It’s time to write an update on AF ablation. Things have changed.
The major change is that I am doing many fewer ablations for AF.
The reason is we have a better understanding of the disease, or should I say, condition? In the last 2-3 years, good science has changed the way specialists see AF. The old-thinking had AF in its own silo. Your ECG showed AF so you had the disease AF. And if you had a disease, we had a fix–say drugs or ablation.
My partners would say, “John, we are sending you this patient with AF; please fix him.” And by fix, they meant drugs or ablation. Like a blockage–make it go away.
That’s not how AF treatment works. I’m surprised it took this long to figure that out.
The new thinking is that AF (often) occurs as a symptom or sign of something else.
Before I expand on that something else, let’s set out that there exists a small (but very vocal) minority of patients with AF that have no underlying disease or cause. This type of AF, the focal kind coming from an isolated source, usually within or around the pulmonary veins, was the type of AF first described by Dr. Michel HaÃ¯ssaguerre and colleagues in the NEJM in 1998. If this was the only AF we ablated, AF ablation would be as curative as it is in supraventricular tachycardia.
It is not.
Most AF in developed countries is not a focal or primary problem with the heart. Most AF has a root cause outside the heart.
“Things” outside the heart that lead to AF include obesity, sleep apnea, alcohol, high blood pressure, inflammatory conditions (infections, trauma), excess exercise and probably stress. A blog post can’t explain the biology of how these signals affect the heart, but most experts now agree that each of these conditions, either alone or together, create the milieu in which AF starts and perpetuates.
The overly simplistic explanation goes like this: the above conditions (with inflammation and excess being the common thread) cause atrial chamber dilation, enlargement of individual atrial cells, loss of atria skeleton, change in cell membrane connections and deposition of scar. In total, we call these effects remodeling, and remodeling favors the development and persistence of AF.
We have always known to look for underlying causes of AF before treatment. In the past, though, this search was limited to conditions like high thyroid levels and valve issues.
What’s new now is the evidence linking lifestyle to disease in the atria. Dr. Prash Sanders and his team in Adelaide Australia have demonstrated that attention to risk factor reduction, such as weight loss, gains in fitness, alcohol modulation, and treatment of high blood pressure reduce AF burden–whether or not a patient comes to ablation. That last phrase is key: risk factor management bolsters AF ablation success rates.
When I see a patient with AF, I check for sleep apnea, discuss weight loss, alcohol intake and make sure we’ve got blood pressure under control. I also inquire about stress. A patient frazzled by the transient stressors of life–care-giving for a loved one, grief, or marital problems–will likely get better when the stress passes. What’s so fascinating about athletes with AF is that the excess exercise can have the same effects on the atria as does obesity–oh the irony.
The first step in AF treatment, therefore, is to focus on the root causes of AF. To do this, you first have to spend a fair amount of time removing fear. Patients with AF have to understand AF. They have to know AF is serious but not deadly.
For patients with ongoing symptoms, these long-term treatments must be combined with something now.
In the short-term, I use temporizing measures to relieve AF symptoms: drugs for rate control, anticoagulants for stroke prevention, and maybe even cardioversion with or without anti-arrhythmic drugs. The key is that these treatments are temporary. We aren’t shocking or medicating an AF patient with the idea that this is the fix; we are doing those things to buy time for risk factor management to work. And it does. I’ve seen it work.
Of course, in medicine not all things work perfectly. Risk factor management doesn’t always succeed. Here is where ablation still has a role–later, after we have given time a chance to heal; after we have given risk factor management a chance to heal, and most importantly, once we have gone slowly enough that patients aren’t having ablation out of fear of the disease or the mistaken belief that putting 60-80 ablation lesions in the left atrium is an “easy” fix.
Perhaps the coolest aspect of this new thinking is that even when we end up doing ablation, risk factor management not only improves success rates but it also makes the person healthier overall.
Since embracing this holistic approach to people with AF, I’ve done far fewer ablations and redo ablations.
The take-home message for patients and doctors alike is that AF ablation remains a reasonable option for carefully selected patients. But we should no longer rush to treat a condition caused by scar by creating more scar.
Go slowly; look for causes; treat these causes; give peace a chance. There is almost always a fix for AF. It’s rarely with a catheter alone.
9 replies on “A cautionary note on AF ablation in 2015”
GREAT post John! Fits right in with my primary care approach to medicine!
I think/hope your “lifestyle improvements” approach is spreading among EP’s, although revenue generation via expensive interventions (e.g. ablations) is probably still all-important to the corporate execs who now often dictate the practice of medicine in many places in the U.S.
Thank goodness M.D.’s like you and Prash Sanders exist. Thank goodness there is still medical research going on in Australia and elsewhere around the world that isn’t solely profit-driven.
Again, thanks Dr. John for your honesty and integrity. I have learned more from reading your blog, over years of having afib, than from any other source.
Dr Mandrola, please, please, PLEASE will you come onto my podcast so that I may interview about this.
I’m up to 30,000 downloads a month, I promise it will be worth your time!
As an EP and recreational athlete yourself, how would you define “excess” exercise for a 60 year old lifetime aerobic activities participant?
Can your average and maximum heart rate during exercise and/or the duration of exercise be used to determine if you have crossed the line into the realm of “excess” exercise?
By the way, your webpage and Twitter feed are wonderful. I wish my physicians followed your sage advice.
The way I define excess exercise is similar to what the judge said about indecency: I know it when I see it.
Seriously. It’s an impossible question.
Paul and Dr Mandrola,
It’s a tough question but I don’t think it is impossible. I think our hearts’ electrical performance can be characterized by a time-intensity envelop within which normal function can be maintained. This envelop does change with other factors (especially altitude and weight). This is certainly the way my heart seems to work.
I’m coming to the realization that a few strange incidents (passing out while running, heart arrhythmia hiking at altitude) that have occurred during my life were probably due to my crossing of that envelop for my heart. I just started working with a cardiologist to figure out what kind of arrhythmia I typically experience but I know I will need to modify my cycling workouts.
Since I became a Pharmacist 35 years ago, I have always believed that less is more in just about every aspect of life. I had one bad episode of AF, four years ago and have made drastic changes in my life since. I have cut down alcohol, increased exercise, reduced BP, and eat and rest properly. I am episode free for four years. Being healthy, in most situations, is a matter of choice and commitment. It is refreshing for a well know cardiologist to practice the old adage, “First do no Harm”. Keep doing what you are doing!
What about persistent typical atrial flutter (AFL)? Are EPs performing too many CTI ablations? Are there lifestyle factors within the patient’s control that can reduce the incidence of AFL? Are the triggers for AFL different than AF triggers? Is there any credible evidence that excess exercise increases the likelihood of AFL?
Dr. Mandrola: After following your newsletter for several years, this update on the potential contributory “causes” of afib (especially in regards to “excess exercise”) has prompted me to comment for the first time.
Back in the “90s”, when Jim Cox (Cox Maze procedure) joined the staff at Georgetown, he directed his assistant, Terri Palazzo, to complete a background profile for every atrial fib patient who was seeking treatment, because he had noticed a high incidence of afib in those who were involved in aerobic steady state exercise and wanted to document his suspicions.
As I recall from a conversation I had with him in June 2002, 1-1/2 years after I had a Cox Maze III successfully performed by Pat McCarthy, at the CCF, Terri’s questionnaire confirmed Dr. Cox’ thoughts that almost (if not ALL) cases of Lone Atrial Fib (a few hundred over several years, as I recall) were found in those who had participated in heavy aerobic exercise.
While there are many steady state aerobic exercisers who never develop afib (at least to their knowledge), I believe and it appears that your “revisiting” the subject certainly raises questions regarding other possible contributory conditions which can influence the possibility of afib development, including all of those you mention.
For years I have thought that some “afib sufferers” probably have a genetic predisposition for afib, and that dehydration, heavy aerobic exercise, alcohol, caffeine, prescription drugs (Z-pack in my case), can all contribute to changes in electrolytes and inflammation in the bodies of some otherwise “heart-healthy” aerobic exercisers.
Keep up the honest, objective “reporting” in layman’s terms. Your voice is a pleasant contrast to those who think an ablations are a “cure-all” for any type of afib.
BTW, I have not had afib for over 14.5 years, but did have “left-sided” atrial flutter which occurred almost exactly 6 years post my Maze III, procedure, which took 2 long ablation procedures to eliminate back in 2007. Subsequently, several other identical Maze vets with whom I have maintained contact, had the same experience, and needed left-sided “touch-up” ablations. I have been back to drinking plenty of mostly red wine, no longer do competitive aerobic exercise (thanks to loss of pulmonary function related to 18 months of Pacerone back in 1999-2000).