For those who like to keep up with research, this paper came through in the list of abstracts I get from Amedeo:
"An endogenous cholinergic system controls electrical conduction in the heart." Xie et al. Pubmed PMID 39437249
Using molecular cell biology techniques they looked at the associated conduction and arrhythmic properties.
Conclusion: "This study identifies an integrated cholinergic system inherent to the heart, rather than external nerves that can effectively control cardiac electrical conduction. The discovery reveals arrhythmia mechanisms beyond classical theories and opens new directions for arrhythmia research."
Still early days, but we can definitely all do with some new ideas
Written by
Cliff_G
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Thanks for posting. About 10 years ago I took part in a world wide citizen’s research project in rare diseases associated who were looking at prevalence of arrythmias in Myasthenia- results showed 30% have arrythmias. I also found that acetycholine esterase drugs I took helped both regulation of BP and fewer episodes of AF.
"... there may be a relationship between acetylcholinesterase (AChE) and the frequency or risk of atrial fibrillation (AF), but it's a complex and emerging area of research.
Key points of the connection:
1. Acetylcholine and Atrial Fibrillation
Acetylcholine is a parasympathetic neurotransmitter that affects the heart.
In the atria, increased vagal (parasympathetic) activity can promote atrial fibrillation, especially vagal AF, a type more common in young, healthy individuals and often triggered at night or after eating.
Acetylcholine can shorten the atrial action potential and refractory period, making the atria more susceptible to reentry circuits that cause AF.
2. Role of Acetylcholinesterase (AChE)
AChE breaks down acetylcholine, thereby limiting parasympathetic signaling.
If AChE activity is low, acetylcholine may accumulate, potentially increasing the risk of vagal AF.
Conversely, higher AChE activity could reduce acetylcholine effects and possibly reduce the risk of vagal AF.
3. Research Evidence
Some studies have looked at cholinergic signaling and AChE levels in relation to AF, especially in contexts like:
Heart failure
Postoperative AF
Autonomic dysfunction
There is no definitive clinical guideline yet connecting AChE levels directly to AF frequency, but it's a subject of investigation.
4. Therapeutic Implications
AChE inhibitors (used in diseases like Alzheimer’s) could theoretically increase parasympathetic tone and might influence AF risk, although this hasn’t been strongly confirmed in clinical data.
Autonomic modulation therapies, such as vagal nerve stimulation, are also being explored in AF management, indirectly tying back to acetylcholine activity."
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...Yet another question for my eventual post-ablation follow-up.
My husband is on a different AChE for Alzheimer’s, I would say his sympathetic, rather than parasympathetic, tone has increased ie: he is a lot more reactive but very hard to distinguish which symptoms are because of disease and which meds. His AF episodes has remained same.
I remember writing a post on this forum circa 2014/2015 after I had been on very high dosage of Pyridostigamine -5-8 x 60mg bd (now down to 1.5-2 60mg bd).
FYI - In Myasthenia Gravis (MG), a primary antibody involved is the anti-acetylcholine receptor (AChR) antibody, which targets the postsynaptic nicotinic acetylcholine receptor at the neuromuscular junction, leading to impaired nerve-muscle transmission.
Indeed. Disopyramide is indicated in vagal AF because of its slightly anti-cholinergic properties. Also other drugs with those properties, like SSRI’s (Sertraline) have a moderating effect on AF.
I was on Disopyramide as PIP back in the 90's before my 2002 ablation. For a short while it was a wonder drug for me. The first time I took it was sitting in a conference and 5 minutes after I took it I felt this wave of calmness and pleasure move from my head down to my feet over a few seconds, as if someone was sweeping a hoop down over my body, and the fib stopped. It worked a few more times over the next couple of weeks, but then it stopped working and never did again. Weird, and what a shame. No cadriologist has ever agreed to try again.
It never fails to inspire me, in what sometimes seems to be an increasingly anti-intellectual online world, when I read of real science testing and pushing at the frontiers of knowledge.
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Interesting to know...
Cardioversion buying time till next ablation.
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