" Boris Schmidt: Hello everybody. My name is Boris Schmidt, I'm an electrophysiologist from Frankfurt, Germany, and today I'm here with Professor Atul Verma from Canada to discuss strategies to address atrial fibrillation after an index AF ablation procedure.
Atul Verma: Thanks so much, Boris. I'm from McGill University Health Centre in Montreal, Canada. It's always such a complicated thing when a patient has had a PVI procedure with an AF ablation, now has recurrent AF, and you bring them back into the lab. What's your approach for that redo procedure — take me through it step by step.
Boris Schmidt: Our strategy is to address voltage. We've never focused on electrophysiological approaches like analysing complex fractionated electrograms or rotor activity — we address substrate. So we cardiovert the patient, perform a voltage map, and then ablate the low voltage areas, ideally with linear lesions, because you can assess conduction block across them and avoid atrial tachycardia recurrences. What would you do?
Atul Verma: I probably start similarly. I do a high-density map to look at the veins and ensure they're isolated — and more and more, I'm finding that the veins are already isolated. So then you're stuck. What do I do outside of the veins? In a persistent patient, I'll often think about empirically doing the posterior wall as well. With PFA especially, it's really invited us to go back to the posterior wall — I'm not worried about the oesophagus and other issues in the same way.
But in particular, I also like to cardiovert the patient back to sinus rhythm and do my mapping there. I'll look for late atrial potentials — similar to how we approach VT. In my mind, these late atrial potentials may represent areas that were previously ablated but not sufficiently, or they may represent progression of substrate over time. I label these points on the electroanatomical mapping system and then target them wherever they may be, including the anterior wall and base of the appendage — especially if the veins and posterior wall are already dealt with.
Boris Schmidt: So if I understand correctly, Atul, it's a mixture of an empirical approach and an individualised approach based on the electrograms you find during remapping.
Atul Verma: Exactly. Empirical approaches such as posterior wall isolation are quite attractive — ADVANTAGE gave us good results with posterior wall isolation using the pentaspline catheter. Do you think other areas of the left atrium should be addressed, like the mitral isthmus line or left atrial appendage isolation? Is there any promising data you're aware of?
Boris Schmidt: As you know, there is data out there on mitral lines and appendage isolation. However, even the biggest advocates for those approaches will often say they reserve them for later procedures. I definitely wouldn't do that on an index ablation. If it's a first redo, I'm not sure I would isolate the left atrial appendage. If there's a mitral-dependent flutter that's obvious, it needs to be dealt with — and I'll go for a mitral line, but most of the time I'll actually go for an anterior line rather than a posterior line. What's your preference?
Atul Verma: It really depends on the voltage. Our experience is that with conventional thermal ablation modalities, in a patient with a healthy anterior wall, it's virtually impossible to block Bachmann's bundle and achieve bidirectional conduction block across the anterior line. With newer ablation modalities — the Sphere 9 catheter, for example — it is more achievable. But if there's no substrate there, I prefer to go for the mitral isthmus line, because with Sphere 9 and dual energy, block can be achieved. And in cases where we cannot achieve block, we also use Vein of Marshall ethanol infusion in selected cases. The acute results are quite encouraging, I have to say.
Boris Schmidt: Excellent. What about artificial intelligence algorithms or other mapping algorithms that have been developed or are being investigated? Do you have experience with any of them for redo procedures?
Atul Verma: Unfortunately not — we haven't had the chance to use them yet. There is encouraging data published by Isabel Diesenhofer on the Volta system, which seems quite interesting. Some data for repeat procedures was also presented during this meeting. We will be part of the so-called OPTIMIZED trial, which uses a basket or array catheter and the Vortex technology — now acquired by Boston Scientific — to detect potential focal sources and rotational activity in patients with persistent atrial fibrillation. I'm really looking forward to seeing what comes out of it.
Boris Schmidt: Yes — before it was acquired by Boston Scientific it was called Ablacon, and it's now called Cortex. I've done a lot of work with it in the past. I think the electrocardiographic flow mapping concept is very interesting. They ran a trial called the FLOW AF trial in redo patients, randomizing them to either re-isolation of the veins — or cardioversion if the veins were already isolated — versus re-isolation plus ablation of areas identified by the system. It was a small, preliminary trial, but it showed much better outcomes in redo procedures with the combination of PVI and Cortex mapping versus PVI alone. Very encouraging.
Atul Verma: So looking at today and perhaps five to ten years from now — where do you see room for improvement? Mapping tools, software tools, panoramic mapping with body surface electrodes?
Boris Schmidt: That's the million dollar question. I personally think there is something real to the concept of drivers of atrial fibrillation — whether you look at them using electrocardiographic flow mapping or other high-density mapping approaches. My belief, even after all these years and after STAR AF2, is that there is something else we can go after. Ultimately I think we need higher resolution mapping — beyond just electrodes on a catheter. We need something akin to optical mapping at that resolution. That's a 20-year plan, perhaps — but I think that's what we ultimately need.
Atul Verma: If I may add one thing — looking at it more holistically, we also need a better understanding of atrial cardiomyopathy. We still don't have the final insights into the pathophysiology of why some patients develop cardiomyopathy and others don't. What are the pathways? Do we have — or could we develop — medications that can slow or stop this process and help us prevent or control atrial fibrillation more effectively?
Boris Schmidt: 100%. Well, this has been a great discussion — thank you very much, Atul.
Atul Verma: Thanks, Boris. Have a great day.”