Help Me Understand Why Atrial Flutter is More Common After an Ablation than A-Fib

I asked this question to Dr. Natale's team during my overnight stay after my recent 3rd touch up ablation and Watchman implant and the answer they gave me didn't help much. They just said it's not uncommon to experience atrial flutter after an ablation vs a-fib because the ablation allows the abnormal arrhythmia to be more regular (but fast).

The part that is missing in that answer is WHY does an ablation allow for a more regular, but fast, arrhythmia (i.e. flutter)?

If the ablation is a success, that means the scar lines are durable and are blocking ALL abnormal signals, correct? If that's the case, then how does any arrhythmia occur (a-fib or flutter)? And if there is a "break in the wall," that is, if something is getting through one of the scar lines, why wouldn't you still just experience a-fib? What happens during an ablation that blocks a-fib but allows atrial flutter?

I'm just having a really hard time understanding why atrial flutter is so much more common after an ablation than a-fib.

Travis

P.S. I ask this because I haven't experienced any a-fib since my Natale index ablation back in 2015. I went almost 8 years before I started having atrial flutter episodes in late 2022, which resulted in my 2nd ablation (LAA ablation). Then I had a few more atrial flutter episodes after that ablation so I just had a third touch up ablation by Natale. They told me that I may experience some "flutter episodes" during the blanking period. I'm just curious why my battle is mostly with flutter now and not fibrillation.

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tvanslooten
If the ablation is a success, that means the scar lines are durable and are blocking ALL abnormal signals, correct?

Yes, after the ablation lines have formed scar tissue and become non-conducting, and that takes a couple of months. Hence, the blanking period.

Flutter happens after an ablation because flutter is caused by electrical barriers in the atrial tissue that aren't perfect, that have holes in them where a signal can pass through and then keep going around and around in a self-perpetuating circle. Imperfect electrical barriers are exactly what your ablation is until it has completely formed scar tissue.

Are you taking Flecainide? It has been shown to cause more Flutter. I and others have posted on our experiences about this.

As for your question, in AFIB the Arrhythmia is a fibrillating chaotic Atria, vs a fast circular re-entry circuit in Flutter. The Ablation often works well enough to inhibit global fibrillation of the Atria, but not well enough to stop the circular re-entry circuit.

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Carey

If the ablation is a success, that means the scar lines are durable and are blocking ALL abnormal signals, correct?

Yes, after the ablation lines have formed scar tissue and become non-conducting, and that takes a couple of months. Hence, the blanking period.

Flutter happens after an ablation because flutter is caused by electrical barriers in the atrial tissue that aren't perfect, that have holes in them where a signal can pass through and then keep going around and around in a self-perpetuating circle. Imperfect electrical barriers are exactly what your ablation is until it has completely formed scar tissue.

after the ablation lines have formed scar tissue and become non-conducting, and that takes a couple of months. Hence, the blanking period.

Is the scar tissue you refer to, that which is formed arround the pulmonary veins?
Also do the ablated scars break down over time, as in Travis case, he had no flutter for 8 years after his first ablation.

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colindo
Is the scar tissue you refer to, that which is formed arround the pulmonary veins?
Also do the ablated scars break down over time, as in Travis case, he had no flutter for 8 years after his first ablation.

Yes, that's the scar tissue I refer to. No, an adequately done ablation line will not heal over, but an inadequately formed one will, which is exactly what explains many ablation failures, including mine. When I finally dumped EP#1 after his 3 ablations all failed months afterwards, EP#2 found no evidence whatsoever I'd ever had an ablation at all. My pulmonary veins were completely unisolated. EP#1 was too timid and didn't burn long enough or deep enough, so my body healed over his ablation lines. I'm certain this explains most failed ablations.

But after 8 years this doesn't explain Travis' recurrence. An ablation line that holds for a full year is permanent and complete. What happened to Travis is simply progression of the disease. That's true for everyone here who's had afib or flutter recur years later. The ablations aren't failing; your body is simply forming new fibrotic tissue all on its own. That's why EPs have come to understand afib as an underlying heart disease known as atrial myopathy. It's also why the term "lone afib" is no longer recognized. Having afib is a form of structural heart disease, so the term doesn't make sense and misleads our thinking.

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Carey
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The ablations aren't failing; your body is simply forming new fibrotic tissue all on its own. That's why EPs have come to understand afib as an underlying heart disease known as atrial myopathy. It's also why the term "lone afib" is no longer recognized. Having afib is a form of structural heart disease, so the term doesn't make sense and misleads our thinking.

If the electrical signals are coming from the gut then it's a gut problem and not the heart. Is that correct?
That would explain why some people like GeorgN, Dean and Steve Carr have been able to stop Afib through diet only.


BTW Dean has a post about Steve Carr on the General Health Forum.

Nothing whatsoever to do with 'the gut'. This is all part of the heart's self-management system, just like your automobile's systems. They work together. Part of the cardiac system is its electrical distribution. In AF, some of the signal migrates through the lining of the pulmonary veins and ends up being 'picked up' by endothelial encroachment of atrial tissue into the 'ostia', or mouths, of the pulmonary veins. By burning a 'stockade' of scar tissue around those ostia, you don't get passage of the electrical signal, the unwanted extra signals, from causing the atrium to beat yet again, out of sequence, with the original signal from the SA node.

The people you name have found that there are apparent triggers to their bouts of AF, when they happen. Some blame caffeine, some swear it's even a whiff of a cork, some blame MSG, and so on, and so forth. There is also considerable evidence that the Vagus Nerve has a significant part to play in AF. The Vagus Nerve is part of the PARA-sympathetic nervous system. It's part of the 'calming network'. It helps to keep your heart slow and steady, and loses the round when adrenaline kicks in. That is why you get beta-ADRENERGIC blockers to help with AF.

Calming oneself, relaxing, meditating, and not eating too much or the wrong foods can help a person's Vagus Nerve keep their AF in check.

I agree with gloaming's answer but let me see if I can simplify it a bit....

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colindo
If the electrical signals are coming from the gut then it's a gut problem and not the heart. Is that correct?

Maybe it would be if electrical signals come from the gut, but they don't. The source of atrial signals is well documented and well understood. In a normal heart all atrial signals arise from the sinus node, as they should. But in someone with afib, there are atrial cells that are firing on their own at improper times, a property heart cells have known as automaticity. Automaticity is an evolved feature that can be lifesaving, but sometimes it can go out of control, and that's what afib is.

If you want to see automaticity in action, just look at someone in third degree heart block. None of the normal sinus node signals are passing through the AV node and yet the heart doesn't stop. That's because cells below the AV node in the Bundle of His are firing via automaticity and that keeps the ventricles pumping (at a much reduced rate, typically 20-40 bpm).

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Carey

your body is simply forming new fibrotic tissue all on its own. That's why EPs have come to understand afib as an underlying heart disease known as atrial myopathy. It's also why the term "lone afib" is no longer recognized. Having afib is a form of structural heart disease, so the term doesn't make sense and misleads our thinking.

Carey - that's sobering. Given the progression of a-fib, does that mean it's impossible to put it to rest for good no matter how many ablations you have and no matter how well those ablations have been done? I remember when I was first ablated 8 years ago the mantra everyone was seeking was, "one and done." That was everyone's goal. It rarely happens it seems.

I'm up to 3 ablations now under Dr. Natale. I know someone else that has had 4 Natale ablations. Are people like us just doomed? Will there come a point where we've had enough "good" ablations that we'll be free of a-fib or atrial flutter, or will it be an endless game of whack a mole where we'll just need an ablation every few years? And is there a point where you can't do any more ablations???

Travis

Travis,

My experience is different. I had my first episode in early July 2004 (nearly 19 years ago). I was having episodes every 10-14 days lasting 9 or so hours and self converting. Around the end of August, an episode started that lasted about 2.5 months. It converted in 20 hours with a 300 mg dose of flecainide. Had one a month later that also took 20 hours to convert with 300 mg flec. I later hypothesized that atrial stunning was still present for this episode. With research, I determined that chronic fitness was a trigger and had been a primary driver for me getting afib.

When my lack of frontal lobe ("sarcasm") let me, I detrained such that for any long duration activity, I let nasal breathing be my governor (and . I also started supplementing with taurine and lots of magnesium and some potassium citrate). When looked at through this lens, my afib hasn't gotten worse. In the first 4 months of afib, my AF burden was 57%. Most subsequent years it has been in the 0.02% range. Around 2012 was materially worse than 0.02% but still < 1%. I learned that excess food consumption of calcium was to blame for that and rectified it. Later, had a family member diagnosed with terminal cancer. I took my eye off the ball for a bit and would miss my magnesium supplements, leading to a slightly higher burden. I refocused and my control returned. More recently, taking mRNA vaccines has been associated with more episodes, to the point I started taking 25 mg flec daily. Had a 0.12% burden in the last 12 months. I've also learned that reducing my PIP dose of flec to 200 mg made it much more effective. I will probably experiment with lowering the daily flec dose to 12.5 mg/day and perhaps try eliminating it altogether & see if it holds. Even a more active afib burden year of 0.12% is still vastly better than 57%. In my case, I'm sure that eliminating the chronic fitness driver was key to not having progression. I can still do short duration very high intensity workouts without it being an afib trigger. For example, I have a fan bike workout where I warm up for 3 minutes, then do 8 rounds of 15 seconds absolutely as hard as I can (and commonly with BFR bands on, restricting venous return and creating mild hypoxia in the muscles) and 15 seconds at 50 watts, then a 3 minute cool down at 50 watts. I know we are all different, but that is my story.

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tvanslooten
Carey - that's sobering. Given the progression of a-fib, does that mean it's impossible to put it to rest for good no matter how many ablations you have and no matter how well those ablations have been done?

I wouldn't put it so bleakly. Like everything in medicine, the individual matters. One person might get an ablation and live out the rest of their life afib-free while the next person who appears similar in every way might find afib returns 10-15 years later. The "why" of that would be almost impossible to pin down.

The reality is that no matter how well ablations are done, new sources of afib can develop later outside the area the ablation isolated. This is a result of aging, genetics, and lifestyle. Things that tend to enlarge your left atrium also tend to create fibrotic tissue over time. Such things include hypertension, endurance sports, and weightlifting. Also contributing are obesity, diabetes, sleep apnea, hyperthyroidism, and of course all the bad stuff like drinking, smoking, etc.

So in the end, it really just boils down to luck and taking care of yourself as best you can.

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Carey



So in the end, it really just boils down to luck and taking care of yourself as best you can.

That makes sense. Thanks!

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tvanslooten
[I'm just having a really hard time understanding why atrial flutter is so much more common after an ablation than a-fib.

Along with everything else said here, to put it simply, atypical a-flutter can coexist with afib, and may or may not be related to the afib:

"LA MRATs [Left Atrial Macro Re-entrant Tachycardias, the arrhythmia class to which atypical a-flutter belongs] are less common than typical AFL and are frequently related to or coexist with AF. LA MRAT is a known complication of surgical and catheter-based therapies of AF, and it can occur in up to 50% of patients following extensive catheter ablation strategies . . . Additionally, cardiac surgery involving the LA or atrial septum can produce different LA macroreentrant circuits. However, LA circuits also can be found in patients without a history of atriotomy or prior ablation. Electroanatomical maps in the latter group often show low-voltage or areas of scar in the LA, which act as a central obstacle or barrier in the circuit. These areas are typically located at the posterior wall (45%), superior region (roof, 28%), or anteroseptal region (27%) of the LA. The pathogenesis of these areas with no electrical signals is not well established. Potential causes include volume and pressure overload (mitral valve disease, hypertension, heart failure), ischemia (atrial branch occlusion), postinflammation scarring (after myocarditis), atrial amyloidosis, atrial dysplasia, and tachycardia-related structural remodeling. These macroreentrant circuits show considerable anatomical variability and frequently involve multiple simultaneous loops." Source: [musculoskeletalkey.com]

I'm a mitral valve repair patient (annulus implant, 1995), and a recent afib/a-flutter patient. The open-heart MV repair itself put me at risk for atrial arrhythmias, though they took many years to develop. It started with transient paroxysmal a-flutter, which I didn't recognize at the time, and progressed to persistent afib, which I also didn't recognize, then CHF with a left atrial thrombus. Long story short, I was evaluated in CCU by three cardio teams, they stabilized the CHF symptoms, dissolved the thrombus, CVed me to NSR, and my ejection fractions and valve functions returned to normal. Since then I've had afib recurrences and have been ablated twice (PVI, then PVI touchup and LA posterior wall). That stopped the afib, but I began having a-flutter episodes (as in the early days) which would give way to afib while I awaited CV (usually takes a week to get one scheduled). Currently I'm trialing PiP Flecainide, which works well (I'm already on supportive Carvedilol). So in my case, it all falls under the category of Valvular Disease, probably congenital. But what first caused the a-flutter -- atrial remodeling from mitral proplapse? Surgical scarring from mitral repair? My EP says currently it's chicken-and-egg. Or maybe precocious vascular cells? Inherited tissue hypermobility? An unnoticed viral infection? Some combination? Who knows?

My personal feeling is we're seeing more atypical a-flutter because we're doing more afib ablations -- not a causative process, but a discovery process.

Regarding (sorry, can't remember where I saw this in the forum) convergent procedures being for afib only, that's not quite true. In the 3D cardiac substrate LA MRATs can travel to or across portions of the epicardium, so there may be a role for convergent procedures for atypical a-flutter case-by-case. In any event, they're working on improved mapping and ablative techniques for LA MRATs, so fingers crossed.

P.S. Thank you all immensely for this forum, been lurking and learning for quite a while.



Edited 1 time(s). Last edit at 05/17/2023 11:03AM by KathyM.

Thanks for this. Your history is interesting KathyM. I developed severe mitral valve regurgitation which was repaired with a transcatheter MitraClip—so presumably no surgical scarring other that the puncture of the atrial wall. But I did have atypical flutter before my ablation and Dr. Natale did need to ablate the posterior wall, the roof and the LAA. He had told me that my history of mitral valve disease would likely mean that I would need an extensive ablation. It is an association that seems to need more attention.

Daisy, absolutely, that makes sense. I'm glad you were able to have a catheter-based MV procedure. I was one of the early patients to receive an annulus repair instead of a full replacement, it was a new technique at the time and my surgeon had learned it at Cleveland Clinic. Over two decades later TEEs show it well-seated and still working. I'm amazed at the catheter-based work they're doing today at every level. Events leading up to my first CV in 2017 saw my first time in a cath lab in over two decades, and my first ablation in an EP lab four years after was mind-blowing, so different from everything back in the day. It gives me real hope, having seen how far the tools and techniques have advanced from 1995 to now.