COMMENTARY

Finding the Least Disruptive Approach to Tachy-Brady Syndrome: AF Ablation vs Pacemaker/Drugs

John Mandrola

Disclosures

September 02, 2013

One effect of becoming an AF ablation doctor is that you implant fewer pacemakers. Why would this be?

Let me tell you about a case, and then an abstract presented here at the European Society of Cardiology (ESC) 2013 Congress .

The text message came from the rounding nurse. It said:

With permission of Dr Mike Cadogen, Life in the Fast Lane

There's a 62-year-old women in the ER having runs of AF and eigh-second pauses. Can you do a pacemaker?

Just a few years ago I would have said, yes, get her ready.

It's different now.

When I went to see this patient, I found a very healthy-appearing woman who came to the hospital with a chief complaint of palpitations and brief near-syncopal episodes. Classic tachy-bradycardia episodes were seen on the monitor. Even for me, the pauses were impressive.

A year before she was put on a low dose of an antiarrhythmic drug for AF. That intervention had worked until recently. The exam and laboratory studies were normal. The ECG was also normal, including a normal p-wave and PR interval.

What next? Clearly this patient required an action plan. Choices included:

  • Stop the drug and let her have palpitations; (living w/disease is always an option).

  • Switch to a different drug.

  • Place a pacemaker, and then continue or increase the current drug.

  • Ablate the AF.

What happened in the past, before I became an AF ablationist, was that a pacemaker was implanted and then AF drugs were continued or increased. More times than not, this proved to be an unfulfilling strategy. Patients did poorly. They recurred with tachy symptoms, or they suffered side effects from higher doses of drugs, or they progressed to permanent AF and never used the atrial lead again, or they had pacemaker complications.

And this isn't surprising. Problems with the pacemaker-drug path include: 1) AF drugs are ineffective, even at higher doses; 2) pacemakers expose patients to significant short-and long-term risks; 3) pacemakers do not relieve tachycardic symptoms; and 4) this strategy has no chance of improving long-term outcomes, like stroke or death.

I now approach the common problem of tachy-brady syndrome much differently.

An abstract at ESC2013 supports the consideration of an ablative approach to the problem.

The abstract

Chinese researchers looked at a nonrandomized series of 100 patients with AF and sinus pauses. These patients met guideline recommendations for pacemakers. In 43 patients, the researchers performed AF ablation alone; the remaining 57 had pacemakers and antiarrhythmic drugs (AAD).

At 20 months of follow-up, the results strongly favored AF ablation:

  • The primary end point (cardiovascular hospitalization) was significantly reduced in the ablation group (five vs 19 admissions).

  • Many more patients in the ablation group were free of AF (36/43 [83.7%] vs 12/57 [21%]).

  • Fewer patients in the ablation were group were on AAD (4.7% vs 40.4%).

The researchers concluded that the strategy of AF ablation seemed to be superior to a strategy of pacing plus AAD. They suggested pacemaker implantation could be waived in the majority of patients after a successful ablation.

Though I am utterly biased and conflicted, I like this study. I believe it. It fits my experience. Granted, this small, single center, nonrandomized study from China is not a practice-changing megatrial. But that doesn't mean it's not useful. This sort of data, modest as it is, should be commended and placed into context.

Follow-up on initial case

The first step was to relieve the patient's anxiety. She was symptomatic, scared, and had been told a pacemaker would be necessary. Also, she was in an ER, a place with noise, bright lights, and beeping monitors. That's not the right place for patients with AF.

I went on to explain that paroxysmal AF episodes were not life threatening. We could stop the low-dose antiarrhythmic drug and the bradycardia would improve. She was admitted to the hospital for monitoring. I told her that yes, she may have continued palpitations, but the pauses would likely improve off the drug. I had bought us some time. Time is good. Remember, AF is not a STEMI, and sick sinus syndrome is not AV block.

A few weeks later she underwent successful PVI. Rapid PV tachycardia was seen at ablation. In the days that followed the procedure, there were no episodes of AF, and therefore, no further bradycardia. I have seen this patient every year for the past few years. There is no hardware in her healthy body.

Take home

I know of no formal comparison between these two strategies. In the absence of formal clinical trial data, one must employ judgment and shared-decision making.

When AF/tachycardia is clearly the cause of bradycardia, an ablation strategy makes sense. It addresses the primary issue—the AF. Compare that with a pacemaker-drug strategy, which uses the device to treat the adverse effect of the drug. Think about that for a moment: using an invasive procedure (pacemaker) to treat a flawed medical strategy (AAD). Really?

Another important factor to consider is outcomes. Here, we don't have a final winner, but I have to favor ablation. Numerous population studies show that AF patients treated with AF ablation fare better than those treated conventionally. These aren't randomized clinical trials, but there's a definite signal of benefit with ablation. The CABANA trial is designed to answer this question, but results will not be available for years. Antiarrhythmic drugs, on the other hand, do not improve outcomes. This we know with certainty.

The final reason why I favor the ablation strategy is that passes the Mandrola rule: As an AF patient, I only recommend therapy that I would undergo myself. In the case of heart racing and pausing, I like the idea of fixing the problem without implanted hardware.

Now . . . to ward off the ablation naysayers and device apostles, I will finish with the all-important caveats.

An ablation strategy isn't easy. There's the assumption that PVI can be done skillfully and safely. This requires an experienced operator and team. But that's not the highest hurdle of a primary ablative strategy.

The hardest part is taking the time with an anxious, frightened AF patient. Undoing fear is not easy—and it encompasses a different skill set than moving ablation catheters in the heart.

JMM

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