John Mandrola, MD


June 20, 2017

Procedures to improve outcomes in patients with atrial fibrillation (AF) come with trade-offs. Moving catheters within the arterial circulation, creating scars on the left atrial endothelial surface, and placing devices in the left atrial appendage are not free.

One such trade-off is the presence of postprocedural MRI-detected brain lesions. Numerous studies have chronicled the presence of these (usually) asymptomatic cerebral lesions after left atrial procedures.[1,2,3] Long-term sequelae from the lesions remain unknown, but brain injury—even if transient—is worrisome, especially if you are the patient.

Two presentations from the first day of the European Heart Rhythm Association (EHRA) EUROPACE-CARDIOSTIM 2017 meeting in Vienna added to the knowledge base of these bothersome white spots.

Post–AF-Ablation Brain Lesions

The first paper, from an Austrian group in Linz, examined the role of AF-ablation anticoagulation on the presence of postprocedural lesions. They compared the use of interrupted non–vitamin-K novel oral anticoagulants (NOACs) vs uninterrupted vitamin-K antagonists (VKA) as periprocedural agents for AF ablation.

Their nonrandomized comparison included 410 consecutive patients (VKA n=314; NOAC n=96) who had AF ablation. All patients had MRI scans before and after the procedure. Brain lesions were seen in 9.6% of patients treated with VKAs vs 17.3% in those treated with NOACs (P=0.049).

In their discussion, the authors raised the possibility that higher rates of brain lesions in the interrupted NOAC group could have been due to baseline differences—eg, the mean left atrial diameter and CHA2DS2-VASc scores were slightly higher in the NOAC group, and the mean activated clotting time (ACT) during the procedure was 44 seconds lower in the NOAC group.

In the end, though, the difference was enough to convince the authors to abandon interrupted NOAC use before ablation.

These are pragmatic real-world data. It's useful because it helps confirm the need for robust periprocedural anticoagulation and, importantly, their evidence changed their practice. I think data collection on AF procedures should be more commonplace.

Also notable in this series is that even with good INR control before the ablation and good anticoagulation during the ablation (ACT=345 seconds) and reasonable procedure times (171 minutes), nearly one in 10 patients in the VKA group had postprocedural brain lesions.

Lead author Dr Michael Derndorfer told me after his presentation that they plan to continue this study and look at MRI scans after ablation with uninterrupted NOACs. We and surely our patients with AF hope uninterrupted NOAC use might reduce the incidence of brain lesions.

It's worth remembering that although any left-sided (arterial) procedure can cause MRI-detected brain lesions, sicker patients who undergo, say, transaortic aortic-valve replacement (TAVR) or multivessel PCI have few other treatment options. In relative terms, post-TAVR brain lesions seem like a smaller issue than new brain lesions found in an otherwise-healthy 55-year-old with intermittent episodes of AF.

And…this is a core problem with AF ablation: it's a big procedure, which is often done in relatively healthy people. Thus, any complication is magnified.

Post-Left Atrial Appendage Closure Brain Lesions

Another paper presented on this first day of EHRA assessed the incidence of brain lesions and cognitive function after left atrial appendage closure (LAAC) in patients with AF.

Lead author Dr Andreas Rillig and coworkers from Charité Campus Benjamin Franklin in Berlin, Germany, used 3T MRI scans and two neurocognitive tests to study 23 patients before and after LAAC.

They observed no differences in cognition, but 12 of 23 (52%) of patients had new brain lesions after the procedure.

This observation is potentially significant because the point of LAAC is to protect the brain.

Consider that appendage closure is usually done in older patients who likely have diminished neurologic reserve. Let's assume this work will be confirmed in larger studies—which seems likely because another small series observed similar findings.[4]

Then the question becomes: what is the significance of adding brain lesions to people with preexisting brain disease? I ask because LAAC is also a big procedure—one that is used to prevent something (stroke or systemic embolism) that may never occur. In fact, and many doctors tend to forget this, the most likely outcome for patients with AF and high stroke risk is that they will not have a future event.

Consider that the flip side of an 8% to 10% yearly stroke-event rate for a patient with a high CHA2DS2-VASc score is the >90% (yearly) chance this patient will not have a stroke. This 90% chance of nothing happening could be compared with a 50% chance of incurring a postprocedural brain lesion.

Again, this trade-off is a core problem with using invasive procedures for prevention. Patients who accept appendage closure must weigh the finite risk of harm from the procedure against an uncertain probabilistic benefit in the future.

Believers in appendage closure will likely take issue with this argument.

But the lead author of the European Society of Cardiology 2016 AF treatment guidelines,[5] Dr Paulus Kirchhof (Birmingham, UK), spent 20 minutes in an opening session today outlining the "incomplete evidence, gaps, and uncertainties" surrounding LAAC for stroke prevention. Boston Scientific sponsored this session. And Dr Kirchhof chose his words carefully.

It says a lot that a person of his stature went to the podium to highlight how little we really know about this increasingly common procedure.

The issue of postprocedural brain lesions and long-term neurologic effects after left atrial procedures deserves our attention. I can't imagine a more patient-centered outcome than how these procedures affect the organ that makes us human.


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