Trials and Fibrillations with Dr John Mandrola

View all posts »

AF ablation: What are we doing?

Feb 17, 2012 14:45 EST


"Atrial fibrillation isn't an immediately life-threatening disease; don't make it one."

So says a good friend, cardiology colleague and master of the obvious.

I wonder about AF ablation. Don't you? Would you have AF ablation? Would you wonder about the long-term effects?

What about the rightness of poking a needle across a beating atrial septum? What of the idea of making 50 or more burns in the delicate left atrium? And those lines?

Yes, I often wonder what we AF ablationists are actually doing?

Are we curing AF? Are we changing the natural history of the disease?

Or . . . is AF ablation akin to placing stents for chronic coronary disease: just a big procedure to reduce symptoms, without improving real outcomes? Similarly, as stents do with their need for antiplatelet drugs, does AF ablation create yet another disease: a poorly contractile left atrium for one, asymptomatic brain lesions, another.

But the treasure of AF ablation is so grand. Freeing patients from the shackles of AF (or AF drugs) feels so good. I tell AF patients this all the time: "I realize that you are the one most invested in the outcome of AF ablation, but I am right behind you."

As heart doctors, our self-esteem demands that we succeed. But AF makes it pretty damn tough. I call this struggle, the AF quandary. Few AF patients can stand (or are best served with) no treatment. Yet sometimes our efforts make matters worse. Blood-thinners worsen bleeding, medicines cause side effects or worse, proarrhythmia, and ablation exposes patients to serious risk.

The Quandary

For the moment, let's focus on the most aggressive treatment of AF—catheter ablation.

A big procedure should have clear goals. Are we aiming to improve survival (acute PCI for heart attack) or just improve quality of life (elective knee replacement)? Or both?

AF patients need both goals addressed. I believe if questioned skillfully, most AF patients will describe living a lower quality of life since the disease struck. It's not just aging; it's the AF. But we also have to consider the long-term risks of AF. Population data, like the Framingham studies, clearly associate AF as a risk factor for stroke and earlier death over the long term.

So wouldn't it be cool if AF ablation did both: alleviate symptoms and lower the risk of stroke and early death? Common sense suggests that it should work this way. The thinking goes: AF ablation eliminates AF, and sinus rhythm means no clots or tachycardia-mediated cardiomyopathy.

Unfortunately, the paradigm of (medically rendered) rhythm control didn't work. The AFFIRM trial showed that maintenance of regular rhythm was associated with lower mortality, but this benefit was neutralized by the negative effects of AF medicines.

But we can all agree that AF ablation works better than meds. Numerous studies show that patients treated with AF ablation, when compared with AF patients on meds, have fewer AF episodes and report higher quality-of-life scores. Yet these studies shed little light on how (or if) AF ablation changes the natural history of the disease.

Ablation naysayers point to these three common post-AF ablation observations:

  • What about the issue of "success?" I hear this often: "Doc, these short episodes are nothing. I feel great. . . . Thank you. I'm good." Does lowering AF burden and improving symptoms equal better outcomes? Maybe not; recent recent data suggest even short episodes of AF may increase stroke risk.
  • Changing the perception of AF. After ablation, patients may not feel AF in the same way. Some may still have long episodes but are no longer bothered by them. I know; it seems strange. I don't understand it either.
    Patient: "Thank you. The ablation worked; my AF is gone. I feel normal."
    Me: "You are in AF."
    Patient: "How is that possible? I felt so bad with AF before, but now I feel great."
  • The downsides of the burns. What are the long-term effects of ablation? The two that come to mind are small brain lesions on MRI scans (most of which resolve) and the possible decrease in LA systolic function. If the atria don't squeeze, what's the point of fixing AF? Although both constitute small risks, one has to remember that many AF patients are at low risk before ablation. Small risks may be amplified in low-risk patients.

 

Obviously, prospective randomized clinical trials are needed to answer these outcome questions. One such study, the CABANA trial, is enrolling AF patients now. Recruitment has been tough, because symptomatic patients want ablation, not drugs. Results will not be available for years.

What can we tell our AF patients now? Is ablation only to relieve symptoms?

As an AF ablation optimist, I think we are doing more than just relieving symptoms. Recent data hint that I may be right.

When Australian and British researchers looked back at outcomes from an AF registry of 1273 patients who had AF ablation, they found encouraging results. Compared with a group of medically treated patients and a hypothetical group of similar patients without AF, those treated with AF ablation had far fewer strokes and better survival. Freedom from AF after ablation lowered the stroke rate by 70%. Females, who typically fare less well with AF, did especially well with ablation. Using historical controls and registry data has important limitations, but these encouraging results align well with other recent look-back trials of AF ablation.

Although the picture is unfinished, a mosaic begins to take shape. As experience and technology make AF ablation safer and perhaps more effective, it becomes plausible to believe in the possibility that our hard-won ablation skills may change the course of the disease.

For now and well into the future, the treatment of AF remains challenging. Getting to the best results for our AF patients requires using all the tenets of good doctoring: knowing the disease, communicating the options, involving the patient in the decision, and then skillfully moving a catheter.

That's refreshing.

JM








Your comments
AF ablation: What are we doing?
# 1 of 19
February 18, 2012 03:57 (EST)
John Hartshorn

The large reduction in stroke risk after a successful ablation seems like reason enough to consider the procedure.

About the AFFIRM trial, didn't the majority of the patients on rhythm control take Amiodarone at some point?  The negative side effects of this drug are so well documented that I wish somebody would break down the results based on which drug(s) the participants were taking. Although the analysis would necessarily lose some statistical power because of reduced sample size it might give valuable information to those considering their options. In over 4 years on Flecainide, 150mg day, I've had only a couple of very brief breaktrough episodes and would not consider ablation unless the drug fails. It would be reassuring to see data confirming the benefits of that choice.

Ablations, no matter how carefully done, will always involve some compromise of atrial function. I've often wondered if anybody is researching/developing a way to control AF with a pacemaker; not a two lead affair that simply delivers shocks at propitious moments, but a network like a mesh cage or something similar that could monitor and correct for the defective impulses that cause AF by short circuiting them near any location where they occur and delivering accurate replacment impulses over as much of the atria as necessary to closely simulate normal contraction. Chip processing power is so good that the challenge would be primarily designing the mesh and contacts to be durable and non-injurious as well as easy to attach, and designing an approriate algorithm to control the device. Just my personal "if only" idea, but it seems so obvious and I've never seen any mention of the idea.

 

 

# 2 of 19
February 19, 2012 10:39 (EST)
Melissa

Howdy neighbor! Really enjoyed your piece and welcome! Great to share the same piece of real estate with you John!

I have been referring patients for afib ablation for nearly a decade.  It's been long enough that a few of my early ablation patients  are coming back around with recurrent afib, proving the same process that begat scarring initially is still continuing. As you point out, though....it now takes a stroke or TIA to get their attention instead of palpitory awareness. 

I still refer for ablation aggressively and believe that my patient's admission rates are dramatically decreased post ablation and their quality of life just as dramatically improved.

Melissa 

# 3 of 19
February 19, 2012 11:09 (EST)
John Mandrola
Thanks Melissa. Aprreciate the welcome.
# 4 of 19
February 19, 2012 11:24 (EST)
John Mandrola

JH,

Thanks for your comment. There is indeed an interesing study that helps to answer your question. 

http://content.onlinejacc.org/cgi/content/full/58/19/1975?maxtoshow=&hits=10&RESULTFORMAT=&fulltext=Cardiovascular+Outcomes+in+the+AFFIRM+Trial+%28Atrial+Fibrillation+Follow-Up+Inves&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

Per their last line: "Death, intensive care unit hospital stay, and non-CV death were more frequent with amiodarone."

# 5 of 19
February 21, 2012 12:17 (EST)
Sarah

John, I have had three cardiac ablations since 2002 (Im now 65) with the most recent one in December 2010, after going 8yrs without symptoms.   However, the re-occurring rate averaged 200bpm, so it wasn't something I could tolerate and I had failed the meds.

As a patient, your description of an implanted mesh device sounds just horrible! I will do almost anything to avoid having a mechanism implanted inside my body.  The idea of mechanical failure, infections and the need for future "parts replacement" and pacing sounds horrifying. As a female minority in the AF club, I was willing to give ablation another try.  I was only 17 when i started tachycardia, and every Cardiologist wanted to put in a pacemaker at some point.  Thank goodness for the advent of EP's and another choice! So far, so good!

 Sarah

# 6 of 19
February 22, 2012 12:43 (EST)
Eric Topol

John,

Great to have you aboard theheart.org. You've got a lot of wisdom to impart to our CV medical community. Welcome!!

Eric

 

 

# 7 of 19
February 22, 2012 08:35 (EST)
GM

The concern that comes to mind regarding ablation is that it may be becoming a version of the hammer for EPs in Maslow's observation, "It is tempting, if the only tool you have is a hammer, to treat everything as a nail."  

The rapidly increasing availibility of this tool could easily overwhelm more benign approaches to the presence of arrythmias where the event, for instance, is short in duration, infrequent, easily tolerated and not accompanied with any other cardovascular condition. There's enough data out there to suggest here that long-term outcomes are similar with or without aggressive treatment. 

# 8 of 19
February 22, 2012 08:57 (EST)
DR.JOE BARRY

Good article. I need to know from the Atria what happened to it and why.I was privy to Juinior Abilskov and Gordon Moe decades ago working on the pathophysiology of AF You need to factor in the  oral ani xa  and anti thrombin thrombin inhibitors in the decision to go for ablation as well as co morbidities. Getting rid of coumadin is half the AF problem.

  Unfortunately AF is very frequently associated with sleep apnea, diabetes, CHD, hypertension, chronic renal failure,and obesity. So to measure success you have to meassure the effect of the remainder of the 6 pack

    I wish I had the time to into this subject because it is a major issue to me a Geriatrician

    Joe Barry,MD,FACP

# 9 of 19
February 22, 2012 11:48 (EST)
Debra

Thank you for this addition of "Trials & Fibrillations."  Many of us A-Fib-ers who try to follow the research will be reading closely.  For many of us, A-Fib is intermittent and entirely related to that cliched term, "sress," and its component parts "anxiety" and "dread" over real ongoing events.  I have records of my intermittent but often severe AFib going back 11 years, which support this reality in my case, which has been called Vagally Mediated AF and has been said to involve the Pulmonary Vein.  So a key question is, are clinicians and researchers anywhere trying to figure out the "front-end" of the ailment in these cases -- what the stress hormones are doing to the relevant atrial node, how to mitigate those adverse effects, find ways of fending off AF episodes, and find ways of cutting them off once they start? A few hours is one thing; several days uninterrupted is another and all of it is quite debilitating indeed.  (Am a propafenone user but have never had a lot of guidance on how much / when to take...)

 Thanks again for coming on the scene!

# 10 of 19
February 22, 2012 11:51 (EST)
Dan Walter

Thank you for this piece. This corporate-driven procedure is riskier and less effective than advertised and people are being hurt -- and killed in some instances -- when inexpereienced operators underestimate its complexity.

Dan Walter, author, "Collateral Damage: A Patient, a New Procedure and the Learning Curve"

 

 

 

 

# 11 of 19
February 22, 2012 12:04 (EST)
Thiago
The risk that young patients with lone AF have a systemic embolism or death that is AF related are close to zero. Thus, any complication from the ablation in this group is completely unjustifiable, eventhough there is a chance of reducing the burden of the arrhythmia. Patients with AF and remodelled left atrial and structural heart disease are those that have increased mortality risk and stroke. However, ablation in this group of patients have poor results, high rates of reccurrences and no definitive evidence of reduction of risks. This scenario is indeed contradictory, because the risks of complications with AF ablation can clearly outweight the risks of the arrhythmia itself. In 2007 in Brazil, we had 2 reported deaths and many myocardial infarctions, strokes, cardiac tamponade, infections, phrenic palsies, oesophageal phistulas etc. Not to say those unreported cases that usually are more frequent than those that are reported. These complications occurred in low risk patients with AF. I will never refer a patient to a treatment that can do more harm to the patient than the disease itself. Furthermore, there is no conclusive evidence in the literature that AF ablation reduces mortality or morbidity from AF. The overwelming majority of patients do fairly well with rate control and anticoagulation. Furthermore, a complication in the lab means several years of wealthy life lost. I also point out that the majority of the studies of ablation in AF are performed by ablationists, not by clinical cardiologists without biased interests in the results. AF ablation still has a long way to prove that is a worthy procedure.  
# 12 of 19
February 24, 2012 08:46 (EST)
Tom Baker MD
  I personally have undergone an ablation.I still have intermittant AF,but it doesn't bother me.What drove me crazy and I couldn't stand was the flutter,which has been cured.Now with rate control and Coumadin,I am doing fine.I would do it again  if it were the first time,but I think repeated proceedures is just asking for a major ccomplication. 
# 13 of 19
February 24, 2012 01:37 (EST)
John G- non medical person

I've had three ablations (UCSF) in 2011 following 8 years of paroxysmal AF during which I went through six meds, including amiodarone with a severe reaction. In the end, my episodes were frequent - couple a week, very symptomatic and lasted 2+ days with 1/2 day for recovery.

In the five months post last ablation I've experienced 3 breakthroughs lasting 6-7 hours, relatively mild. They respond to fleckanide -pill in a pocket.

I strongly endorse ablation. The quality of my life (70 yrs) has improved  dramatically and I cannot believe I will not live longer as a result. I have significantly more physical and mental energy, my exercise level is up considerably and I am my old optimistic self again.

This is very anecdotal, I realize. I have come to appreciate that AF is so variable in it's manifestations that individual experiences make generalizations unreliable. Thus views on rate vs. rhythm vs. ablation must be patient or analogous group specific.

# 14 of 19
March 2, 2012 12:19 (EST)
Alvise Bernabei, MD

The discussion of AF has been very interesting.  The cardiology and medical community also needs to consider minimally invasive ablations for AF.  I recently attended the AF Symposium in Boston and spoke with several EP physicians.  They were very enthusiastic supporters of surgical ablations.  The FDA recently has approved a surgical device for AF ablation.  I am a surgeon that has been performing concomitant ablations with either coronary or valvular surgery for ten years.

New minimally invasive techniques for surgical AF ablation have comparable risk to cath lab ablations, however, the effectiveness of the ablation is far superior.  Stand-alone surgical AF ablations have come of age.  We need more head to head studies comparing EP catheter ablation versus surgical ablation.  Not only do we need to determine which is more effective (short and long term) but do they affect QoL, mortality, and morbidity rates in patients suffering from AF.

# 15 of 19
March 5, 2012 09:50 (EST)
flutterfib

I have both, Aflutter and Afib.  Cardiologist has tried 4 different meds.  They were not working as I was in Afib all the time for 3 weeks.  He did a cardioversion.  Lasted 2 days.

He then increased my rythmol and referred me to an EP.  The EP explained the ablation process to me.  Said he would do one for the Aflutter hoping it would also stop the Afib. That was almost 2 weeks ago.  My flutter and fib stopped just before I saw the EP.  At the same time I did a sleep study.  No sleep apnea but I was not getting enough 02.  Have been on the 02 machine for about a week.  I have had no flutter or fib.

That is the longest that I have not had either Afib nor Aflutter.  Hopefully this will last.  

I was also placed on xarelto. 

# 16 of 19
March 5, 2012 10:43 (EST)
Gary
I had a full-tilt cath-lab ablation done 15 years ago back when the procedure was done by the electrophysiologist cardiologist aka "Mad Scientist". My Atrial Flutter episodes, pre-ablation, were stimulated by my endogenous catecholamine levels.....adrenaline from being a chronic type A, mach 5 "hair-on-fire" type of personality. I personally believe that the chronic catecholamines, endogenously produced, caused my atria to develop new SA nodes to respond to my catecholamines....well, after the ablation....I was instructed to take Propranolol for the rest of my life....being a FP/ER kind of guy, I did what I wanted and decided that I would avoid the side-effects of the nonspecific beta blocker propranolol. I decided to take the cardiac-specific bisoprolol fumarate 5mg....and only prn. Well, that has worked just fine for me for 15 years. I have learned to "cool-my-jets", take life a little less-seriously, slow the hell down and smell the flowers a bit more. I've learned to control my circulating catecholamines and reserve them for "fight-or-flight".....in essence teavhing myself to adopt a more type-B personality. This has helped tremendously....I rarely have what I consider "breakthrough" flutter episodes....usually when stressed emotionally or when overly-tired physically. 1 tab of bisoprolol fumarate 5mg has been shown to flat-out Stop the flutter and eradicate the episode within 15-30 minutes. Take this testamonial as from an experienced insider.....Gary
# 17 of 19
March 9, 2012 01:44 (EST)
Dr. Vince Williams

I have had A-fib for 7 years; now I am 71 years old. For the first five years I was on Amiodorone with varying degrees of success. Then in 2008 I was switched to sotolol/flecinaide with disastrous results. On Amiodorone I always felt "uptight" and extremely tired but all my tests were "normal". Then with the new regime of medications after about two weeks everything seemed to go wrong. Losing weight, very high HR and great difficulty to be mobile. My cardiologist wanted to switch me back to Amiodorone. I refused and discovered from a wide array of tests that my symptoms were traced to an extremely active thyroid. After stopping all medications and about three months in time, everything became normal. Normal thyroid and back to my "old self". In late 2009 I was experiencing periodic A-fib and A-flutter so I elected CA rather than medications. This was repeated in late 2011 because of episodes of mild A-flutter and suspected A-fib. Today, I am free of AF symptoms. I am taking daily Rhythmol and Pradaxa but if all is well in the next month or so and The EKG shows good, then I expect to be medicine-free.

From my experiences, the quality of life issue is paramount. Drug therapy almost killed me. So even if CA has some risks, my quality of life in the last two year, following CA, is far superior to that from drug regimes....Vince W

# 18 of 19
March 15, 2012 01:37 (EDT)
Paul Macnamee
Based on AFFIRM, I do hope you are takign an anticoagulant to reduce your stroke risk. Pradaxa (if non valve), warfarin, etc. You need AC on board, regardless fo rate or rhythym control strategies.
# 19 of 19
March 23, 2012 04:20 (EDT)
David

As an AF ablating EP, I would agree entirely with your comments.

IMHO ablation should be considered a symptom relieving procedure when other methods have failed.  I cannot in good conscience recommend an asymptomatic patient undergo AF ablation, no matter how young.  I share your concerns that the more LA we ablate (first PVI, then CFAE, then lines, etc....) in an effort to get persistent AF patients back to SR (most asymptomatics seem persistent or we would not have found them), the more likely we are to end up with "fried atria" that don't contract.  The surgical Cox-Maze data supprot this fear, with about 1/3 of patients having impaired atrial transport function post-op despite SR.  This could even be worse than AF as the patient and doctor won't know about it from routine examination and ECG, so anticoagulation will not be given. 

Again intolerable symptoms are the only current justification for AF ablation.  If you believe otherwise, show me the mortality data!


You must be a member (with full membership) to post a comment.
Already a member?
Enter your login information below:
 Remember me on this computer
Enjoy all the benefits of theheart.org

With full membership, you can check out our educational and editorial content, search the site, receive our newsletters, join discussions, download slides and much more.

Membership is free!

About the author

Dr John Mandrola practices cardiac electrophysiology in Louisville, KY. He finished training at Indiana University in 1996. His practice encompasses catheter ablation, including an eight-year experience with AF ablation, device implantation, and consultative EP. Outside of the EP lab, Dr Mandrola's two hobbies include competitive cycling and writing. He has maintained a medical, fitness, and cycling blog, Dr John M, for the past two years.