Today is the third and final day of the Boston AF symposium. (My editorial comments in italics.)
Dr Hugh Caulkins started the day by reviewing the major clinical trials of AF ablation. A lot of these I have written about previously. One of the most pivotal trials to mention is CABANA. Here, investigators are enrolling symptomatic AF patients to either ablation or continued drug therapy. They seek to discover whether ablating AF reduces hard endpoints like stroke or death. It’s been hard recruiting because many patients want ablation. Another challenge for investigators is that technology is changing quickly. So once this data is published, the procedure will surely have been advanced.
Dr David Wilbur spoke about late recurrences of AF after ablation: Most late recurrences are still related to PV connection. But…Very late recurrences may be from non-PV sources. As time goes on after ablation, non-PV sources of AF become more important. Also relevant to long-term results is disease progression. High blood pressure, obesity, sleep apnea and advancing age all contribute to recurrent AF long after ablation.
Possible solutions for limiting late recuurences Dr WIlbur suggested, should be multifaceted: attention to blood pressure, obesity, stress, and sleep. These are the so-called “upstream” therapies. His biggest advice: “These are your patients for life; prepare them for that.”
Of course that line hollers at me–as I tell patients of the ‘journey,’ that is AF treatment.
Dr Gerhard Hindricks (Germany) presented more information on late recurrences after AF ablation. He is famous for his intense follow-up. They use ILR (Implantable Loop Recorders) to assess for AF recurrences. Their 10 year data shows that AF continues to recur over time. But he asks, are late recurrences of AF really late, or are they persistence of early episodes?
Basically, his ILR data show that ‘true’ late recurrences of AF are uncommon. Most of the AF that occurs late was picked up in the earlier period of monitoring. He called this information ‘encouraging.’ The message is that if patients make it through the early period without any AF, they will likely do well in the long term.
He also mentioned monitoring products that may come available in the future: one was a better ILR–the other an injectable ILR.
In the Q/A, he said that ILR recordings are a tool for research, not routine clinical use. Dr Jais raised an important point: He suggests that the use of only 30 seconds of AF to define failure of ablation is too rigorous. “We should not expect ablation patients to have less AF than the age-matched peers. He rightly said that monitors done in normal people (without AF) often show more than 30 seconds of arrhythmia
Good point here.
Dr Young-Hoon Kim (South Korea) addressed the issue of whether (or when) we should recommend AF ablation in patients with typical flutter. (Remember: flutter ablation is easy and low risk, AF ablation is much higher risk and much more complicated.)
He went on to tell us some important facts about AFL and AF. The likelihood that AF develops in cases of atrial flutter not treated with ablation approaches 60%. Secondly, ablation of AFL does not eliminate the chance of getting AF. More than 30% and up to 80% of patients who get AFL ablation develop AF. Importantly, there are risk factors that predict the chance of AF after AFL ablation. These include: a prior history of AF, congestive failure, advanced age and large atrial size.
This was an important issue because it comes up a lot in the real world. It’s even more pressing in South Korea because patients can have only two ablations in their entire life. (Think government control of healthcare. ) If a Korean AF patient has one ablation for flutter that leaves only for when they develop AF.
My thoughts on this matter our changing. As AF ablation gets easier and safer, I more often recommend that flutter patients consider having AF ablation if they have had AF episodes along with flutter. An important issue about doing AF ablation preventatively is that many patients will not ever get AF, and thus we risk over treating patients–a bad thing.
The next sessions dealt with ablation strategies to treat persistent AF: A very controversial topic.
First up was Dr Frank Marchlinski: He presented the UPENN approach to persistent AF. They do pulmonary vein isolation (wide circles), give adrenaline to look for non-PV triggers and do right AFlutter lines when indicated. They don’t do lines nor do they chase complex fractionated electrograms (CFAE). They do not believe in substrate modification.
He reviewed their RASTA study: (Circ A and EP; 114 (3) 91-95): A comparison of three ablation strategies: PVI/triggers, PVI/triggers + burns at common sites of triggers, PVI/triggers + CFAE. Group 2 had a slightly higher success, but the real message was all patients taken back for second procedures had reconnection of PVs. “To really change success rates for any kind of AF ablation, we need to achieve more durable PV isolation.” He also added the obvious: all other strategies to ablate AF cannot be assessed until durable PV isolation becomes commonplace.
Dr Pierre Jais presented the Bordeaux approach to ablation in persistent AF: Their approach is called the stepwise approach, where they do PVI, CFAE ablations and then they make lines. They like to terminate AF or at least organize the fib to flutter and then target these more organized rhythms. Not much is changed in their approach from last year. It’s an aggressive approach that entails doing a lot of ablation. They feel that PVI alone is not adequate in advanced AF.
The sense that I get though is that the AF ablation community is moving away from the Bordeaux approach of making lines.
He was asked about rotors and the future–as he ended his talk with FIRM-guided videos. Dr Jais posited the future of AF ablation will incorporate mathematics and engineering.
This is cool. I think this was a subtle shout out to Dr Narayan’s work.
Dr Moussa Mansour (Mass General) spoke on the role of terminating AF during the ablation. He gave the MGH approach which is to ablate extensively in the left atrium until they get termination. It’s a similar approach to Bordeaux.
Not much new here. MY problem with these extensive strategies are numerous. One that we have seen, when we were using the extensive ablation approach, was the recurrence of atrial flutters, which are really bothersome to the patient, and frequently led to more complicated second and third procedures.
Dr Karl-Heinz Kuck reports on five-year outcomes after ablation for persistent AF using the Hamburg approach. The Hamburg approach includes mostly just PV isolation alone. They rarely ablate any other areas, unless there is spontaneous arrhythmia or the patient cannot be successfully cardioverted. On redo procedures, they do repeat PV isolation and rarely do extra ablation. This is a true minimalist approach.
He reported a 200+ group of patients with very advanced persistent AF (mean duration of AF 4 years, 60% had failed Amio). They found long-term success with one procedure to be quite low at 26%. WIth multiple procedures, the success rates increases to 45%. They also added a finding that patients who had more than 2 years of persistent AF have a much lower chance to maintain SR with a minimalist approach. (Not surprising.)
When asked about the future, Dr Kuck said that his dream (“a small dream”) was that earlier intervention will prevent progression to more advanced AF. Along these lines, he announced a brand new European AF ablation trial called ATTEST. The investigators have introduced a new endpoint: the time to conversion into persistent AF. They want to know whether early ablation of AF may help reduce the progression to persistent AF.
My take: Dr Kuck’s thesis is that efforts to intervene with catheter ablation in later stages makes little sense. Not only are success rates lower, but the amount of ablation needed defeats the point of getting the patient to regular rhythm. What’s so appealing about his early intervention strategy in AF is that it parallels the best approach for coronary heart disease. It’s always better to prevent severe disease rather than trying to treat it after the fact.
Dr Andrea Natale presented data on AF ablation in patients with prosthetic heart valves: Patients with prior MV surgery do poorly with just PVI. He admonishes ablators to look for other non-PV triggers of AF in these difficult patients. Dr Natale still persists in advocating for isolation of the left atrial appendage. This is a very controversial topic, as most (a clear majority) feel that it is a bad idea to render the appendage non-contractile.
Dr Ralph Damiano (St Louis) presented the surgical approach to persistent AF. Surgical ablation data from St Louis, where they use the Cox-Maze procedure is impressive. They take on all forms of AF, failed catheter ablation patients and even those with huge left atria. Despite dealing with more advanced AF, the Cox-Maze procedure boasts near 90% long-term success. The problem of course, with Cox-Maze is that it includes major open heart surgery on bypass.
He also reviewed the much smaller evidence base for less invasive approaches to surgical ablation–approaches that get to the heart through the side of chest and without the need for bypass. These smaller studies hint that success rates are good, but the data is scant. He cited the FAST trial, which I have written about previously. Dr Damiano mentioned that the learning curve for surgical ablation is quite steep and bleeding with ‘less-invasive’ surgery can be catastrophic.
My bottom line: Surgical approaches to AF offer more durable lesions and probably higher long-term success, particularly in more advanced cases of AF. The problem is that these procedures are clearly not less-invasive.
The next sessions were on lesion monitoring and new technologies:
Dr Larry Chinitz presented encouraging data on using contact force sensors to guide more effective lesions. It will be awhile before US doctors get to use contact force. That’s too bad because it looks promising.
Dr Pierre Jais spoke about the use of intracardiac ultrasound to guide lesion formation. This too, is futuristic. One thing that he emphasized was that just using impedance measurements and electrograms to assess burn quality isn’t ideal. Again, more technology for the future.
Dr Mousa Mansour presented the data on systems that allow direct visualization of the burn. These were mostly animal studies on new catheter designs. Future stuff.
Dr Kuck again presented early data on a new way of measuring temps during burns. They are testing a novel catheter that uses microwave technology to measure and control power during burns. Again, more technologic attempts to make better burns.
Dr Nassir Marrouche (Utah) reviewed the role of MRI imaging in assessing and improving burns. I have the same comments as his previous talks: widespread use of MRI is way in the future.
Dr Keane (Ireland) talked about the utility of making lines with ablation catheters. He reviewed the current technological limitations of making continuous and durable lines by making single RF burns. (Think how hard it would be to draw a line by making dots.) Dr Keane then reviewed the current evidence base supporting line-making. Despite citing huge numbers of studies, he admitted there exists no real answer.
Like all of AF, the ability to sort out the incremental value of adjunct techniques is limited by the inability to get durable PV isolation.
I don’t make lines unless I need to.
That’s all folks. Heading to the airport.
As always, I learned a ton.
15 replies on “Day 3 Boston AF Symposium: More rough notes.”
John, thanks for the 411. See you next week.
Thanks, John. Excellent summary of the meeting, even better than last year..
…we really should be contributing towards your meeting registration fees!
That would be nice, because Boston AF costs more than an iPad!
Thanks for the summary, very useful. When is anyone going to agree that we should stop ablating persistent af? (46% success with 2 procedures?!)
For the 46%, it was good. This is the problem–knowing the 46%.
As always… terrific synopsis and written in a way that a non-doc can understand. Thanks.
Thanks for saying.
Nice and balanced report.
However your statement on the the appeal of an early intervention for AFib (resembling prevention of CHD) is not fully appropriate since in AFib, the intervention involved is highly invasive (in contrast with quitting smoking, taking statins, …).
Your are correct. Though not all early intervention of AF has to be invasive. I should have mentioned effective interventions like getting adequate sleep, managing stress and avoiding ingestion of cardiac irritants.
I think there is a typo here, but I can’t figure out what’s missing or incorrect:
“He went on to tell us some important facts about AFL and AF. The natural history of flutter without ablation approaches 60%.”
What is that 2nd sentence communicating?
Pretty impressive pick up for a business guy. I fixed it.
Basically, if you leave flutter unablated, fib is highly likely to occur, but even if you ablate AFlutter, this does not eliminate the chance of having AF. Here’s the thing though: in cases of flutter alone, sometimes fib develops into an issue and sometimes it doesn’t. You don’t know until flutter is gone.
my perceptiveness is perhaps aided by my 2 ablations for AFlutter and my quest for knowledge that has accompanied. I have some clients that might be amused by the “business guy” description. (I’m a lawyer, but at least a business lawyer.)
Thanks for all the info. This blog is a great resource.
Firstly, thanks so much for posting the info & insights into Boston 2012. Absolutely fascinating for someone who is interested in the science as well as in not ever going back into AF!
I also checked out the symposium program along with your notes, and with what looks to be a representative and broad view in the sessions of the current state-of-the-art, one thing stuck out so strongly for me – absolutely no mention of further work on neural influences.
My AF started in ’94 and by 2002 was almost permanent, before I had a PVI & top-up in Bordeaux, now 9 years of almost freedom from AF. Both before and after the ablations, my AF was strongly and classically vagally-mediated, and having read deeply starting with Coumel’s papers, found I could have more influence on episodes than drugs, statistically speaking. I KNEW and still know from long personal experience of the effects of a tendency to a low resting HR, being a pretty fit individual (though not an elite athlete by any means), a long standing IBS-like situation, triggers from eating, sleeping, learning tricks like jogging up the stairs to raise my heart rate to tip me back out of Fib, etc. It’s still like this 9 years after ablation – if I get indigestion, I get ectos, short tachy runs, I clear the indigestions it all stops. Disopyramide was a wonder drug for me at one point (pre-ablation). One reversion to AF 2 years ago for several hours during a period of stress, one near-episode 1 year ago similarly under stress, and the last 3 months being on the edge of AF due again to very high stress levels at work, with probably an ANS “on fire” and sympathetic and para-sympathetic fighting each other for this period before I stepped out of the role I was doing at work and it has all settled back to what it was – minor ectos and a smile on my face.
I know many others over the years who have similar influences. Neural influences have made it into current AF Guidelines whereas they were barely recognised when I first presented, but they don’t appear to be a major focus.
With what, to me as a sufferer, is such an obvious and influential factor, why does there appear to be so little work apparently done on neural influences? One or two abstracts I have seen suggest that even the neural influencs in the heart can even *create* the conditions for the heart tissue to tip into AF susceptibility.
I just feel that a trick is being missed here. I’d be interested to hear your thoughts, if you have time. Thanks again
You and one of the most famed electrophysiologist, Dr Sonny Jackman see eye to eye. Sonny and my former mentor, Dr Douglas Zipes, have been proponents of studying the neural inputs of the heart.
No doubt, vagal influences are very important in AF. And also as you suggest, vagal inputs are especially prominent in many athletes. For awhile there was a push to ablate specifically to target neural inputs. This hasn’t panned out, but it does not mean neural influences are not important.
Glad your new life changes have settled the AF–a scenario I hear often
Dr J, Thanks. Glad to hear research is still being done. And that’s a couple more names for me to plug into pubmed!
Since my post, I found a short biography of and interview with Phillipe Coumel on hrsonline.org He described AF as a: ” â€œtriangleâ€ of arrhythmogenesis with three main factors interacting to produce arrhythmia: the arrhythmogenic substrate, the triggering factors and modulating factors, the dominant one being the autonomic nervous system.” Nice way to think of it. In the interview he also says that when he started looking at it, “all of them [the other researchers] totally ignored” this area. “This was wrong”.
So I really look forward to new developments in due course.