Essential Autonomic Dysfunction - The Root Cause and an Essential Ingridient in Atrial Fibrillation

One wise man said that autonomic nervous system is to paroxysmal atrial fibrillation is what the accessory pathway is to the Wolf Parkinson White syndrome. Why do seemingly anatomically healthy atria have such an amazing ability and such a strong desire to fibrillate? Why do seemingly healthy hearts of young people who have lead healthy lifestyles behave worse than those of hard drug users and 90 year old long-term care residents? We do not have complete answers to these questions yet, but we taking steps in the right direction.

I have recently read an Italian study which evaluate cardiac function and morphology of heavy cocaine users. Of the 30 cocaine addicts studied, 16 (53%) were polydrug addicts (nine cocaine and opioids, six cocaine and ethanol and
one cocaine, opioids and ethanol). The mean drug abuse duration was 12 years (range 3-24), and average self-reported
street cocaine daily consumption was 7,5 grams. Ten subjects reported intravenous use of cocaine, 18 by inhalation (sniffing) and two by smoking (crack). There 24 Hour Holter monitoring results were unremarkable - no
episodes of significant bradyarrhythmias, supra-, ventricular tachyarrhythmias or significant transient ST-segment changes were recorded. The average number of premature ventricular beats was 277 and one subject only showed a Lown >II classification (more than 30 PVCs per any given hour). All patients were asymptomatic and had no cardiac complaints.

Lets analyze this data for a moment. This is population which leads a very unhealthy lifestyle. They consume 7.5 grams of coke a day (!!!!) and have been doing so for an average of 12 YEARS! I am a Social Worker and have volunteered at a homeless shelter before. Many of our clients were cocaine and heroine users. They are a skinny bunch. They might eat once every few days if they are on a binge. I highly doubt that they pay attention to their Mg, K intake. However, despite their extremely unhealthy lifestyles, the drug users in the study did not have any sustained arrhythmias. Furthermore, they did not even have many PVCs, only 1 person out of 30 had more than 30 PVCs per hour. Nobody in that group had symptomatic AFIB, or any sustained arrhythmia. Furthermore, most of them showed signs of fibrosis on their MRIs. Their hearts weren't anatomically healthy, as cocaine induced ischemia caused silent heart attacks, oedemas and toxic necrosis. However, despite all of that they did not have any major heart rhythm abnormalities(1).

The point of this exercise is to underline the secondary importance of lifestyle choices in development of lone atrial fibrillation. Even though 30 people is too small of a sample, it is telling that none of them had symptomatic afib, and none of them had a high arrhythmia burden by any means. I would bet that most people on this board have more PVCs then people in that study. Furthermore, there is no direct correlation between degree of anatomic substrate and arrhythmia burden. Atrial fibrosis does not guarantee AF, just like ventricular fibrosis does not mean one will have VT of VF, or even frequent PVCs for that matter.

Essential autonomic dysfunction is necessary ingredient, if not a primary root cause, of lone atrial fibrillation. The intrinsic cardiac autonomic nervous system serves as more than a relay station for the extrinsic projections of the vagosympathetic system from the brain and the spinal cord to the heart. It functions as an integrative system which acts cooperatively with the extrinsic innervations, but can act independently to modulate numerous cardiac functions (automaticity, contractility, conduction). The intrinsic control centers of this system, known as ganglionated plexi, are located in epicardial fat pads. Pulmanary veins are situatated adjacent to 4 GPs and are highly innervated with both sympathetic and parasympathetic nervous fibers, as they have different electrophysiological properties relative to the surrounding atrial myocardium. Numerous studies show that high frequency stimulation of the GPs lead to shortening of action potential duration in PVs in response to parasympathetic neurotransmitter emission and also causes rapid ectopic bursts from the PVs caused by triggered activity modulated by sympathetic neurotransmitters. Rapid and extensive release of both sympathetic and parasympathetic neurotransmitters caused by GP hyperactivity create favourable substrate for AF - triggering focal firing from PVs serve as a trigger and the rhythm is maintained by functional re-entry (rotors) and ectopic enhanced automaticity (focal beats) which are located in areas corresponding to major release of neurotransmitters (where major GPs are located).

What causes GP hyperactivity? Experimental evidence suggests that the loss of signal from the brain (via the vagosymathetic trunk) results in GP hyperactivity. You can think of GPs as backup generators that turn on when the external source of electricity goes out. However, they end up generating too much power, damaging the circuits and setting the house on fire. For example some evidence indicates that up to 21% of heart transplant patients develop AF within 3 years after transplantation, and only 0.3% of age matched controls develop AF. As the heart is transplanted the signalling from the brain is lost, however the GPs remain in epicardial fat. Furthermore, other animal studies demonstrate that dogs that had their vagosympathetic trunk disconnected from their hearts, developed autonomic hyperactivity. AF could be induced by rapid atrial pacing in these animals more easily than in animals with intact sympathovagal trunks. Endurance sports participation also contributes to ANS dysfunction, as such training routines lead to prolonged hyper-activations of both branches of the nervous systems. Furthermore, the increased baseline vagal tone associated with endurance conditioning can be particularly arrhythmogenic (or rather pro-fibrillatory), as atria have higher concentration of parasympathetic nervous fibers than the ventricles. Nightly AF episodes associated with increased parasympathetic activity occur when Ach concentration excedes a specific threshold, creating islands of fibrillatory heterogeneous conduction in areas of greatest concentration of parasympathetic nervous fibers.

The association between PVCs and AF is also interesting to examine. Idiopathic PVCs commonly encountered in clinical practice usually originate in Right Ventricular Outflow Tract (RVOT). Autopsy and animal studies have demonstrated that RVOT is richly innervated with sympathetic nervous fibers; more so than surrounding ventricular tissue. Therefore, sympathetic stimulation can result in triggered activity from this region, as it is exposed to more catecholomines than the surrounding tissues. Thus, one can have both vegal AFs and adrenogenic PVCs concurently, as both phenomenon can be explained hyperactivation of intrinsic cardiac autonomic system. As parasympathetic fibers are more numerous in the atria and sympathetic fibers are more numerous in the ventricles, the hyperactivation of one of these branches will produce the associated arrhythmia.

References:

STAVRAKIS, S., JACKMAN, W.. Atrial Fibrillation and the Autonomic Nervous System. Hospital Chronicles, North America, 7, jun. 2012. Available at: [hospitalchronicles.gr]. Date accessed: 06 Nov. 2012.

Giovanni Donato Aquaro, et al. "Silent myocardial damage in cocaine addicts." Heart 2011;97:24 2056-2062 Published Online First: 20 June 2011 doi:10.1136/hrt.2011.226977

Heart Rhythm. 2012 Sep;9(9):1393-4. doi: 10.1016/j.hrthm.2012.05.025. Epub 2012 May 30.
Trials and tribulations of stimulating human cardiac ganglia for autonomic intervention.
Lemery R.



Edited 1 time(s). Last edit at 11/05/2012 07:46PM by Namor.

Namor,

Are you an EP or cardiologist? You seem to have a doctor's level knowlege of the heart. In any case, your knowledge is impressive.

A question for you: In your opinion, would de-training help? If I am an endurance athlete, what if I give up bike rides of a certain length (say nothing over 20 miles, and when I do ride, don't ride too hard). Or maybe give up bike riding completely for a month and see how my heart responds.

One of the studies about detraining I read about on this site said that the study participants showed significant improvement after detraining in just 4 weeks. Another study I read about, done in rats who were over-exercised, showed that they actually made a full recovery after detraining (including repair of fibrosis).

Diane

Namor,

You sound like you have been talking to Dr. John Sirak, the surgeon that developed the Five Box procedure (and did mine on January 20.)

The initial step of the five box is a "disection" of the left atrium. Dr. Sirak calls it "autonomic ablation" as he strips the GPs off. I was in a junctional rhythm as a result (however my sinus node recovered as is typical), but for my situation, in all likelihood this is what fixed my LAF. My autonomic system was essentially like having a "cross-wired" heart.

This is an important difference between the Five Box procedure versus CA (or even compared to a Wolf Mini-Maze); during my post op time with Dr. Sirak he talked in detail about the autonomic ablation as the key success factor in the procedure. He told me that most of his patients have failed one or more CAs.

Anyone interested in the Five Box can view videos online at ohioafib.com. The videos are graphic.

EB

Namor:

You are, in my opinion, 100% correct. I came to the same conclusion many years ago and have hesitated to get an ablation because I felt they (the EP's) we're not quite there yet in understanding what is stated clearly and concisely in your post. It seems so damn obvious to any thinking person that it is the ANS that is responsible. Yes, it could be genetic at it's root. Yes, it could be a mutation of genes triggered by a low grade virus or such. There's still a great deal to figure out. But what's with people who get lost seeing the trees and not the forest? Insanely driven marathoners and athletes or those that for whatever reason have an elevated 'flight or fight' response , anxiety problems, etc. It's really the same thing; the ANS gets torked, out of balance, incapable of finding permanent balance unlike 99% of society, and the result is the barometer of the ANS (the heart) goes looney. I know this is stated very unscientific like, but it is no less accurate. BALANCE THE ANS, OR ELIMINATE AN UNBALENCED ANS'S EFFECT ON THE HEART AND THIS AFIB PROBLEM IS NO MORE. PERIOD!!! I have much anecdotal evidence in my own life to substantiate thisand will not recite it here. But for those that read Namor's post--get out the books (now the internet) and research the ANS and how your symptoms, life history, and timing of these afib events fit's with this picture. I've had many years of following the evidence as an attorney, and I'm volunteering to anyone who will listen, this is where the smoking gun is.

WELL SAID NAMOR! YOUR POSTS SHOULD BE MANDATORY READING BY ALL!

Great news, now we know the cause how do we fix it?

I got a PVI. So far it seems to be working



Edited 1 time(s). Last edit at 11/06/2012 03:05PM by afhound99.

Namor,

Great work! I certainly agree.

In my case, my ANS is very much not static. The interesting question is modulating it in a favorable direction.

The electrolyte balance is part of the equation. If my electrolytes are out of balance, a strongly vagal status will result in afib. If they are in balance, I am much more likely to stay in rhythm. Presently I have more tools to play with electrolytes than I do with the ANS (except for flec, which is a crude vagolytic tool and one I don't like to use). I've not played with Propantheline Bromide or its cousins that are antimuscarinic agents and vagolytic.

George

Namor,

Thank you for this most interesting and thought-provoking post. I am looking forward to Part 2. I totally agree that ANS dysfunction play a very major role in LAF. That this is so was first discovered in 1982 by Professor Philippe Coumel of the Lariboisiere Hospital in Paris. Pr. Coumel was, until his untimely death in 2004, considered to be one of the world’s foremost authorities on cardiac arrhythmias. He proposed that there are two radically different forms of LAF, an adrenergic form and a vagal form [1,2].

Pr. Coumel proposed that three conditions need to be met for LAF to develop:

1. The autonomic nervous system is dysfunctional
2. The heart tissue is abnormally sensitive and capable of being triggered into and sustaining an afib episode
3. A trigger or precipitating cause capable of initiating an afib episode is present.

Unfortunately it has taken the medical establishment an awful long time to recognize this crucial involvement of the ANS as evidenced by the still common practice of prescribing beta-blockers and sotalol to vagal afibbers. [www.afibbers.com].

As far as the folly of continuing strenuous endurance exercise once afib has reared its ugly head Pr. Coumel made this comment in his foreword to my first book Lone Atrial Fibrillation: Towards a Cure: [www.afibbers.org]

When asked what must be done to prevent further attacks, I usually tell my patients it all depends on them and that the answer lies in their own observations. This is, in particular, the case for sports, whether on an occasional basis or with the major issue of professional training; excessive training is harmful when it exaggeratedly modifies the ANS balance beyond the sympathetic and parasympathetic physiological values [3]. It is a major mistake to think that the man in the street must be as trained and fit as the professional sportsman. Any common sense driver knows that if he wants to make his car last he must avoid handling it as a rally or Formula I driver.

Finally, in regard to ablation of ganglionated plexi, this is not new. It was an integral part of my 2005 catheter ablation in Bordeaux.

For more on the connection between LAF and dysautonomia you may be interested in reading the proceedings of Conference Room 59 (Dysautonomia and LAF) [www.afibbers.org].

1. Coumel, Philippe. Paroxysmal atrial fibrillation: a disorder of autonomic tone? European Heart Journal, Vol. 15, suppl A, April 1994, pp. 9-16
2. Coumel, Philippe. The role of the autonomic nervous system in atrial flutter and fibrillation, chapter 6. In Atrial Flutter and Fibrillation: From Basic to Clinical Applications, edited by N. Saoudi, et al. Armonk, NY, Future Publishing, 1998
3. Kolb, C., et al. Modes of initiation of paroxysmal atrial fibrillation from analysis of spontaneously occurring episodes using a 12-lead Holter monitoring system. American Journal of Cardiology, Vol. 88, No. 8, October 15, 2001, pp. 853-57

Hans



Edited 1 time(s). Last edit at 11/06/2012 07:48PM by Hans Larsen.

George,

Have you tried D3?
I think your Oz friend may be on to something in the right direction.

DGM Wrote:
-------------------------------------------------------
> Namor:
>
> You are, in my opinion, 100% correct. I came to
> the same conclusion many years ago and have
> hesitated to get an ablation because I felt they
> (the EP's) we're not quite there yet in
> understanding what is stated clearly and concisely
> in your post. It seems so damn obvious to any
> thinking person that it is the ANS that is
> responsible. Yes, it could be genetic at it's
> root. Yes, it could be a mutation of genes
> triggered by a low grade virus or such. There's
> still a great deal to figure out. But what's with
> people who get lost seeing the trees and not the
> forest? Insanely driven marathoners and athletes
> or those that for whatever reason have an elevated
> 'flight or fight' response , anxiety problems,
> etc. It's really the same thing; the ANS gets
> torked, out of balance, incapable of finding
> permanent balance unlike 99% of society, and the
> result is the barometer of the ANS (the heart)
> goes looney. I know this is stated very
> unscientific like, but it is no less accurate.
> BALANCE THE ANS, OR ELIMINATE AN UNBALENCED ANS'S
> EFFECT ON THE HEART AND THIS AFIB PROBLEM IS NO
> MORE. PERIOD!!! I have much anecdotal evidence
> in my own life to substantiate thisand will not
> recite it here. But for those that read Namor's
> post--get out the books (now the internet) and
> research the ANS and how your symptoms, life
> history, and timing of these afib events fit's
> with this picture. I've had many years of
> following the evidence as an attorney, and I'm
> volunteering to anyone who will listen, this is
> where the smoking gun is.
>
>

I think there may be more to it than that. ANS is (was?) certainly a large part of my afib issue toward the ablation end of my current afib journey, but doesn't seem to be for many other afibbers I know. Balance the ANS..OK. (if that's even possible)..but what about the foci that are already permanently changed...and irritable beyond repair - the ANS seemed to lack relevance to afib occurances during my early afib years. That's where an ablation or other means comes in handy! What I've noticed is my post-ablation heart does not over-react to the very same ANS stimuli that had caused all sorts of late-progression problems (both systems) including non-atrial arrhythmias in the form of multi-focal PVC's. So where does the ANS fit in, as the cart or the horse? The same question can be asked of so many aspects of afib; fibrosis, ion-balance etc.

It has been noted by many that an accelerated heart rate immediately post ablation is a sign of a successful procedure.

My local EP explained it in fairly simple terms; your adrengenic sympathetic system is the accelerator pedal for the heart; the parasympathetic system is the brakes. With the Five Box, the surgeon strips the GPs right off (removing the brakes) which allows a rebalancing of the ANS. Catheter ablation of the GPs would cause a similar effect.

Tom B's post illustrates that rebalancing that is occuring during the blanking period.

This just reinforces the idea that when you decide to get the CA, don't just go for the straight PVI- you need an experienced EP with the ability to map and zap the hot spots-

Here is a fairly current study on this subject:

http://www.ipej.org/1106/katritsis.htm]

EB



Edited 1 time(s). Last edit at 11/06/2012 03:54PM by FiveBox.

George,

You do not need drugs in order to balance the autonomic nervous system (ANS). L-theanine is highly effective in dampening an overly exuberant adrenergic (sympathetic) response [www.ncbi.nlm.nih.gov], while ginger is effective in dampening an overly vagal (parasympathetic) response [www.afibbers.com] and [www.ncbi.nlm.nih.gov].

So, if you have a Freezeframer or similar program/instrument that will show you your autonomic system balance in real time you should be able to balance it with theanine and ginger. Of course, you would have to experiment to find the optimum dosage, timing and frequency of administration.

For an example of the effect of theanine administration click here. [afibbers.org].

Hans

PS. For those not familiar with the Freezeframer and similar programs/instruments I would recommend perusing Conference Room sessions 52 and 52a [www.afibbers.org].

Thank you guys for your replies and comments! I am glad that some of you found this information useful and though provoking. The more I read about cardiac electrophysiology, the more I realize how little we know and how crude and primitive our treatment options really are. That being said, I firmly believe that in the next decade or two, our understanding of cardiac arrhythmias, and more specifically the complex interactions between the brain and the heart via the autonomic nervous system will improve significantly. This will ultimately translate into better treatment options for AF sufferers, which will address the root cause of their ailment. Furthermore, the advancement of personalized genetic medicine will one day unable us to offer a much needed individualized approach in managing AF.

I definitely have a sympathetic hyperactivity. My PVCs are definitely adrenergic atrial fibrillation, my AF is largely mixed and adrenergic. I was born with a cerebral hemotoma, which could have damaged my medulla oblongata. I have always have had a fast heart rate and developed AF after a heat stroke. I believe that in my case, the birth trauma has left me with an impaired ANS and the subsequent heat stroke did more damage, which lead to my AF. However, this is only my personal hypothesis and I have no means to prove or disprove it.

Hans can you please recommend me a good brand of L-theanine and a good supplement routine? I have never heard about this supplement before, but I would be interested in trying it... Thank you in advance.

Namor,

I use (and used for the experiment) Stress-Relax by Natural Factors. It is available in the afibbers.org vitamin shop [www.afibbers.org]. I would suggest that you try 500 mg (2 capsules) about an hour prior to your most vulnerable period on a day when you can stay home and observe the results (it may make you drowsy). After that you can experiment to find the optimum dose, timing and frequency for your particular case. Please let us know how it goes.

Hans

Hans,

I tried the ginger the other night. I used 2 tsp of the powdered spice I had in the cupboard. It worked quickly, however it did not last the night. Maybe I need "timed release" ginger...

George

Question for Hans:

To your knowledge, does Dr. Natale go after the ganglionated plexi, or just standard PVAI and LAA? I want the PVAI and per prior posts obviously believe the GP areas are crucial. Am informing Dr. Natale and staff not to do LAA, just map it. Self defeating to be at a higher clot risk and forced to be on blood thinners the rest of my life. Thanks in advance for your response.

I turns out the essential oils Cajeput (Melaleuca leucadendron) and Lavender (Lavandula officinalis) are also vagolytic. [www.dankennerresearch.com] I've not tried them yet.

DGM,

I don't know if Dr. Natale routinely ablates the ganglionated plexi. Perhaps Shannon will know the answer to that. He will certainly do a PVAI and will likely also ablate around the crista terminalis, the superior vena cava and perhaps do a right flutter ablation. He will also, especially if your episodes were longer than about 24 hours, go looking for for clusters of rogue cells (focal areas) and ablate them. I think it is unproductive to try to second guess what he will do in any individual case. Just be assured that you could be in no better hands in the US.

Hans



Edited 1 time(s). Last edit at 11/07/2012 01:14PM by Hans Larsen.

DGM,

Is your ablation already scheduled? You should have an opportunity to ask Dr. Natale that question.

Regarding George's good comments, he may recall that I experimented with Propanthaline Bromide and had a fairly long period with no afib. The problem was that the PB blurred my vision and I could not tolerate even a very small dose. I was a mixed afibber, so even if could have tolerated the drug I am rather doubtful that it would have resulted a "cure" for me. Several others have attempted PB use and I only recall seeing one person who claimed success.

I think it is very interesting that the subject of Autonomic Dysfunction is covered in an older conference room proceeding. There is so much information in those CRs that it becomes virtually impossible to separate the wheat from the chaff. A couple of months ago fibrosis was the hot topic of interest and we were all focused on how to eliminate that.

But to continue our current line of thinking- for many people, GP ablation (or ANS ablation as Dr Sirak calls it) will be a difference maker. If you are just getting a simple PVIA, your odds of success are much lower. Just thinking out loud, I would think that the FIRM system would be one means of mapping the GPs- maybe FIRM will make it a part of the "routine" CA (rather just the PVs).

EB

I got to thinking about other vagolytic agents.

The following may be a source of novel agents for this purpose.

Michael Tierra's review of Botanical Medicine: by Dan Kenner, L.Ac. and Yves Requena, MD (there are probably many other practitioners using similar approaches too). There is much in there of the neuroendocrine approach common in Europe with four nervous system types: sympathetic dominant, parasympathetic (vagotonic) dominant, sympathetic insufficiency, and vagal (parasympathetic) insufficiency. Drugs, herbs, essential oils are classified as to whether they are sympathotonic, sympatholytic, parasympathoimetic (vagotonic), or parasympatholytic (vagolytic). {I just ordered this book}

From: [www.planetherbs.com]

Here is the book: [www.amazon.com]

Most vagolytic meds are anticholinergic.

"pancuronium and gallamine inhibited significantly the bradycardia induced by electrical stimulation of the vagus or injection of DMPP; gallamine was found to have greater vagolytic action. "
[www.ncbi.nlm.nih.gov]

Also:
Atropine, Propantheline bromide, Glycopyrrolate
[www.provet.co.uk]

Propatheline has been used for this purpose successfully. There are posts on using it and references to papers about using it for afib purposes in past forums here. Anticholinergics do have some side effects, most, but not all users say these side effects are manageable.

George

Namor - on the L-theanine, the brand I've usedfor many years is that from Hans' vitamin link with iHerb and is the Jarrow brand - 100 mg. It's just an amino acid with remarkable results. I've shared my success with several other afibbers who have found it to be extremely helpful and several have been able to ward off a full-blown AF event when they take it at the first sign of ectopy.

Naturopathic physician, Michael Murray, writes this about dosing:

L-theanine has been approved for use in Japan as an aid to conquer stress and promote relaxation. It is a very is a popular ingredient in function foods and beverages as well as dietary supplements designed to produce mental and physical relaxation, without inducing drowsiness. L-theanine is fast-acting. Generally, the effects are felt within the first 30 minutes, and have been shown to last up to 8 to 12 hours. For the best results, I recommend taking L-theanine in a chewable tablet (e.g., Crave Relax from Natural Factors) as it seems to produce quicker results via nearly immediate transport to the brain.

Based on the results of clinical studies, it has been established that L-theanine is effective in the range of 50 - 200 mg. If a person has higher levels of stress it is often recommended that they take at least 100 to 200 mg one to three times daily. Although L-theanine is completely safe and without any known adverse drug interaction, as a general guideline it is recommended to take no more than 600 mg within a 6 hour period and no more than 1,200 mg within a 24 hour period.

At typical dosages, e.g., 100-200 mg L-theanine does not act as a sedative, but it does significantly improve sleep quality. It is also an excellent synergist to melatonin and 5-HTP (5-hydroxytryptophan) in promoting sleep. On its own, L-theanine at a dosage of 200 mg was shown in a double-blind trial to produce statistically significant improvements in sleep efficiency, an index of actual sleep time enjoyed between the time of falling asleep and nighttime awakenings.

Jackie

I take Atrovent inhaler for a low grade asthma condition - it is ipratropium bromide, a derivative of atropine, and is vagolytic. I am a vagal affiber (with a pulse in the low 50's), but it doesn't seem to help as far as I can tell - I take it every night and every week or two I have an episode in the middle of the night. The reason it doesn't seem to help is that supposedly it doesn't disperse into the bloodstream (a reason it has few side effects and is considered a safe drug), so I assume it isn't impacting the ANS. Too bad I guess.

Hi DGM and George,

Yes indeed, Dr. Natale addresses GPs as and when they are found to be trouble spots in each patients. Some of the anatomical areas he addresses and ablates outside the PVAI also include areas of GP overlap and involvement. The same is true for rotors area which often overlap these over focal hot spots beyond just the PVAI. Dr. N also addresses other focal hot spots like CAFEs when they too are found to be active triggers as well as ablation of the SVC, CS, mitral isthmus, roof line across the top of the LA, back wall of the LA and Crista terminalis when needed.

He also will do a right atrial flutter preventive ablation on the way out as well when it is warranted, especially if the person has had persistent AFIB and/or required a complex long ablation to begin with. Finally, he now maps and often addresses any significant trigger sources around or inside the LAA, including in some cases full isolation of the LAA when that is required to stop the main source of AFIB/Left Flutter. THis is usually the case with when the main or only source of arrhythmia is located around the mouth of or within the LAA itself.

Its not so common for there to be significant LAA involvement out side of persistent Afibbers or those with long episodes after many years of increasing paroxysmal AFIB. If you are mostly a pure paroxysmal when you get you ablation with Natale its uncommon that LAA will be an issue he would have to deal with. It can be, but its relatively rare in those easier patients.

For those that would arbitrarily instruct Dr. Natale not to do any work around the mouth of, or inside, the LAA for fear of having to possibly deal with lifelong anti-coag or have to go for a Lariet-II or similar new procedures in the future to block off the LAA mechanically such that no drugs would be needed you might want to think this decision through a bit more?

I suspect that most people with that thought don't have persistent AFIB or a very difficutl symptomatic case yet as it is? Keep in mind that if the LAA is one of your main problem areas and it is not dealt with teh odds are extremely high for having on going and increasing breakthroughs until possibly persistent AFIB arrives as a conseqence of too much remodeling?

And keep in mind that persistent AFIB, in most cases, would eventually demand anti-coag anyway at some point when left unsuccessfully treated. Once you have a very symptomatic persistent AFIB, dealing with Coumadin, or Apixiban, as much of a hassle and unwanted thing to have to address, its a walk in the park compared to ongoing 24/7 symptomatic AFIB/ Flutter or even dealing with atypical left flutter taht originates ONLY from the LAA after a first successful AFIB ablation .. and thus those periodic flutter episodes always will require same day ECV at a local ER to get out of it and back to NSR every time!

The question you need to ask yourself before seeing Dr. Natale is, what if he discovers that either THE major source.. or even the ONLY source ... of your arrhythmia is within your LAA??? Should he then just pull the catheters and let you fend for yourself?? Think about it ... I realize its not what anyone would prefer, but some manifestations of this beast don't leave one with all the most appealing options and achieving much greater periods of NSR is a real blessing when it is there for the taking. In any event, there are now newer options like the Lariet-II that can free you from the drugs too, even after an LAA isolation. But first you might not even need any blood thinner drugs long term nor a lariet-II procedure and might well be free of the whole show if and when a TEE six months later confirms your velocity of blood flow out of the LAA is high enough to all you to safely stop all blood thinners. The odds of that after successful full LAA isolation are about 50/50 according to Dr. Natale's extensive experience.

But back to the main thread topic Namor and Hans have clearly noted that the ANS is a major issue at the core of our problem and no doubt further understanding will pay major dividends in more and more targeted treatment methods to address this all too common dysfunction in our group of people on a case by case basis. That will likely be a huge help when greater progress is made along these lines as well.

Shannon

Shannon: Thanks for the instructive post. But if the LAA is such a potential trouble spot, why, in my understanding, is Dr.Natale the only EP that ablates this area? Many other 'difficult' AFIB/flutter cases seem to be successfully addressed by other EP's without doing the LAA, (e.g, Hans in France, if I'm not mistaken.) Also, I ride quarter horses and do ranch work on them--and yes I get banged and bruised sometimes. Lifelong blood thinners, a mechanical device (lariet et. al.,) or removal of a body part (LAA) god/nature put there for a reason is sort of a non-sequitor for me. Also, are you saying that left flutter after an otherwise successful ablation ONLY arises from the LAA?

Thanks in advance for your amended and further answer. I appreciate your input.

DGM

Dr Reddy at Mt Sinai told he he rarely touches the LAA doesn't see much of a problem there.............

Hi DGM,

First of all I want to answer your last question from your reply above.

No. I am not saying that all left flutter after a first ablation arises only in the LAA. As noted below, in less than 30% of patients requiring a follow-up ablation was any LAA involvement discovered at all, and that includes people with both AFIB episodes and left flutter. So you are not at all automatically fated to have to deal with LAA issues in any event. Its much more commonly found in people with a long history of AFIB that has evolved into persistent 24/7 AFIB/Flutter for some time. Another good reason for not waiting too awfully long if and when you have exhausted all of your more natural options for controlling this.

And I hear you on not wanting to have to rely on blood thinners or Lariet procedures to insure your stroke risk is minimal after such an ablation. I felt exactly the same way until requiring 13 ECVs in 15 months for left atrial flutter and then learned that my LAA was the only culprit left that triggered those flutters. Nevertheless, rest assured Dr. Natale is in no hurry to isolate your LAA either and would only do so should he find during mapping that it is the main or sole source of your problem...

I brought up the issue for you to consider during your decision making .what if he finds the LAA in your case IS your only trigger area?? If you are not persistent AFIB that is not likely to be the case at all, so take heart in that. But I do want you to think about such a scenario prior to telling him to forget addressing your LAA under any circumstance. Nevertheless, I'm sure he will honor your wishes on the matter but he will likely explain the consequence if yours turns out to be such a case and he then can do nothing really for you outside of a more preventative kind of ablation around the PVAI.

Alas, we cant always pick and choose the parameters of what should work well for us as each of us have different manifestations of this beast.

And Dr Natale is definitely not the only EP, by any means, who ablates around and within the LAA! A number of Japanese and European EPs do so, in addition to most of Natale's group as well whenever it is clearly indicated. Also Dr. Jais and Haissaguerre at Bordeaux frequently address the LAA when they find it a trigger source ( though as of last year they mostly stuck with focal ablation within the LAA , which in some cases can do the trick but not in all cases and not always as reliably .. especially when the LAA is the only source of trouble.. in which cases LAA isolation is the only way to skin that particular cat.

Keep in mind too that LAA is not at all the most common trigger source for the average Afibber and even among persistent Afibbers roughly only 27% have significant hot spot action from the LAA.

You will find that many even up and coming EPs who are starting to develop a name for themselves, will be somewhat selective too in the type of cases they try to take on. Natale and Bordeaux get a larger percentage, by far, of the really difficult repeat cases than most other busy EPs without the same level of experience. From what I have heard, and can easily imagine as well, a good percentage of these up and coming EPs are understandably not as eager and willing to be quite so exposed on the cutting edge of development and feel more comfortable sticking with the more tried and true technigues while leaving it to the guys with more mileage under their belts to press the envelope of ablation technology first.

Its not surprising then when you hear such remarks as "We haven't found it that common yet" when quite possibly their own inherent selection screening criteria for choosing patients might well filter out a fair number of those who are more likely to have LAA involvement and thus make them less likely to recognize its presence in the broader class of persistent patients.

Not surprisingly, the average success rate for persistent AFIB ablation in the past has ranged from 40% to 50% for typical decent EPs with some experience ... up to around 70% for more elite EPs when their procedures did NOT include mapping and addressing the LAA.

Isn't it interesting then that in the 970 some odd patient study of people needing a repeat ablation that this well done study found 27% had ongoing significant firing from the LAA region! Perhaps that is a not such a coincidental finding? At least common sense would say there certainly appears to be a correlation between what Natale's group have found to be the approximate prevalence of LAA involvement in those needing a repeat ablation at 27% (note: in roughly 8% of those LAA was the ONLY source of arrhythmia) in comparison to the 30%, best case, of persistent afibbers who still have unacceptable arrhythmia episodes often after several ablations, simply due to their EPs avoiding even looking at, much less ablating around, the LAA during those follow up ablations!

This can lead to 3rd and 4th and 5th and 6th ablations .. and so on .. with what amounts to dancing around the increasingly large elephant in the room, trying to zap newly found hot spots in the Left atrium, just to avoid going to the LAA where the going requires a bit more care and confidence in their skill with a catheter.

Its no surprise that many less experienced EPs are still leary of even looking at the LAA at all as it does require more skill and dexterity and they fear pressing too hard and possibly causing a tamponade through the somewhat thinner wall of the LAA than is found in most,, but not all .. sections of the LA itself.

Hence, many of those EPs at this point are still waiting for more studies to come in to convince them they need to buck up and get with learning how to do this. And in the meantime, they will very likely be stuck at around 60% to 70 % at the very best outcome for persistent afibbers, even with repeat ablations factored in.

Nevertheless, the more difficult cases where perhaps more LAA involvement is the culprit , by the shear force of the stress and hassle of having to live with this beast like that, will most often drive these folks (me among them) eventually to either Natale's table or one of his colleagues or to Bordeaux. And that's one reason why these top centers remain at the cutting edge of development too in this field. They constantly see the most difficult and challenging repeat cases and thus don't have quite the luxury of most other front line EPs still climbing their experience ladder with less than a couple thousand ablations under their belts and who can still cherry pick their patients more easily to help pad their 'success' stats.

DGM, this article posted earlier in a different thread by researcher a couple weeks ago, is one of an increasing number of case reports and studies now starting to come out that are shedding more like on the LAA involvement issue. So, it is very much becoming a hot topic in AFIB research and development. AFIBSustained tachycardia in the Left Atrial Appendage

Natale is at the very forefront of this research as well and as such, its not surprising that many other EPs have not yet caught up with the lead wagon on this issue. There is still much to be learned and that is understandable.

Another thing you will find too in this EP world, is some real competition within such a number of EPs, some of whom reflect a bit of a 'not invented here' mentality.

In any event, I go into all this to hopefully help shed some light on the more typical human side of these docs, and we all know how it goes in many such competitive fields. Its not uncommon for experts to disagree, particularly in such a rapidly growing and complex area as AFIB electrophysiology and many will not always keep up with those at the forefront of progress. The majority.. as in every technical field I know of.. will typically lag behind the relatively few true leaders in any given field, and many less informed members will, during periods of new development, often disregard or dismiss those new newer developments that they are not so familiar with or that prove extra challenging, but that may well become standard of care procedure a few years hence.

Its a good idea, I feel, to keep this dynamic in mind when trying to sort through such conflicting claims. Take a look at the level of experience those opinions are arising from? No one is infallible of course, and even the best EPs make mistakes and have some unexpected outcomes in some difficult patients, but my bet will be on those Doc's who have established themselves at the forefront long ago and have remained at that cutting edge for well over a decade now running.

Another key point about the LAA ablation, Natale started to recognize this issue some time around 2006 and slowly started working focally around and within the LAA. Starting in late 2008 to 2009 he and his larger group in the US and Italy began doing full LAA isolation when the focal-only approach within the LAA proved insufficient for a fair number of persistent afibbers. He started to do LAA isolation in selected patients either during the first ablation when LAA was clearly the only or the major trigger, or more commonly he would reserve full isolation for follow up ablations so he could see how well the patient did with the comprehensive first ablation before adding any burns in or around the LAA. Only then in many cases does he address the LAA at all to deal with on-going arrhythmia once it is demonstrated during that follow up ablation that all other source areas like the PVs and other focal spots ablated the first time were still solid and had developed no leaks.

At the end of 2012 now, Dr Natale and his group have been doing LAA isolations quite frequently for four plus years due to the many challenging cases that get referred to him, in particular, every week. And I know from our conversations about it that he is even more convinced now after all of this experience of the importance in addressing the LAA in those who have significant LAA firing. Anyway, I hope that gives some more nuance on the situation for you to sort through in your decision DMG.

Shannon



Edited 3 time(s). Last edit at 11/13/2012 03:37PM by Shannon.

Shannon,

An EXCELLENT post. Thank you for your time and effort in writing it!!

George

Thank you for your thorough and informed post Shannon. Definetly food for thought. Like all, I'm weighing and balancing each fine point to attempt to get the optimal result with the least downside. I do greatly appreciate your time.

DGM

You are most welcome DGM and George,,

I know all too well that it's a complex subject and trying to thread the comfort needle for each of us is a challenging and personal task. If you wish to discuss it further or in more detail, you can PM me and we can chat on the phone about it if you like.

Shannon

This post should be required reading for anyone getting serious about addressing their afib. It would be an interesting study to compare ablation success rates of patients with PVI only versus patients with ablation that address the GPs; obviously my money would be on the latter having a significantly higher success rate.

To address one comment in Shannon's excellent post (where he talks about having 3-6 ablations); before anyone has the third ablation they should seriously consider an alternate procedure such as the Five Box. As I said earlier, the Five Box does an "Autonomic Ablation" (Dr. Sirak's term), as well as addressing the LAA (with an atriclip). That's how he gets a 90%+ success rate.

Thanks to Namor for bringing it up-

EB