Atrial fibrillation in the structurally normal human heart: a hypothesis
All the recent clinical and laboratory findings combine to provide a compelling, if somewhat challenging, hypothesis for the initiation and perpetuation of atrial fibrillation in the structurally normal heart, which, if proved, may provide a possible framework for understanding and managing this arrhythmia. That is, atrial fibrillation triggered by an atrial tachyarrhythmia, which may initially be focal, induces atrial remodelling in susceptible individuals leading to a perpetuation of the tendency to fibrillation.3 The reason some patients experience paroxysmal atrial fibrillation and others rapidly progress to having chronic persistent atrial fibrillation may relate to the duration and periodicity of the early arrhythmic episodes and the rate of progression and regression of the atrial remodelling during and between arrhythmic episodes.
According to this hypothesis, once atrial fibrillation is established, the apparently random propagation of multiple simultaneous wavelets of reentrant activity within the atrial myocardial mass11 12would mean that any evidence of an underlying focal or regular tachycardia involving the atria might tend to be lost in the advanced fibrillatory activity and remodelling of the atria. However, patterns of right atrial activation in patients with chronic atrial fibrillation have revealed that atrial activation, even in the chronic phase, is not entirely random and may have a repetitive pattern suggesting some organisation of atrial activation in most cases.13Furthermore, in a proportion of patients in whom atrial fibrillation is terminated by the largely experimental procedure of creating multiple lines of conduction block throughout the atria by linear catheter ablation, when fibrillation ceases a persistent focal atrial tachycardia is revealed.14
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saulger
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Interesting . May be a partial explanation . Think there can be different causes . My AF episode was triggered by an electrolyte imbalance caused by a painkiller when my normal heart rate was 58-60 ( unmedicated ) ) . My dad had AF when he was older than me so it’s possible I have a genetic focus for AF waiting to be irritated. Am doing my best not to irritate it
No not really . Wasn’t a drinker either. Maybe 5 glasses of fizz in a year . I did have several episodes of SVT nearly 35 years ago but my AF really was caused by an electrolyte imbalance caused by an NSAID. Any heart can have AF induced in clinical settings every heart has the potential
It is the sustained strain on the heart which causes enlargement and therefor stretching of the atrium. Professional athletes seldom have the problem as they tend to retire and de-train in their late thirties but the overly keen amateurs who keep pluging on into their dotage are the prime candidates for AF. Interstingly a second group who have a disproportionate percentage of AF are fast jet pilots, in their case caused by the strain of fighting g forces. One of my acquaintance regularly saw +9g in his Typhoon.
Thanks, Bob. I am in the dotage amateur category. Luckily, my AF is paroxysmal and lasts a couple of hours or less. The problem that I have is that I can be rowing steady state (700 Kcals hour) at under 120 bpm and suddenly it will shoot up to 175 without warning.Naturally, I stop and wait for another day. I find that it may be linked to the regularity (or lack ) of toilet habit.
Mine was ultimately induced by chemotherapy & herceptin. However underlying problem with b12 uptake caused by gluten ultimately affecting the cellebellam may have been another underlying cause. My heart has settled loads since going gluten free and b12 injections. Wonder if anyone has researched this? Low b12 affects heart rate amongst many other things....... many medics dont take much note of vitamins & minerals mores the pity. Peoples ability to absorbe b12 declines after aged 50yrs so many older folks have low b12.......
I am sorry to hear of your past issues and am happy that you are better now. I also feel that an imbalance of vitamins and minerals plays a part in AF.Since taking 200mg of Magnesium Taurate and 1000mg of Taurine daily, my AF episodes are less frequent and less debilitating.
In my case, I also plan to investigate whether oesophageal irritation (proximity to the left atrium of the heart) exacerbates my condition.
I will check whether I am getting enough B12 vitamin with food. Thank you for suggesting.
Salger for me it was the gluten that made my heart race.....it also caused tremors (postural) so its good to check out your b12 & make sure its over 500 but also have a look at gluten.....
You can get all the B12 in the world through food. If you have lost the bulk of your intrinsic factor in your stomach, you won't be able to use it and be deficient. Best way is to test it. Use a Medichecks test if GP won't. It's best to test Active B12 anyway and NHS only does Serum. Pernicious Anaemia Society say anything less than serum 500 is deficient, where as a GP will say we are all fine provided we just scraped into the range (which is huge). To be optimal we need to be towards the top of the range.
Sadly, if we can't process the B12 from food, we won't do a very good job with tablets either. So the best supplements are injection (not easy to get) or sublingual tablets and sprays. Basically, avoid the stomach.
Thank you. I checked the B12 food sources and I eat them all regularly. Fish, chicken, cheese, milk, some egg, etc. in moderate portions. I don't eat too much bread (2 thin slices a day) so maybe Gluten is not an issue ? I do feel that it's a GI trigger with me and must explore it more with specialists. Thanks again.
As I said, you can eat all the B12 in the world and get zero benefit from it if your intrinsic factor levels are too low in the stomach. We loose intrinsic factor as we age. That was the main point and explanation of my message above.
For the first 20 months of my afib, I found if I went running with a high heart rate it TERMINATED the Afib! I am aware of a number of other people on this forum who used exercise for this purpose. Bizarrely my Afib was always characterised by a fast resting HR anyway, typical 165 but often variable 130 to 195. This HR increased when running. So 7 to 10 mins of high HR stopped the random high HR! (???)
Unfortunately this trick stopped working after my 12th (ish) attack.
Yes we are all different with AFIB symptoms . As BobD says mongrel condition. I was completely asymptomatic with AFib . However I know what you feel as after i was cured ( for now anyway) of AFIB I developed Atrial flutter and just walking into the kitchen had me breathless, much further gasping, and I definitely could not have ran anywhere!
Yes I had an RF ablation for it which was one month after my first ablation which was a PVI Cryo ablation for the AFIB. I only developed flutter after I had stopped the AFIB.
FYI. For the article, the way move to a more recent date is to put the article into google scholar, and click on "cited by" gives only 16 articles but they will all be more recent, and "related articles". Some of the articles will be behind a pay barrier, but the abstracts should be visible.This is an interesting topic. I have ECG records where I went backwards and forwards between AF and tachycardia.
Google scholar is a hidden gem, especially the way it helps to find similar and more up to date articles. I use it more than Pubmed, which does a similar job but only for medical material.
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RE:recent posts triggers and ectopics...
Sinus tachycardia causes?
This may be of interest to those with persistent AF considering ablation
More On Rate Control Meds
The outcome of permanent AF 
