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.
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FIRM ablation: So much hope and excitementJul 23, 2012 16:30 EDT
You have likely seen the exciting news concerning AF ablation. More than a year after it was presented at HRS 2011, the Conventional Ablation for Atrial Fibrillation With or Without Focal Impulse and Rotor Modulation (CONFIRM) trial has now been published in the Journal of the American College of Cardiology.1
This might be a turning point in the treatment of AF ablation. AF patients and doctors have been waiting a long time for a treatment more satisfying and successful than pulmonary vein isolation. Patients often ask me: "What causes AF? How do you know my pulmonary veins are causing my AF?"
Yes, these are good questions.
Some thoughts from the real world on focal impulse and rotor modulation (FIRM) ablation:
When I talk with family members immediately after an AF ablation, they often ask what I found.
That's the thing about contemporary AF ablation: In most cases, we don't often find things; we simply use ablation to isolate the pulmonary veins--areas that often (but not always) initiate or drive AF. It's an anatomically based procedure, and mostly, it's the same. This one-procedure-fits-all approach differs greatly from focally targeted procedures used to ablate all other arrhythmia. In atrioventricular nodal reentry tachycardia (AVNRT), we target the slow pathway; in Wolff-Parkinson-White (WPW) syndrome, the accessory pathway; and in ventricular tachycardia (VT), important areas in and around the scar. That's because, unlike in AF, we understand the mechanisms of these arrhythmias.
Thanks to the work of Dr Sanjay Narayan and colleagues, our understanding of human AF may have expanded. The old thinking of AF perpetuation had multiple wavelets propagating through structurally diseased atria. AF persisted as long as enough wavelets continued. For more advanced cases of AF (persistent AF), this theory led to treatments that aimed to debulk the atria into smaller sections of tissue, which would then prohibit propagation of wavelets. As a strategy, surgically debulking the atria is limited by its invasive nature and the potential for disrupting long-term atrial transport function. Similarly, attempts to debulk the atria with catheter techniques have been severely limited by poor durability of ablation lines. Gaps in conduction leading to electrical reconnection predispose to postablation atrial flutters, which are often more problematic than AF. Alas, these aggressive ablation therapies risk making AF therapy worse than the disease.
And another unknown: Not all post-AF ablation patients with gaps in pulmonary-vein (PV) connection have recurrent AF. What's happening here? In these cases, ablation has stopped AF without isolating the PVs. What have we ablated?
In the spirit of "learning while burning," Dr Narayan and colleagues have described and, perhaps, confirmed an alternative mechanism for AF perpetuation. This second theory of AF depends on the importance of areas of the atria that harbor focal impulses or localized reentry. On software-generated optical maps of AF, these areas appear as electrical rotors. But, are these rotors important for human AF perpetuation?
As has been the case in the history of electrophysiology, one of the best ways to confirm the (causative) importance of an area or impulse is when ablation of that area terminates the arrhythmia. In the EP lab, we often ask: "Was that the spot?" If the burn terminates the arrhythmia and renders it noninducible, than yes, that was indeed the spot.
Herein lies the beauty of Dr Narayan's work. The 92-patient CONFIRM trial tempts us to make three game-changing conclusions:
- Human AF may be sustained by localized sources in the form of either electrical rotors or focal impulses.
- Brief ablation (FIRM) at these patient-specific sites can terminate or slow AF.
- Adding FIRM ablation to standard pulmonary vein isolation (PVI) may markedly improve the long-term success of AF ablation.
As pointed out in a well-written and extremely helpful accompanying editorial written by Drs Erik Wissner and Karl-Heinz Kuck, these data are both exciting and early.2 These experienced and practical ablationists highlight the obvious limitation of CONFIRM: that this entire concept (the secret sauce, if you will) turns on propriety software, the details of which have yet to be published or reproduced by other labs.
I wrote hopefully and enthusiastically about FIRM ablation a few months ago when it was presented at HRS. I was stirred by the comments of Dr Sonny Jackman: "This work could turn the AF-ablation community upside down." At HRS 2012, we learned that FIRM ablation is now ongoing in EP labs outside of Southern California, and the preliminary results are consistent with and as equally encouraging as the results of the CONFIRM trial.
The AF community eagerly awaits confirmation of this novel and mechanism-based approach to AF ablation. It's so much smarter and more elegant a strategy than blindly ablating areas that we think to be important in causing AF.
It's been so long. It's time for a jump in knowledge--and success. It's time for AF ablation--"to be easy."
Gosh, if this works. Now that would be something.
1. Narayan SM, Krummen DE, Shivkumar K, et al. Treatment of atrial fibrillation by the ablation of localized sources. J Am Coll Cardiol 2012; DOI: 10.1016/j.jacc.2012.05.022. Available at: http://content.onlinejacc.org.
2. Kuck KH, Wissner E. A FIRM grip on atrial fibrillation. J Am Coll Cardiol 2012; DOI: 10.1016/j.jacc.2012.06.009. Available at: http://content.onlinejacc.org.