Ablation After Pulmonary Vein Isolation: Chase the Triggers or Modify the Atrium?

Discussion With Bradley Knight, MD, and Philipp Sommer, MD, FHRS, FESC, FEHRA 

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Edited by Jodie Elrod

Bradley Knight, MD, talks with Philipp Sommer, MD, FHRS, FESC, FEHRA, about the roundtable session entitled "Ablation After Pulmonary Vein Isolation: Chase the Triggers or Modify the Atrium?" at Western AFib 2026.

Bradley Knight, MD: I'm Brad Knight, Editor-in-Chief of EP Lab Digest, and we are here at the 2026 Western Atrial Fibrillation (AFib) Symposium in Salt Lake City. I am delighted to be joined by Professor Phillip Sommer, who gave a talk today on what to do beyond ablation of the pulmonary veins (PVs)—whether to chase triggers or modify the substrate. Maybe we can start by asking you to define trigger. What does a trigger even mean?

Philipp Sommer, MD, FHRS, FESC, FEHRA: Starting with the most difficult question right away! In this context, triggers refer to sites within the atria—likely both the right and left atria—that initiate AFib. The most well-known triggers are within the pulmonary veins (PVs), which led to the strategy of pulmonary vein isolation (PVI). However, similar trigger mechanisms that initiate this arrhythmia may also be located in other areas that we know exist. Some of these may be found in locations such as the coronary sinus (CS) os or the appendage. There are multiple ways to identify these triggers, but at least in my view, there is still no single technology that can provide clear insight into exactly where they are or even confirm their presence. Various strategies are used to provoke, identify, and localize these triggers, which makes the overall process quite complex.

Bradley Knight, MD: So your definition implies, in some ways, that the patient is in sinus rhythm, not AFib, and then a trigger initiates AFib. The early data from the PVs suggested frequent premature atrial beats, which then somehow trigger AFib, possibly by initiating reentry. It may also be that there is rapid firing originating from those sites. So do you think a trigger is an individual premature beat? Is that capable of inducing AFib, or is it more consecutive drivers from that site?

Philipp Sommer, MD, FHRS, FESC, FEHRA: It’s probably more than single beats, at least like in the early phases when the atria may not yet be susceptible to maintaining the arrhythmia after just a single triggering beat. But yes, you make a good point, because this understanding of a trigger is the classical one—there are some extra beats. 

Bradley Knight, MD: I think that is what people are looking for when they give isoproterenol and look for triggers.

Philipp Sommer, MD, FHRS, FESC, FEHRA: Right. And of course, there are also strategies that may be more easily applicable, which look for sources—whatever you may call them—during AFib. 

Bradley Knight, MD: Tell me more about that. It is really a whole different concept.

Philipp Sommer, MD, FHRS, FESC, FEHRA: It is, and at least for me, it makes the whole concept much more difficult to understand. If a patient is in sinus rhythm and you see AFib initiated from a specific site, you may be able to locate and ablate it, eliminate that trigger and thereby eliminate AFib. But chasing and identifying those trigger sites during ongoing AFib is, I would say, intellectually more challenging. In that setting, you are mapping AFib, processing signals, and using different algorithms and tools to direct you to certain spots. There are various technologies for this—some of them have been demonstrated quite nicely at this meeting—and some of them are based on intracardiac electrograms. Some are even based solely, I would say, on 12-lead surface ECG data, which makes it harder for me to fully understand how to reliably get to the right target. 

Bradley Knight, MD: The theme of your presentation was that it probably will not be one key that unlocks everybody's AFib.

Philipp Sommer, MD, FHRS, FESC, FEHRA: Yes, that is my take on that. 

Bradley Knight, MD: There are surface ECG techniques and intracardiac ECG techniques. What have you used, and what is your take on these other tools?

Philipp Sommer, MD, FHRS, FESC, FEHRA: Honestly, with all these approaches and technologies, if you talk to the companies, they often promise that they have found the holy grail—that this is the solution. You can use this algorithm, it will work for everyone, it will terminate all AFib, and it will never come back. But I’m concerned that AFib involves multiple pathophysiologies. Each patient may, in a sense, have their own “secret.” There may be groups of patients triggered by, for example, an extra stimulus from the CS os. Others may benefit from posterior wall isolation because their triggering substrate lies within the posterior wall. So I think there are multiple underlying mechanisms, and we need to be prepared to identify those different mechanisms.

Bradley Knight, MD: There's clearly a need for it. Over the past couple of years—at least in the US—we've been overwhelmed by the availability of pulsed field ablation (PFA) tools. The last 2 years, in particular, have seen a complete shift toward PFA. That approach has largely been anatomically based, but now we have many patients who have undergone an anatomically-based approach and still have paroxysmal or persistent AFib. So moving forward, there is going to be a need for some of these mapping systems.

Philipp Sommer, MD, FHRS, FESC, FEHRA: Definitely, there is a need. And to me, the question remains: if we use these mapping tools and identify focal areas to ablate, do we then end up expanding beyond those targets? For example, if we find a few focal sites in the posterior wall, do we proceed to isolate the entire posterior wall—essentially creating a full “box” lesion set? Some even suggest extending that all the way down to the CS. Then we move to the anterior wall and think, “I should probably connect the mitral annulus to the right superior.” And at the end of the day, you’ve essentially ablated the entire left atrium. 

Bradley Knight, MD: The presentation at Western AFib 2026 by Devi Nair looked at another mapping system that identified certain hotspots, but she then targeted them using a pentaspline catheter. So this also raises the issue of safety, because if these tools begin identifying additional areas for ablation—areas we do not typically target—it becomes an important consideration. For example, ablating near the CS os raises concerns about heart block. What are the areas you would be concerned about going after?

Philipp Sommer, MD, FHRS, FESC, FEHRA: I'm quite confident working on the left side. I have seen temporary AV block when creating septal lines when I was supposed to ablate, such as longer connecting lines between the annulus and the left side. But overall, I'm much more concerned about the right side, honestly—particularly the risk of sinus node dysfunction. This becomes especially relevant with superior vena cava isolation or when targeting focal activity in the right atrium. Of course, as you mentioned, the CS os is another area, that if you have the wrong tool in your hands—potentially PFA—you could affect atrioventricular (AV) nodal conduction, which is something you definitely want to avoid. You might identify a site that seems important, ablate it, and then end up creating a pacemaker-dependent patient.

Bradley Knight, MD: Yes, even on the left side. We participated in the duty-cycled radiofrequency (RF) Ablation Frontiers studies, and we had that powerful septal ablation tool with RF, and there were never any cases of heart block. But now that we have these PFA tools, when ablating on the other side of the AV nodal area, I am aware of some cases of heart block. What is your expectation for when we might have something available that you would use regularly—1 year, 2 years, 5 years?

Philipp Sommer, MD, FHRS, FESC, FEHRA: That's very difficult. We're currently using Volta Medical’s system as a bailout strategy in our labs, which focuses on identifying areas of dispersion—spatiotemporal dispersion areas where something might be going on, let's put it that way. 

Bradley Knight, MD: There has been some criticism of that approach, because the primary trials didn't show an overall reduction in atrial arrhythmias—even though they did show a reduction in AFib—which may be a case of throwing the baby out with the bathwater. There is probably still something to it, and ongoing trials are exploring this further. Do you still think there is value in targeting dispersion?

Philipp Sommer, MD, FHRS, FESC, FEHRA: Yes, I'm not sure. As I said, I need to try everything and build my own experience. I don't put too much weight on registry data, retrospective data, or reports where people said they treated 100 patients and now they are all in sinus rhythm and doing well. I need to be able to reproduce those findings myself. For example, I rarely see termination of AFib. Even during the Topera era, there were claims that ablating those rotors would consistently terminate AFib, but I was never able to reproduce that.

Bradley Knight, MD: So we have talked about triggers, but you may also identify other findings that visually. For example, you're performing a PVI with Farapulse (Boston Scientific) or a pentaspline catheter and you encounter electrograms that seem interesting—such as fractionation or scar. Are there other features you subjectively notice that would lead you to ablate?

Philipp Sommer, MD, FHRS, FESC, FEHRA: I'm a big fan of voltage mapping and scar modification. I truly believe that most of these tools, in our hands, guide us to areas that I would also detect using simple voltage mapping. The question is whether voltage information alone is sufficient, especially when using relatively large bipole catheters rather than dedicated mapping tools like a pentaspline, which is probably not providing ideal mapping information, but more or less a rough estimate. 

Bradley Knight, MD: Ken Ellenbogen presented this new system that Peter Spector had been working on, using very tiny electrodes, and showed epicardial recordings from the operating room of what looks like AFib, but with these tiny electrodes, they look more like highly multifocal atrial tachycardia. So the electrode sizing and spacing will clearly evolve. Anything else from your presentation that you think is worth mentioning?

Philipp Sommer, MD, FHRS, FESC, FEHRA: Yes, the frustrating summary is that it's not going to be easy. There will not be a one-size-fits-all solution. We need to stay open-minded, consider different technologies, and be ready—even within a procedure—to switch gears and adjust our approach. Sometimes the case may be different from what we anticipated, so we cannot be too fixed on a single strategy or concept. We really need to keep our focus on the patient and their clinical needs. And ultimately, we need more robust data.

Bradley Knight, MD: Is there anything you identify on preprocedural imaging—or even something like left atrial enlargement—that influences your approach? Are there features you notice in a patient during clinic that shape your procedural plan going in?

Philipp Sommer, MD, FHRS, FESC, FEHRA: Left atrial size, and also the shape of the PVs, of course influence my choice of device. I also try to tailor my ablation approach based on the patient’s history. If it's a third or fourth ablation, I know the veins are already isolated, and if there are flutters, I may use a different tool than if the recurrent arrhythmia pattern is AFib. So yes, I try to look at the whole picture—and still, I’m regularly wrong with my choice.

Bradley Knight, MD: Thank you for your time and insight. Safe travels back to Germany. 

Philipp Sommer, MD, FHRS, FESC, FEHRA: Thank you. 

The transcripts were edited for clarity and length.