Thoughts about preventing recurences of AF after ablations

In my earlier blog on oral Mg I mentioned I have been fortunate converting my long-standing persistent AF (2 years duration) to SR with my low risk, low cost protocol for almost 18 months.. As I described previously the protocol involves careful titration of a well absorbed, fast acting, oral Mg that maintains stable blood Mg levels needed for 20 weeks to convert to SR. The protocol emphasizes daily self monitoring of EKGs; remaining hydrated and testing my urine specific gravity occasionally (it should remain 1.020 or less) and monitoring potassium needs. All of it sounds routine and familiar except I made a deep research dive into the medical literature to discover underappreciated observations to support my protocol. I have wondered since I have been able to accomplish this without the need for ablations , medications, electric cardioversions whether my protocol could be implemented before interventions and continued after they are done to determine if AF recurrence rates might reduce. In order to determine if my thought has plausibility, individuals with planned ablations might help themselves by introducing my protocol to their EPs. That would mean the EPs would be willing to take time to read the protocol and determine whether their patient is a candidate for the protocol. I imagine they will likely defer reading it because it will be viewed as quackery and non-scientific because it describes the experience of one individual. Reading the medical literature and the stories on this forum, recurrences of AF occur frequently. Would a low-risk protocol be helpful in this regard? For those who do not know I am a physician who wrote about my heart story in a book on Amazon titled "Atrial Fibrillation: How a physician converted his atrial fibrillation with a low-risk, low-cost protocol". On line the cover shows a doctor holding binoculars . All of the above is conjecture but so far I haven't read about treatments that have been successful preventing AF recurrences . just thinking out of the box.

Having yet to read your book, I assume your ECG monitoring was to see if your persistent afib ended?

My hypothesis has always been that my consumption of electrolytes would have a much higher efficacy keeping me in NSR rather than conversion. Hence my own approach, subsequent to my 2.5 month persistent episode 20 ish years ago (with some exceptions for experimentation) has been to take a loading dose of flecainide as soon as I know i'm in afib (I also learned after quite a few years that reducing this dose by 1/3 materially lowered conversion time). I also chew the foul tasting pills to increase the rate of absorption, sometimes holding the chewed pills in my saliva for.sublingual absorption. This way I minimize my time in afib (median conversion time is sub two hours) and any remodelling that occurs. Having very few episodes also contributes to a low AF burde

George first yes to the EKG daily self monitoring (3-4 times for 30 sec each- only 2 minutes a day), and substitutes for Holter but obviously not 24/7. The other self monitoring I look at is the end of the week reporting of AF on the iPhone which reads less than 2% AF. That; is because it can not detect every heartbeat. Being a little OCD I also do Kardia or Apple phone depending which is available for the day time. Lastly I mentioned that the heat rate variability percentage is a canary for me as to developing asymptomatic AF. When the heart beat intervals are short msec (under 20 msec) I don't have AF but when there is a wide separation between two heart beats(up to 140 msec) then I have AF. I believe there are AF individuals who when they are not symptomatic may have asymptomatic AF. Self monitoring will tell one if that is occurring and if it is, then there is an increased risk for stroke even on anticoagulants Obviously the goal is to remain in SR.

I have no experience with flecainide. My reading on it , although rare is it can prolong the QTc interval calculated on the EKG which makes one susceptible to a life threatening ventricular arrythmia . Since I have always been asymptomatic I have not been confronted with the need for it as I remain in SR with my protocol.

Flecainide kept me in NSR until it didn’t 15 years later.

I did get a flecainide overdose that caused V-Tach because I exceeded the dosage based on my weight. If one weighs less than 154 pounds, the maximum dosage in a 24 hour period is 200mg. If your weight exceeds 154 pounds, the maximum dosage in a 24 hour period is 300mg.

[www.afibbers.org]

From your other thread.

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Hugging
Another part I didn’t discuss has to do with % Heart rate Variability ( HRV) which is time between successive heart beats recorded without my awareness on my iPhone. When the interval in msec is large like as high as 140 msec, I have AF. In contrast when the interval is short between heart beats it ranges around 14 msec and I don’t have AF. I can use the HRV as a canary to tell me I am having asymptomatic AF. I have not seen that reported in medical articles.

I agree that HRV can be a metric. However the actual values will depend on age, sex and will vary significantly between individuals. Here are some data on the mid 50% of HRV by age. At 69, my normal overnight HRV tends to run between 30 & 70 ms with a median around 45 ms. My 35 year old daughter runs between 120-140 ms overnight.

I've also found that devices that rely on plethysmography aren't particularly accurate during afib. I have some examples where I had on a recording ECG grade heart rate monitor chest strap as well as a recording plethysmograph device and the peaks & troughs are much greater on the strap than the pulse waveform device during afib. During afib, there is not a lot of RR (beat to beat) time in ms variability, there is also a lot of variability in pulse wave amplitude. This amplitude variability makes it difficult for plethysmograph devices to "see" each beat.

Also, one app I have will monitor HRV for 2.5 minutes. A few PAC's in the sample can dramatically increase the HRV. The app is supposed to "see" and correct the ectopics, but does a poor job of this.



Edited 1 time(s). Last edit at 02/07/2025 01:19PM by GeorgeN.

Hi George

Here is my literature validation for my own observations that when I have attenuated HRV (short msec intervals between successive heart beats) no AF occurred and when I have unattenuated HRV (wide variations between each consecutive heart beat )i it correlates with AF occurrence. See attachment for photos.

After reviewing the medical literature, I discovered three articles consistent with my observations. One article37 reported reviewing Holter monitor readings on twenty-one hundred individuals, of whom seven hundred and eighty-two had hypertension. During a follow-up of approximately one year, forty-four individuals developed AF. A higher unattenuated HRV correlated with occurrences of AF. I don’t have hypertension, but it seemed supportive of my observation. Another study38 reported that HRV may be a prognostic marker for the recurrence of AF after cardiac ablation. All AF-afflicted individuals had unattenuated HRV preoperatively. Those who continued to have unattenuated HRV patterns postoperatively eventually had recurrence of AF, requiring another catheter ablation procedure. The AF-afflicted individuals who developed post-operative attenuated HRV did not have recurrences of AF and did not require another catheter ablation. This provided more support for my observation. Animal data is often used to support therapies and medical applications in humans. A study on horses39 observed HRV before and after electrical cardioversion for AF. Unattenuated HRV correlated with the incidence of AF. Conversely, after electrical cardioversion of AF to SR, the HRV was attenuated.

It seems curious that this is what I noticed and it was recorded without my awareness on my iPhone/Apple Watch App.


37. Kim SH, Lim KR,Seo JH et.al. Higher heart rate variability as a predictor of AF in patients with hypertension. Sci Rep.2022; 12: 3702.

38. Seaborn GEJ, Todd K, Michael KA, et.al. Heart Rate Variability and Procedural Outcome in Catheter Ablation for AF. Ann Noninvasive Electrocardiol 2014;19(1):23–33

39. Broux B, De Clercq A., Decloedt A. Heart rate variability parameters in horses distinguish AF from sinus rhythm before and after successful electrical cardioversion. Equine Vet 2017; 49: 723-728.

I heartily agree that a high unattenuated HRV can be indicative of afib. My only point is what is unattenuated or attenuated for you may not be the same for another person. Probably around 2007, when a number of us were recording R to R data for various rhythms, an optometrist from the UK, Mark Robinson, sent me a file of annotated R to R heart rate vs time (tachogram) charts. Visual inspection will show that what you are saying is correct, at least for afib, but maybe not for atrial flutter as HRV tends to be low for flutter.

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GeorgeN
Visual inspection will show that what you are saying is correct, at least for afib, but maybe not for atrial flutter as HRV tends to be low for flutter.

It's going to be low for all the supraventricular tachycardias (SVTs) with the sole exception of afib, and that's simply because the hallmark of afib is an irregularly irregular pulse, so that's naturally going to have a high HRV. All the other SVTs (flutter, atrial tach, AVNRT, AVRT) produce a regular pulse, and that's going to have a low HRV.

HRV seems to me to mainly just be a proxy for regularity.

I agree it’s application is only.for AF based on my personal experience and the supporting articles I cited. The photos I attached are consistent for me so I am curious if anyone with AF has observed the same pattern. For me it’s the canary for recurrence of asymptomatic and symptomatic AF.

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Hugging
I agree it’s application is only.for AF based on my personal experience and the supporting articles I cited. The photos I attached are consistent for me so I am curious if anyone with AF has observed the same pattern. For me it’s the canary for recurrence of asymptomatic and symptomatic AF.

I'm sure there would be a marked difference for HRV in and out of afib, for anyone. This issue is what is "normal" would be very individual. I just looked at 8 months of my HRV average during sleep. The range was from 23 ms to 81 ms with an eyeballed median of about 45 ms. Zero afib during that time. I'm not sure how a doc would implement this clinically, because they wouldn't have a baseline unless they had a patient who was very self aware. Perhaps a patient could be provided information about this for future reference and if they observed a marked increase to see that as a sign they should investigate further, perhaps with their own or a medical ECG?

If my HRV was up in my daughter's range of 130 ms, I'd probably view it as a signal. However, though not symptomatic, I always have a "knowing" of when I'm in afib and confirm with a manual pulse check (I can usually tell within 4 beats) and then with a Kardia or even viewing my pulse with a plesmograph phone app, where I can see it in the pulse amplitude waveform.

Hi George N
My premise for correlating unattenuated HRV with AF idepends on being compulsive and record your EkGs for 30 sec every morning,noon, late afternoon ,and at bedtime. Depending on symptoms as an alert can be misleading as if one follows my routine, asymptomatic AF will be more likely detected. Doing that provides data to determine if AF correlates with unattenuated HRV, and conversely attenuated HRV correlates with no AF.
Hugging

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Hugging
Hi George N
My premise for correlating unattenuated HRV with AF depends on being compulsive and record your EkGs for 30 sec every morning,noon, late afternoon ,and at bedtime. Depending on symptoms as an alert can be misleading as if one follows my routine, asymptomatic AF will be more likely detected. Doing that provides data to determine if AF correlates with unattenuated HRV, and conversely attenuated HRV correlates with no AF.

Oh, I get that for sure. In my case, I can identify afib in myself with 4 beats of a radial pulse. In fact, all I need to do it put my attention on my heart and notice my pulse for 4 beats and can detect it that way as well.

George
You maybe misleading yourself without objective data as I described. Decisions based on symptomatic impressions will miss asymptomatic AF.

Hugging said:

George
You maybe misleading yourself without objective data as I described. Decisions based on symptomatic impressions will miss asymptomatic AF.


Some of us are highly symptomatic, and with my over 200 documented episodes of afib (while awake), I know it immediately when it kicks in within seconds. A quick check of my carotid pulse confirms it. I find it strange that someone can have afib and be asymptomatic. I wonder why some can be so aware and others totally unaware. Possibly? - I was a competitive athlete at the highest level and have a BMI of 22.4. Now age 79 and still VERY active, ski, golf, windsurfing, hiking, weight training, scuba diving.

Now, two successful ablations and all is well, at least until IT returns. It all started 30 years ago.



Edited 1 time(s). Last edit at 02/19/2025 07:32PM by Ken.

I. too was a runner all my adult life, and even did snowshoe 'races' when I was in the military. I cycled aggressively when I took cycling up in a big way around 40. In fact, it was while confronting an aggressive driver that I had my first sensed tachycardia. It was purely an adrenergic response....but boy did I feel it! So, I have leaned heavily toward George's orientation to the asymptomatic/symptomatic AF; people who are highly in tune with their body's activity and sensations are more likely to notice when their heart rhythm is abnormal.

Having said all that, I know a retire professor, also very active, who only learned of his flutter when he went to his physician for another purpose. Flutter, mind you, and not AF. AF is a whole 'nuther beast, as those of us who know it's bite can aver.