Trials and Fibrillations with Dr John Mandrola

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10 facts about catheter ablation of atrial fibrillation in 2012

Nov 13, 2012 09:19 EST


Earlier this year, I wrote (on DrJohnM and theheart.org ) that catheter ablation of atrial fibrillation had become an easier journey. The short story is that AF ablation is a heck of lot easier now.

In May 2012, at the Heart Rhythm Society meeting, a study called RAAFT 2 reported that ablation of AF, performed as a first-line strategy, was superior to rhythm-control drugs. This was news, because most experts believed ablation should be recommended only after a trial of AF drugs had failed. Although markedly positive, this abstract has yet to be published in a peer-reviewed journal.

Last month, a similar study was published as the lead article in the New England Journal of Medicine. The MANTRA-PAF study compared an initial strategy of AF ablation vs rhythm drugs in patients with low-risk but bothersome AF.

The results of this small study, which recruited patients from 2005 to 2009 (in AF ablation time, eons ago) and employed an outdated ablation strategy, were less positive than many expected. Using an intention-to-treat analysis, the northern European researchers found no difference in overall AF burden between patients treated initially with ablation vs drugs. After two years, however, ablation looked better, with 85% success in the ablation group vs 71% in the drug group. Adverse events were similar in both groups, although one death occurred as a result of the procedure. Notable details include:

  • Crossover was common: 36% of those in the drug arm crossed over to ablation. Intention-to-treat analysis means they are still counted in the drug-treatment group.
  • Well more than a third of those in the ablation arm required two procedures. And more than two procedures were required in nearly 8%.
  • Patients enrolled in this trial had low-risk profiles and intermittent AF. Those with coexistent diseases or more advanced cases of AF (persistent) were excluded.
  • The ablation strategy was outdated: The end point of ablation was diminution of electrograms inside the line of ablation. It is now universally accepted that complete pulmonary-vein (PV) isolation is critical for success. Perhaps equally important was that linear ablation across the left atrial roof and other lines were used. This is no longer the accepted practice for intermittent AF. Routinely adding ablation outside of PV isolation increases the risk of proarrhythmia and paradoxically, probably decreases the success rate.

When the procedure that dominates your practice makes the lead article in the NEJM, it seems a good time to reflect on focus points that come up in the shared decision-making surrounding the decision to ablate in the left atrium.

Here are 10 basic principles of AF ablation:

1. AF ablation works by electrically isolating areas of the atrium that are important for the initiation or maintenance of atrial fibrillation. Usually these areas involve the muscles sleeves surrounding the pulmonary veins. (Why these areas are so important is a bit of a mystery.) Exciting research looking into finding other important areas to ablate in the atrium shows great promise.

2. After more than a decade, AF ablation has evolved into a routine procedure. Ablating AF encompasses the overwhelming majority of my practice. It's normal. We easily do two AF ablations in a day. In our lab, what was once a four- to five-hour marathon is now a two-hour well-practiced procedure.

3. For patients, AF ablation is still a very serious procedure. It means being under general anesthesia for two to three hours in the EP lab and having 40 to 70 ablation lesions (burns) made in the left atrium of the heart.

4. The safety of the procedure has improved over the years. This stems mostly from the growing experience of human operators. Yes . . . in something as intricate as AF ablation, the safety of the procedure depends mostly on another human being, not a checklist.

5. Point-to-point delivery of radiofrequency lesions in a beating heart took a really long time to learn. It's all about feel, and neural pathways from hand to brain and then back to the hand. It's rewarding because it exemplifies the best of medical practice: a hard-learned skill delivered skillfully in the right patient can make a difference. Every day in the office, I see multiple patients who used to have AF.

6. One of the greatest drawbacks of AF ablation is the need to redo the procedure. Recurrent AF occurs in too many ablation patients—up to 30% to 40% in honest reports. In nearly all redo procedures, the problem is gaps in conduction block between the pulmonary vein and left atrium. Again, it's not exactly clear why these gaps occur, though lack of transmural burns is the leading hypothesis. Good AF ablationists understand the importance of making each burn effective and continuous, but the technology is not quite there yet. It's hard to make continuous lines with dots.

7. The good news about redo procedures is that they frequently are easier than the first. The reason is that closing gaps often entails doing just a couple of burns. I like to say the majority of the electric fence is made; all we have to do is close a few areas of leaks. The exception here is when AF recurs in diseased atria. Then, extensive ablation lines may be needed to curtail atrial flutters.

8. In addition to well-honed neural pathways of the operator, the success of AF ablation depends on patient selection. Electrically isolating the pulmonary veins works to control AF when those areas are driving and maintaining AF. This is most often the case with intermittent AF, less often with persistent AF, and rarely with long-standing AF. Structural disease of the left atrium predicts lower success rates with catheter ablation .

9. Less is more also applies to AF ablation. A truism: one can always burn more, but one can never undo a burn. Ablation in the left atrium cuts both ways. On the one hand, it's important to thoroughly isolate the areas causing the AF, but on the other hand, it's now clear that doing extra ablation—with point burns or lines—only increases the risk of arrhythmia. Also, too much ablation-related scar can limit atrial contractile ability, which defeats the purpose of a "rhythm-control" strategy.

10. On severe complications like stroke, cardiac perforation, damage to the esophagus, and paralysis of phrenic nerves: although increasingly rare and dependent on operator skill, these are important statistics to acknowledge. Last year I presented our AF ablation experience as an abstract at the American Heart Association meeting. We detailed four major complications that occurred in 282 procedures. The rate of complications of an operator and institution should be a knowable number. The published data suggests a 2% to 5% risk of complications. Common thinking has it that academic centers of excellence have lower rates of complications because of experience. Perhaps yes, but it's also possible that real-world AF ablation centers, which have small numbers of dedicated operators who are not involved in training young doctors and have grown in experience, may now be capable of producing competitive outcomes.

Take home:

The decision to ablate atrial fibrillation must be a shared one between an empowered patient and enlightened ablationist. Nobody needs an AF ablation. Patients with refractory AF must know that to rid themselves of symptoms and improve their quality of life, they must endure the procedure and risk a complication. They must also know that AF responds best to ablation in its earlier stages.

We know a lot about AF ablation, but much remains to learn. The main question: Will ablation of AF improve long-term outcomes, like stroke, heart failure, and death? Preliminary data look favorable, but for now, we simply don't know. We also don't know what to do with nonsymptomatic patients. I recently saw a 38-year-old man with newly discovered nonsymptomatic AF that persisted after drug therapy and cardioversion. He had a tough choice: be in AF for the rest of his life or have a couple of AF ablations and sinus rhythm? It's been only six months, but he is sinus rhythm after two ablations.

JMM








Your comments
10 facts about catheter ablation of atrial fibrillation in 2012
# 1 of 6
November 13, 2012 05:29 (EST)
Michael Safani

I would appreciate it if you send me the abstract you presented at the AHA meeting as referenced above.

 Thank you

# 2 of 6
November 14, 2012 12:00 (EST)
Dr. Val
Excellent summary. I have a "loved one" who has a complicated cardiac history. About 7 years ago he c/o shortness of breath and was found to be in heart failure from rapid a. fib. He was heparinized and cardioverted and remained in (we think) sinus rhythm for about 5 years. Then two years ago he was found to be in a fib/flutter on a regular EKG. He was cardioverted and NSR lasted a couple of months. The cardiac electrophysiologist felt that flutter was the underlying trigger for the a fib, so he underwent a flutter ablation procedure. He remained in NSR for a year until he was found to have a new right-sided MI on EKG. A stress test revealed severe blockages and he had a CABG x3 with a left atrial appendage removal while they were at it. After the CABG he has had paroxsysmal a fib ever since. He is asymptomatic, and the a fib seems to be slower than previously. He's on a beta blocker and aspirin. My concern is the possibility of the heart failure returning if he is left in a fib, and I wonder if a fib ablation could reduce that risk? Our educated decision at this point is to simply go the "watchful waiting" route. Are there any additional risks related to waiting that I may have missed?
# 3 of 6
December 3, 2012 12:00 (EST)
Cardiology Resident

The "patient" had 3 vessel coronary artey disease. Probably also other risk factors for heart disease. FA was caused by these pathologies. The heart failure was part FA, part CAD.

FA paroxysms in the present stage are less dangerous now that the myocardium is revascularized via grafts. Also myocardial ischemia is not causing FA. Amiodarone is probably the only possible drug treatment apart from betablockers to inhibit FA but may be contraindicated for other reasons. The future therapeutic intervention is probably not FA ablation because it sounds like this may not be ideal patient for that (LA size? age?) but AV ablation + pacemaker if FA paroxysms are detrimental to health. 

# 4 of 6
December 13, 2012 02:59 (EST)
David Ward
Blog taken down
I was looking for my comments on this article but they have been taken down including John's reply and some others. Why is this?
Author's disclosure (Dec 13, 2012)
I have no relevant disclosures to make in connection with this topic.
# 5 of 6
December 13, 2012 09:02 (EST)
Steven Rourke
migration to new platform
Dr Ward - we transferred the blogs to a new platform and have had a couple of technical glitches including the temporary misplacement of some blocks of comments. We are working to bring them back and apologize for this mishap.
Steven Rourke
theheart.org
Author's disclosure (Dec 13, 2012)
Editorial director, theheart.org
# 6 of 6
March 20, 2013 07:44 (EDT)
David Ward
Where is my blog?
Hi Steve, I enjoy this column but would like to see my blog back up. Can you point me please?
Author's disclosure (Dec 13, 2012)
I have no relevant disclosures to make in connection with this topic.

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About the author

Dr John Mandrola practices cardiac electrophysiology in Louisville, KY. He finished training at Indiana University in 1996. His practice encompasses catheter ablation, including an eight-year experience with AF ablation, device implantation, and consultative EP. Outside of the EP lab, Dr Mandrola's two hobbies include competitive cycling and writing. He has maintained a medical, fitness, and cycling blog, Dr John M, for the past two years.