I have read quite a few of the responses in this forum regarding afib. I also suffer from paroxsymal lone afib and have obviously
been searching for answers. There seems to be some discussion regarding vagal vs other types of afib. I know that the vagus nerve is responsible for many things in our body. It does exhibit a parasympathetic effect on the SA node of the heart. I would assume this might result in sinus pauses that could trigger afib. Regardless of the cause is it correct to assume that afib is afib and therefore its onset is the result of an abnormality in the myocardium.
A cardiologist recently recommended that I try, as an experiment, taking the anticholinergic drug (scopolamine) to see if by inhibiting the vagal effect I could reduce the amount of focal atrial tach. I was experiencing. I have noticed that I have very high vagal tone probably due to a combo of genetics and aerobic conditioning. When my resting rate is low (typically 50) I can experience a short burst of atrial tach every time I swallow. I recently suffered an intense cold which made my resting heart rate rise into the 70's. I found that the atrial tach basically disappeared for several days while I was ill. As I started to feel better the resting rate dropped back to the 50's and along with that came the atrial ectopics upon swallowing.
So my question is - can you explain how the vagus nerve may precipitate afib/focal atrial tach. If in fact I find that by inhibiting the vagal effect the problem is solved, how can I make this a permanent situation? Are there drugs/procedures that can do this?
Thankyou for your response
You are asking a very good question and one that there is not well researched answers. It is true that people with higher vagal tones and lower heart rates are predisposed to afib. Possibly this is because the foci where the afib starts does not have time to discharge at a higher heart rate. There are no trials of scopolamine for this and I would be rather leary of taking it on a regular basis. A pacemaker set to a higher rate would be one option I suppose but your best option is to have an afib ablation. Yours would probably be amenable to this procedure. We are doing afib ablations here and if you would like to be considered for this procedure please make an appointment with Dr. Andre Natalie by calling the number below.
When you say afib ablation exactly how would that be done? I understand the ablation idea after having gone through an EP study with no ablation. I understand that afib is a tough thing to attack throught this procedure. Usually procedures such as Maze etc are considered. I suppose it may be due to the presence of a single foci which is targeted for ablation.
You are correct that afib ablation is not an easy thing and is still in its early stages. However, in some individuals the afib starts from a single focus, usually in the pulmonary veins, that can be ablated using special techniques. A large academic center near you should be doing it and if not we are doing it here and you can make an appointment in the electrophysiology clinic for evaluation.
Thank you for that piece of information. How does tissue in the pulmonary vien initiate afib? Perhaps that is a difficult question to answer. I would have thought the stimulus would be confined within the heart tissue itself.
One other observation I have noticed and would appreciate your thoughts on - as I said earlier I recently suffered a decent cold where my resting heart rate elevated significantly. This is still the case although I am getting over it now. The swallow trigger has shut off completely since this cold came on. Now that I am getting better I am starting to experience muscle twitches especially concentrated in the left Pectoral region. I sometimes wonder if they are cardiac twitches or skeletal. I suspect skeletal in that they seem very surficial and the beat of the heart does not react to them. Is there some connection that could account for this? I sometimes wonder if some neuromuscular disorder could in fact be at work here.
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