and showed slides of heart cell tissue which showed in his analysis that:
- The hypothesis that fibrosis progresses systematically from paroxysmal to persistent A-Fib was not confirmed.
- While there was a tendency of increased mean fibrosis level in patients with persistent vs paroxysmal A-Fib, the variation within the two groups was very high.
- No correlation at all could be detected between patient age and increase in the extent of fibrosis or fatty changes in atrial tissue.2
- Atrial samples taken from age-matched A-Fib-free patients contained negligibly low amounts of fibrofatty tissue despite similar clinical high-risk profiles.3
Similar to Dr. Nassir Marrouche’s Utah Stages I-IV, Dr. Kottkamp showed slides of paroxysmal patients with No Fibrosis (no FACM), Mild Fibrosis (FACM I), Moderate Fibrosis (FACM II), Severe Fibrosis (FACM III).
WHAT DR. KOTTKAMP’S RESEARCH MEANS FOR A-FIB PATIENTS
According to Dr. Kottkamp, what FACM means for patients:
- In patients with “Focal” paroxysmal A-Fib (no or almost no fibrosis [No FACM], PV isolation can (almost) be considered curative. Though there are relatively rare cases of extra-PV foci in these cases.
- In patients with FACM I AND II (similar to Utah Stages II and III) the ablation cannot really “cure” the underlying disease FACM. However, in many of these cases, ablation can effectively treat the arrhythmia A-Fib which in many patients is the only clinical manifestation of the FACM disease.
- While patients in FACM III (similar to Utah Stage IV) are very hard or impossible to cure with today’s standard catheter mapping and ablation techniques.
Dr. Kottkamp’s conclusions:
- Circumferential PV isolation is a cornerstone treatment for most patients with paroxysmal A-Fib.
- The concept of FACM as a primary atrial disease explains recurrences of paroxysmal or even persistent A-Fib after a period of stable Sinus Rhythm after a previous PV isolation by the potentially progressive nature of the FACM disease (which is independent of the arrhythmia).
- In patients with A-Fib recurrence after durable PV isolation, the ablation strategy can be targeted to the individual substrate localization.
- In patients with more advanced substrates (FACM II-III), additional substrate modification may be reasonable in patients with persistent A-Fib already in the first ablation session.
Dr. Kottkamp’s concept of Fibrotic Atrial Cardiomyopathy may become important in our understanding of A-Fib, though it needs further studies to determine how it develops and progresses, how it differs from fibrosis measurements like Utah Stages I-IV, how best to quantify and measure it, etc.
Dr. Kottkamp’s concept that Lone A-Fib may come from Cardiomyopathy, that “Lone” A-Fib isn’t really lone or idiopathic but may come from a form of Atrial Cardiomyopathy may be an important thesis for future research. It may explain why some paroxysmal A-Fib patients have extensive fibrosis, while others don’t. (Though there are other factors which may produce fibrosis as well as Cardiomyopathy.)
Dr. Platonov’s finding that age doesn’t relate to fibrosis is certainly good news for patients. It indicates that just because we are getting older, our hearts aren’t automatically developing fibrosis. (Though we do know that A-Fib is associated with aging of the heart. As patients get older, the prevalence of A-Fib increases, roughly doubling with each decade.4 This suggests that A-Fib may be related to degenerative, age-related changes in the heart.)
Contrary to Dr. Jalife’s experimental studies with sheep which showed that A-Fib produces fibrosis, Dr. Kottkamp’s studies indicate that in the real world fibrosis doesn’t progress systematically from paroxysmal to persistent A-Fib. But his studies did show that there was more fibrosis in persistent vs. paroxysmal A-Fib patients. And that people without A-Fib compared to age-matched patients with A-Fib, had “negligibly low amounts of fibrofatty tissue (fibrosis) despite similar clinical high-risk profiles.”
Even though animal models like sheep aren’t perfect, studies like Dr. Jalife’s are scientifically sound and very convincing. Sheep hearts seem very similar to human hearts for all practical purposes. As patients with A-Fib, we have to base our medical decisions on the conclusion that A-Fib produces fibrosis (Dr. Kottkamp disagrees with this conclusion); that if we stay in A-Fib over a significant period of time, we will progressively develop fibrosis which is currently irreversible. However, as Dr. Kottkamp points out, it isn’t inevitable that everyone will develop fibrosis to an equal extent. This is consistent with Dr. Jalife’s studies in which even sheep with the same environment, diet, similar gene pool, etc. did differ in how fast they developed fibrosis.
Return to Index of Articles: AF Symposium: Steve’s Summary Reports
Last updated: Wednesday, September 2, 2015
- Mahnkopk, C. et al Evolution of the left atrial substrate in patients with lone atrial fibrillation using delayed-enhanced MRI: implications for disease progression and response to catheter ablation. Heart Rhythm. 2010 Oct. 7(10):1475-81 http://www.ncbi.nlm.nih.gov/pubmed/20601148 doi: 10.1016/j.hrthm.2010.06.030. Epub 2010 Jul 1.↵
- Platonov, PG et al. Structural Abnormalities in Atrial Walls Are Associated With Presence and Persistency of Atrial Fibrillation But Not With Age. J Am Coll Cardiol 2011;58(21):2225-2232. Last accessed 4/1/14 http://content.onlinejacc.org/article.aspx?articleid=1147757. doi:10.1016/j.jacc.2011.05.061↵
- Calkins, H, Berger, R. Atrial Fibrillation: Management Strategies. Scientific American Special Health Reports. Last accessed August 24, 2015. URL: http://tinyurl.com/Calkins-A-Fib-Mgmt-strategies, p. 9.↵
Live via Satellite—Seven Catheter Ablation Cases: Impressive Educational and Technical Achievement
By Steve S. Ryan, PhD The most impressive technical achievement of the Symposium was seven live satellite ablation cases including one from Siberia. The satellite cases alone were worth the price of admission.
In previous Symposia two or three satellite cases would be interspersed with pre-recorded videos. But this time they scheduled seven live cases back to back and for some events, even intercut between locations. Note: Throughout the Symposium doctors would often describe a particular device but not name it or the company which produced it. They probably wanted to avoid any conflict of interest or didn’t want to appear to favor one device or procedure over another. But I did research after the presentations and for the most part, I have identified and noted the name and manufacturer of particular devices that were demonstrated.
- The Netherlands: part 1. part 2
- Siberia. Russia
- Bordeaux, France: part 1, part 2
- Milan, Italy
- Frankfort, Germany
- Michigan, USA
- Boston, USA
Drs. Mark La Meir and Laurent Pison of Maastricht University Medical Center in the Netherlands performed live a hybrid surgical and catheter ablation. The patient was a very large man with significant body mass, exactly the type of patient often referred for surgery by EPs. It’s difficult for current ablation mapping technologies such as fluoroscopy to see clearly through significant body mass. Several ports were cut in between the rib openings on one side of the chest. (I neglected to count how many and apologize for this oversight.)
The robotic camera and operating instruments were inserted through the various ports. With this system the patient did not have to go on bypass. His heart was still beating when the surgical lesions (RF burns) were made. He did have to have one side of his lungs deflated and re-inflated in order to fit the AtriCure bipolar RF clamp around the pulmonary veins. This same procedure was repeated on the other side of the chest after the live presentation.
The images transmitted by the robotic camera were remarkably clear and vibrant. The clamp was inserted around each vein. 5-6 burns at a median output of 10 to 15 W were made on each vein to ensure transmurality. A roof line was also made. [I apologize for not being able to follow what additional lesions or burn patterns were made.] It was remarkable how big the patient’s Left Atrial Appendage was and how active and rapidly it pumped into the ventricle along with the left atrium. It was fascinating to watch the surgeons position the AtriClamp on the LAA and close it off.[After the LAA is closed off, I’m told it eventually shrivels up like a dried grape. Partially because his LAA was so large and active, this patient will likely experience a significant loss of pumping volume in his left atrium after closing off his LAA. But he probably wasn’t very active any way and may not even notice the change.] They did not perform ablation of the ganglionated plexi areas. “There is until now too little evidence to advocate a systematic ganglionated plexi ablation strategy.”1
Probably one of the most technically difficult cases to schedule and coordinate was a live presentation from Siberia. (One can only imagine the effort it must have taken to pull this off!) Dr. Evgeny Pokushalov and his colleagues at the State Research Institute of Circulation Pathology in Novosibirsk, Russia worked on a 55-year-old female patients who had high blood pressure that couldn’t be lowered by drugs or other methods and who had A-Fib. She had a moderately enlarged left atrium (5.2mm) and a CHA2DS2-VASc score of 2. (Hypertension [high blood pressure] is a well-recognized trigger or cause of A-Fib, probably because of the extra pressure and stress it puts on the Pulmonary Veins where most A-Fib develops. This patient’s A-Fib probably was caused and sustained by high blood pressure.)
Dr. Pokushalov and his colleagues first did a normal PVI checking for Entrance and Exit Block and waiting 40 minutes to see if recurrence occurred before completing the PVI. They then mapped and developed a 3-D image of the artery and its branches leading to the kidneys just as EPs do when mapping and doing an ablation of the heart’s left and right atria. They made ablation burns within the artery branches leading to the kidneys (renal denervation) at 10 Watts for 6 seconds thereby reducing Sympathetic Tone (the functioning of the Sympathetic Nervous system). They made four burns in each artery branch, but they acknowledged that this field is so new they don’t know if this is the best technique. “What is a clear end point? How many burns are enough?” It’s not like doing a PVI catheter ablation where one can see the patient return to sinus rhythm.
They said they’ve done over 100 of these renal denervations with no complications. They use the same catheter as for PVI ablations. They said they need to use more sedation than with a normal Paroxysmal PVI ablation. (Research has shown that when one partially ablates the nerves going to the kidneys, this can significantly reduce blood pressure in people who can’t otherwise lower their hypertension. It also seems to diminish A-Fib attacks. These four burns in each artery branch didn’t seem to affect the integrity of the arteries.)
Later in the Symposium different presenters discussed the just released findings of the Medtronic Symplicity HTN-3 trial which basically found that Medtronic’s system – though safe – was no better than a sham procedure for reducing office systolic blood pressure through six months. What this means is that renal denervation, although performed frequently in Europe and in other parts of the world, will not be approved in the U.S. in the foreseeable future. (The clinical trials Symplicity 1 and 2 seemed to produce good results and had a clear therapeutic effect. Other data have shown that renal denervation reduces blood pressure in animal models and in smaller human trials. One doctor speculated that the artery nerves are very deep and that in the Symplicity 3 trial the energy level used may not have been high enough to penetrate to the nerves.)
Attendees seemed shocked and disappointed at this news.
Everyone, both doctors and patients, expected and hoped renal denervation would work. For some patients, who had tried everything else, it was their only hope to reduce their high blood pressure. There are many other methods being tested to denervate the renal arteries. But because of this news, one company has already announced it’s halting its trial. Until the data from Symplicity HTN-3 can be more thoroughly examined, renal denervation may be dead in the water.
Editor’s comments: This ultimately may not be a bad thing. It points out the importance of well-performed trials to prevent the premature adaption of therapies [whether procedures or drugs] until they are thoroughly studied. It’s difficult when the expected benefits of renal denervation are so high, when patients know about it and request it, and when the procedure is recognized as safe. But in spite of its promise and the data coming from Europe, preliminary findings from the Symplicity HTN-3 study indicates that renal denervation doesn’t work.
They then cut back to the Netherlands to show the catheter ablation part of the operation. The EP used a Lasso catheter inside the heart to confirm that the pulmonary veins were indeed isolated.
The EP basically continued the lines inside the heart that the surgeon had created outside the heart. The EP also ablated the right atrium for Flutter which current surgical approaches can’t do. The EP also ablated the Coronary Sinus. They mentioned that if someone has been in Persistent A-Fib for over three years, the success rate drops by 25%. If someone has had a previous heart operation, they generally can’t undergo this Hybrid Operation. Their goal is to return a patient to sinus rhythm during the operation. If they have to cardiovert someone to return them to sinus rhythm, the operation isn’t as successful.
They talked about making a box set of lesions in the posterior left atrium to “debulk” that area, to stop A-Fib signals from propagating through the left atrium substrate which is often necessary in cases of persistent A-Fib.
Dr. Mélèze Hocini of the Centre Hospitalier Universitaire De Bordeaux was introduced with her arms poking through arm holes in what looked like a Plexiglas type of shield, undoubtedly to protect her from radiation during the ablation.
In the beginning Dr. Hocini couldn’t hear Dr. Ruskin and Dr. Mansour in Orlando. But that problem was soon resolved. (She was very poorly lit with low production values.) Dr. Hocini’s 61-year-old male patient had been in Persistent A-Fib for four months. Such cases are generally the hardest to cure. Someone in Persistent A-Fib has usually been in A-Fib for a long time and has often developed many A-Fib producing spots throughout the left and right atria. In this type of case, a simple Pulmonary Vein Isolation Ablation (PVI) usually won’t terminate A-Fib.
The patient also had a huge left atrium (59mm) and a lot of fibrosis (22%). In the MRI fibrosis scale he would have been classified as a Utah 3. All the attendees recognized that this was a difficult case.
This was a truly ground-breaking presentation and historically an important milestone in the treatment of A-Fib.
For the first time the world saw the ECGI (body surface) imaging and mapping system in action and in practical, day-to-day use. Instead of having to spend a great deal of time and effort [and radiation exposure] mapping and hunting down the multiple A-Fib-producing spots in the heart, this was all done beforehand for Dr. Hocini using ECGI.
The day before his ablation, the patient simply laid down with a special vest on his chest like having an ECG exam with 256 electrodes rather than just twelve. These electrodes, imaged on the patient by a CT scan, produced an exact 3-D image of his heart and, what was most innovative, identified and labeled the location of all the spots producing A-Fib signals. This 3-D rendering of the left and right atrium with CT scan showed many different foci and rotors in the patient’s heart, but they seemed to cluster in three distinct areas. ECGI established a hierarchy of where to ablate. One starts where the most foci and rotors are.
Fibrosis doesn’t guide the procedure or change this hierarchy at the present time. Rotors are generally found next to or bordering areas of fibrosis in preliminary data. We then saw Dr. Hocini ablating the areas that showed up on the ECGI. For an extensive discussion of ECGI, see my reports under the 2013 Boston A-Fib Symposium.
From Milan, Italy. Drs. Claudio Tondo, Gaetano Fassini and Antonio Bartorelli of the Centro Cardiologico Monzino, University of Milan, Italy did a live insertion of a new Left Atrial Appendage (LAA) closure device available in Europe but not currently approved in the US. The patient receiving the device was a 72-year-old man in Chronic A-Fib who had a history of intestinal and cerebral bleeding. He also had a stroke risk score of four which meant he needed to be on anticoagulants and protected from having an A-Fib stroke.
The Coherex WaveCrest occluder they installed looked like a piece of white foam with little barbs or hooks which attached the device to the LAA but were small enough that they wouldn’t puncture it. The device collapsed so that it fit on the end of a catheter which they maneuvered into the left atrium and into the LAA using fluoroscopy (X-ray) imaging and ICE (Intracardiac Echo).
They had different sizes and shapes of these occluders to fit patients’ different LAA openings. Once inside the LAA they opened up the device, like opening up an umbrella, and attached the hooks. They weren’t happy with their first two tries and re-collapsed the device and repositioned it in the LAA a third time.
To check that they had good contact and closure, they injected dye from the tip of the catheter to see if any would flow past the device into the left atrium. Then they simply withdrew the catheter, leaving the occluder in place in the LAA. This whole procedure seemed really simple to perform, though these doctors developed this facility only after years of study and experience. And it didn’t take long to do. (I know an EP in Los Angeles who installs the Watchman device in an average time of 20 minutes.) Anyone thinking of having a LAA occluder device installed could benefit from seeing this Left atrial appendage (LAA) Animation by Coherex. It’s reassuring to see how apparently easy it is to install.
Editor’s comments: Regarding A-Fib Stroke Risk, Blood Thinners and Occlusion Devices
One of the most difficult tasks of a Cardiologist/Electrophysiologist (EP) is to determine, along with the patient, whether or not someone in A-Fib has a real need to be on anticoagulants. Blood thinners are not benign drugs. They’re not like taking vitamins. Current anticoagulants have their own set of risks and, in spite of the ads you see on TV, they are not to be taken lightly.
This 72-year-old man had a high A-Fib stroke risk score and certainly needed protection from an A-Fib stroke which can be a fate worse than death. In A-fib the upper part of your heart (the left atrium) doesn’t pump out properly but instead fibrillates. Large clots can form usually in the Left Atrial Appendage (LAA) where 90%-95% of A-Fib clots come from. These clots are usually much larger than a “normal” clot. When they break loose and are transported to the rest of the body, they can completely close off a vein branch and cause a lot of damage.
But when this 72-year old man took blood thinners, he suffered intestinal bleeding and cerebral hemorrhaging. This unfortunately happens all too often when one has to take anticoagulants especially as one gets older, and is part of the risk/reward ratio doctors and patients have to agonize over. Since he couldn’t tolerate blood thinners, this 72-year-old man decided to have his LAA closed off, where 90%-95% of A-Fib clots come from. It’s not an absolute guarantee he will never have an A-Fib stroke. There’s still that 5%-10% chance. But it’s probably his best option.
If you can’t tolerate blood thinners or just don’t want to take them, you may want to check out LAA occlusion devices like the Watchman, Lariat II or AtriClip. Your doctor can discuss with you the strengths and weaknesses of each device. The Watchman is still in clinical trials in the US, but was recently approved by an FDA advisory panel.
LAA occlusion devices do reduce blood flow in your heart which may be a concern if you are young and exercise regularly. But if you’re in your 70s or 80s and/or aren’t very active, this probably isn’t something to worry about.
Dr. Hocini in France and Drs. Michele Haissaguerre and Pierre Jais in Orlando pointed out that many foci in persistent A-Fib patients are found in the left and right atrial appendages. This patient’s inferior left atrium, as is often the case, had the highest number of rotors.
They discussed the fact that rotors do seem to drift somewhat. But they can be broken up or stopped from rotating by cross hatch ablations or other techniques such as using the newer circular wide area ablation catheters to encircle and block off the rotor areas. Thanks to ECGI this procedure used much less RF energy and needed much less RF burns than the old five-step protocol, which was good both for the patient and for the operating doctor. Later in the day Dr. Ruskin announced that this patient’s persistent A-Fib was eventually terminated and that he was in normal sinus rhythm.
They then cut to Frankfurt, Germany. Drs. Boris Schmidt and KR Julian Chun of the Cardioangiologisches Centrum Bethanien performed a CryoBalloon ablation (“ICE T concept”) using the new, second-generation Arctic Front Advance Cardiac Cryo Ablation catheter (Medtronic) with eight cooling ports instead of four.
The patient was a 61-year-old female in Paroxysmal A-Fib for two years. They used a temperature probe in the esophagus (as in RF ablation) The temperature in the esophagus should not go cooler than +12°C. Therefore they stop the freeze at +15°C. In contrast, if the CryoBalloon temperature goes beyond -60°C, they stop the freeze rather than complete the ablation. In Germany they have been using the CryoBalloon catheter for years before it was approved by the FDA for use in the US. Their results have been very good. The process of making the CryoBalloon ablations seemed amazingly fast.
We then were transported to Royal Oaks, Michigan. Dr. David Haines of William Beaumont Hospital performed a thermal balloon ablation for paroxysmal A-Fib. The Toray Satake Hot Balloon Catheter is named after its inventor Dr. Shutaro Satake of the Hayama Heart Center in Japan who was with Dr. Haines.
The balloon is filled with a solution of saline. When radio frequency energy is applied through a coil electrode in the balloon, this heats the saline. Dr. Haines maneuvered the balloon into a pulmonary vein opening. When he pressed the balloon into the PV opening, the compliant material of the balloon seemed to mold itself to the shape of the opening. He would apply heat to the PV opening for around 2½ minutes and heat it to 70 degrees Celsius. He used an esophageal probe to measure heat and a special cooling system in the esophagus. He also paced the phrenic nerve to make sure it wasn’t damaged by the heat.
Dr. Satake has performed over 500 ablations in Japan using this Hot Balloon catheter. One would expect applying this much heat to an extensive area of the PV openings would carry an increased risk of stenosis, a swelling of the pulmonary vein opening restricting blood flow. But Dr. Haines says this has not been the case. (For a detailed description of the thermal balloon catheter, see the subheading “Radiofrequency ‘Hot’ Balloon” in the article, “Balloon Catheters for Ablation“.) In an interesting juxtaposition during Dr. Haines’ presentation, the satellite program cut back to the Frankfurt group who were doing CryoBalloon ablations. They had completely isolated all four pulmonary veins in 60 minutes. That’s a very short time to do a catheter ablation PVI.
They then cut back to Dr. Haines who finished his ablations with the Hot Balloon catheter. NOTE: Dr. Haines and three other centers are recruiting patients for preliminary clinical trials of the Hot Balloon Catheter. The other centers are Mount Sinai in New York (Dr. Vivek Reddy), Texas Cardiac Arrhythmia Institute in Austin (Dr. Andrea Natale), and the Medical University of South Carolina in Charleston (Dr. J Marcus Wharton).
Editor’s comments: As a patient you may be asking which of these different catheter balloon strategies would be the best for me. It’s far too early to tell with the Thermal Balloon until it gets further along in clinical trials. But from what I’ve seen, I’m willing to speculate. Because the thermal Balloon is more compliant and flexible than the CryoBalloon, when it’s pushed up into a pulmonary vein, it probably burns higher up into the vein than the CryoBalloon. This combined with the RF heat would seem to be more apt to produce stenosis than the CryoBalloon. And stenosis is something patients need to avoid if at all possible. Unlike most other catheter ablation complications which are temporary and fixable, stenosis is permanent and usually irreversible. If you develop stenosis, your life is wrecked.
CryoBalloon catheters are more rigid than the Thermal Balloon and, when sized properly, usually only freeze on the outside edges of a pulmonary vein. Because pulmonary vein openings aren’t perfectly round, it may take two or three CryoBalloon placements and freezes to completely isolate around a vein. But this is relatively easy to do.
Freezing creates a different kind of ablation than thermal RF. One advantage of Cryo is that, if the Balloon is improperly positioned, the preliminary freezing can be stopped and the area allowed to defrost and return to normal. This isn’t possible with thermal RF.
A freezing ablation looks different than a thermal RF ablation. There is no burn scarring. Frozen ablated heart tissue looks very similar and seems to have an integrity similar to that of normal heart tissue.
When the CryoBalloon is positioned against a vein opening, the preliminary freezing action sticks the balloon to the opening (like a kid sticking his tongue to a frozen lamp post). It’s harder for flowing blood to push the CryoBalloon away from the vein opening or create gaps.
Someone asked me why most of the world leaders in A-Fib ablation haven’t moved to CryoBalloon ablation, since it seems to be easier, faster and safer for patients than regular RF ablation. Most likely because they are so experienced and skillful with RF point-by-point ablation and get such good results, that for them RF ablation is as easy and fast as CryoBalloon ablation. And they generally work in the antrum and don’t get near the pulmonary vein openings. But this is definitely a question I need to ask these A-Fib leaders. Right now I don’t have the answer.
The last live case was from Massachusetts General in Boston with Drs. Kevin Heist and Moussa Mansour. The title of their presentation was “Radiation Reduction Strategies During Catheter Ablation of AF.” The patient was a 61-year-old female with a history of persistent Flutter. She also had three right veins instead of the normal two. (I have the same unusual anatomy.) The doctors used an innovative Electromagnetic Navigational System integrated with fluoroscopy (X-Ray). (Mediguide system, with NavX mapping, an externally irrigated ablation catheter and a pent array mapping catheter.)
It produced 3-D color images of the left and right atrium. You could see in real time the catheter electrode making burns. The doctors explained how this system used only 2-3 minutes of fluoroscopy compared to a normal ablation which could produce 38 minutes of radiation exposure. This was most welcome news for the attendees doing catheter ablations.
Editor’s comment: Radiation Reduction is a concern not just for patients, but especially for doctors, nurses and staff in the cath lab during ablations. I was recently in a cath lab and observed several ablation procedures. I and everyone there had to wear a leaded waist belt, vest and thyroid protector. The doctor doing the procedure wore special anti-radiation glasses to protect him from retinal radiation damage. These leaded protectors are not light. The floor is padded to make it easier for the EP to stand with all this weight. Doctors may do 3-4 ablations a day and are exposed to a lot of fluoroscopic radiation. Doctors and others in the cath lab worry about being exposed to so much radiation and its long-term effects. Anything that will lower exposure to radiation in the cath lab is important both to patients and particularly to doctors.
SUMMARY OF THE SATELLITE EVENTS
These live satelite events were extremely informative and educational. And as a five-and-a-half hour event, quite an accomplishment. Having worked in broadcast television and on several Live TV events (i.e.; the live EMMY Awards Presentation show, broadcasting of the 1984 Los Angeles Olympics and numerous sporting events for NBC), I know this was an incredibly complex event.
The staging teams had to coordinate and intercut between multiple satellite and trans-oceanic optical fiber video feeds. But before that, the planning teams had to schedule and coordinate multiple locations, with multiple cameras, audio and lighting personnel and equipment in order to video the numerous doctors working in their respective operating rooms and EP labs. (Not to mention dealing with the multiple languages spoken by the doctors and their staff).
Frankly I doubted they could pull it off, especially since the Symposium was held at a new conference site. But, WOW! From the audiences’ perspective the presentations were seamless and, except for some audio problems, the presentations came off perfectly. (Though I’m sure the behind-the-scenes people were pulling out their hair trying to make everything work.)
Return to Index of Articles: AF Symposium: Steve’s Summary Reports
Last updated: Wednesday, September 2, 2015
- Pison, L. et al. Hybrid Thoracoscopic Surgical and Transvenous Catheter Ablation of Atrial Fibrillation. Journal of the American College of Cardiology, Volume 60, Issue 1, July 2012. http://content.onlinejacc.org/article.aspx?articleid=1208681↵