Strategies for Managing Atrial Fibrillation in Patients on BTKi

EP: 1.A Review of Treatment Options in CLL

EP: 2.Key Safety Considerations

EP: 3.Baseline Testing Prior to Initiation of BTKi Treatment in CLL

EP: 4.Balancing the Risk and Benefit of Anticoagulation in Patients on BTKi

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EP: 5.Strategies for Managing Atrial Fibrillation in Patients on BTKi

EP: 6.A Real-World Case of a Patient with CLL and a Cardiac History

EP: 7.Strategies for Managing Hypertension in Patients with CLL

EP: 8.Experts Answer Audience Questions Related to Adverse Events of BTKi

Farrukh Awan, MD: Atrial fibrillation [AFib] is the most common issue with these patients [with chronic lymphocytic leukemia]. Another thing I learned the hard way is that when patients without a history of AFib got on a BTK inhibitor, with a rapid ventricular rate, they got admitted to the hospital through the ER [emergency department] in the middle of the night. The first instinct was to zap it—shock it, cardioversion them, stop the BTK inhibitor, put them on anticoagulation, shock it, get it back, put them back on a BTK inhibitor later. Every time I’ve done that, the minute they go back on the BTK inhibitor, AFib comes right back. It was almost to a point that I was fighting the cardiologist. I do not want to cardioversion this person. That’s been my practice. I might be wrong or correct in this, but I’ve found that rhythm-controlled strategies don’t seem to be very effective, No. 1. Amiodarone or other such agents have too many adverse events and interactions with that drug, so you have to constantly worry about the dosages and the toxicity because of the interactions. I’m not a fan of that. I tend to focus solely on rate control. That’s question No. 1. I’d love to hear what you have to say about rate vs rhythm control.

The second thing was that 1 of the cardiologists I was talking to—and we did do a few patients on that; I don’t know how this is panning out in the cardiology side—was to do pulmonary sinus trial therapy ablation or some procedure like that. I’m not sure what the technicality is. There were a few patients in whom they did this trial ablation procedure, and apparently that worked better. Maybe those were just unique patients who have an aberrant rhythm, and they had maybe some other type of SVT [supraventricular tachycardia]. But those are just some personal experiences from the ablation side. Maybe that’s something we should consider. This is different from the watchman strategy because that’s mostly for anticoagulation based. What do you think about these strategies, the rhythm rate and then this ablation?

Carrie Lenneman, MD, MSCI: You’re exactly right. I approach a patient with new-onset AFib who’s been on a BTK inhibitor by asking, “Are you symptomatic with it or are you not? What are your rates?” My bottom line is if they’re not symptomatic with their AFib, they don’t feel bad with it. If it’s not causing heart failure, I always go for rate control. I’m with you. I don’t think rhythm control really works. Not without either doing some ablation or having them on some heavy drugs.

You bring up great points that I need to emphasize. There are a lot of drug interactions, especially in the cardiology realm of BTK inhibitors. We already talked about the anticoagulation and some of the challenges with that. But with diltiazem, there are interactions with BTK inhibitors. I usually have to reach out to my oncology colleagues and say, “I’m putting them on diltiazem, so we may need to do a dose adjust,” because it will cause adjustments in their overall therapeutic levels of that. I tend to try to do mostly a rhythm control strategy. I’m usually looking at beta-blockers or calcium channel blockers. I favor beta-blockers because they’re cleaner. They don’t have the drug interactions. The calcium channel blockers, like diltiazem and verapamil, can cause drug interactions that become a problem, and we have to adjust the BTK inhibitor.

I totally agree that with amiodarone and digoxin, there’s more drug-drug interaction, and it becomes a complicated circle. Unless a patient is symptomatic, I always use rate control strategy. If they’re symptomatic, then I think about doing an ablation. We typically do a pulmonary vein isolation ablation, which is standard if you’re talking about anything else new or novel from an EP [electrophysiology] perspective. I definitely think an AFib ablation is reasonable. Unfortunately I’ve seen people who we’ve done an ablation on with a BTK inhibitor, who then unfortunately get AFib again. Usually they’re easier to control, and they’re maybe a little less symptomatic.

In general, for AFib ablation—in a normal population, not on BTK inhibitors—the likelihood of them staying in normal sinus [rhythm] is about 75%. AFib ablations aren’t perfect. But then you take a person who’s got CLL [chronic lymphocytic leukemia], and you add back their medicine, which increases the automaticity of the cardiac myocytes. People probably aren’t going to be part of that 75% of responders remaining in sinus rhythm. They probably have a 50% or 60% chance of staying in normal sinus after an AFib ablation. It’s real world, different from what we know from other data. I use AFib ablation, and I rely on my EP colleagues to take care of these challenging patients when I have a person who needs a rhythm-controlling strategy.

This transcript has been edited for clarity.