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Introduction
1.   What is Vagally Mediated Atrial Fibrillation?
2.   What do "Adrenergically-mediated" and "Vagally-mediated" mean?
3.   What is the relevance of Vagal AF ?
4.   I have often seen the words "Paroxysmal" and "Lone" - What do they mean?
5.   What are the characteristics of the two forms?
6.   What are vagal manoeuvres and why do I get conflicting information about them?
7.   I think I may have vagal AF - how can I be sure which form I have ?
8.   I've had ECGs - surely there must be a machine to test specifically for vagal AF?
9.   Why does resting or sleep trigger vagal AF?
10. How and why does exercise affect vagal AF?
11. How and why does stress affect vagal AF?
12. Why does the digestive system, eating and propensity to wind and bloating have an effect?
13. I have heard of other links between AF and gastrointestinal problems, etc.  Is this right?
14. Are there any other abdominal  conditions where AF could be a side-effect ?
15. Why do fit people get vagal AF?
16. Monitoring heart rate can familiarise you with your own tendencies
17. Conclusion: What is the prognosis if I have vagal AF?
18. Further information
 

Introduction

This FAQ follows personal experience of this form of Atrial Fibrillation. This web site is an information resource only.  The author is not medically qualified, and you should only act, or not act, on anything contained here after proper consultation with your qualified medical carers.  However, it is believed to be accurate. The FAQ contains some material which could be said to be subjective, and this is probably fair criticism.  However, over the years many topics included seem to address issues that constantly recur amongst different people, hence their inclusion.

This FAQ assumes a basic understanding, or a pre-existing diagnosis, of atrial fibrillation, for which more guidance is being sought.  It is aimed at a better understanding of vagal AF and is not designed to inform on adrenergically mediated AF.

The FAQ was originally based largely on the work and papers of Professor Philippe Coumel of L'Hopital Lariboisiere in Paris.  It has been written since experience suggests that the importance of the vagally mediated form of AF has not yet propagated as widely throughout the medical world as would be appropriate relative to the prevalence of the condition. However, a recent (Dec 2001) Medline survey indicated that recognition of the importance of the autonomic nervous system effects on AF is increasing, at least within the research community.  Further, the recently published (Oct 2001) ACC/AHA/ESC "Guidelines for the Management of Patients with Atrial Fibrillation" (Ref 23) explicitly includes the vagal form.  It remains my opinion, however, that in spite of an increasing appreciation of the existence of vagal AF, it is still under-recognised, particularly in the way that vagal stimuli can probably render a previously healthy heart fibrillatory.

Suggestions for additions or comments/correction should be sent to the e-mail address on the home page - many thanks.  Thanks as always for all the comments and helpful information which have been received over the years, and which continue to be supplied by readers of this FAQ.

1.  What is Vagally Mediated Atrial Fibrillation?

A simplistic classification of AF is as follows.

Atrial fibrillation can occur for a number of reasons including after heart surgery, with various forms of heart disease, or with problems such as thyroid imbalance.  However, some AF is apparently without any such attributable cause - known as "lone" or "idiopathic" AF.

However, in spite of having no apparent cause, lone AF can still be sub-divided according to certain influences.  The most common of its forms influenced by the autonomic nervous system, or rather the form often believed to be the most common, is "adrenergically-mediated".  The vagally mediated form, however, can differ significantly in its triggers, potential causes, and preferred treatments. 

The author's experience is that historically there seems to be a general lack of knowledge among non-specialists (and some specialists) about vagal AF. The two forms are often not differentiated, and even when this possibility is recognised, they can be difficult to distinguish between.  The overall prevalence of vagal AF is unknown - one set of published figures (Ref 1) states "2% - 31%" of all AF, which confirms this uncertainty. Ref 5 indicates that idiopathic PAF may in fact be predominantly vagal in origin.  Some other studies have not found such clear demarcation.

There can, of course, be a vagal component to non-idiopathic AF that has other attributable causes.

If you suspect you might have vagal AF, you should definitely discuss it directly with your medical carers.  If after discussing it, you feel they have insufficient specific knowledge of this form, it is your right to seek out a specialist familiar with it.

The heart's rate control system consists of inputs from the two branches of the autonomic (involuntarily controlled) nervous system.  The cardiac nerve is the sympathetic branch of the autonomic nervous system; stimulation by this will speed the heart rate up (adrenergically- mediated).  The vagus nerve is the parasympathetic branch of the nervous system, and slows the heart rate.  These two controls respond to and balance the body's requirements such as speeding up blood flow during exercise or calming it again afterwards. 

Overstimulation of either branch can cause Atrial Fibrillation due to the resultant, and similar but not equal, nerve impulse transmitter chemicals' effects on changes in the heart's electrical status.  This may or may not occur in the presence of other predisposing factors - i.e. it is suggested that some autonomic activity can cause fibrillation even if there is nothing wrong with the heart. It is a fallacy that AF is always caused by excessive cardiac nerve activity; this is unfortunately a persistent misconception among some.

Given no external control an isolated heart would adopt its own rate, controlled by the sinus node, which would be higher than the usual resting heart rate of around 65-75 bpm (beats per minute).  Thus, in a normal heart, the vagus nerve is active. This is called the "vagal drive".  Thus in a "normal" heart (with no underlying heart disease) any AF is more likely to be vagal.

Traditionally, much literature and practice concerning lone atrial fibrillation has either been implicitly based on the adrenergically mediated form, or has not differentiated between these essential sub-types of AF.  The treatments developed for this form are well established, (although it has to be said that AF can be a difficult problem to treat and though immediate success is often achieved, sometimes a great deal of experimentation must be tried before a suitable drug regime is established).  However, there is a significant group of people who do not have adrenergic AF, but in fact have vagal AF, and for whom the "usual" treatments may not help at all, or may actually make their AF worse.

Paroxysmal means a sudden occasional occurrence. ("PAF" - Paroxysmal Atrial Fibrillation). 

Lone, as in Lone Atrial Fibrillation (sometimes "LAF"), means having no apparent cause (also called idiopathic).

Vagal AF may well be a predominant mode for lone and paroxysmal AF. Ref 5 indicates that in their study 63% of idiopathic AF was of vagal origin. Various other papers on the references page support this, though not all research agrees on it.

Note that these characteristics are guidelines only, and are not absolutely fixed criteria.
 

These are sometimes advised to AF patients as a means of helping to control  attacks.  Classically they are to apply pressure to the carotid artery at the side of the neck (one side only!), or to the eyeballs (eyes shut!), or the valsalva technique which is to hold the nose and mouth shut and 'blow out', raising the airways' internal pressure.  Drinking very cold water or sucking an ice cube are also mentioned.  Straining on the toilet also can have similar effects. 

(Note this FAQ is NOT advocating these moves, which can have significant risks of their own). 

These moves stimulate the vagus nerve, which, in the adrenergically-mediated form, are intended to slow the heart down again from its adrenergically-stimulated fibrillation, thus stopping the attack.  Hence, it may be seen that in the vagal form, such manoeuvres may actually precipitate an attack.  Thus if vagal moves do set off an attack, or fail to stop them, suspect vagally-mediated PAF.

However, as vagal AF, and AF in general, can be seen to be quite sensitive to the balance between vagal and adrenergic drives, even in Vagal AF these moves may sometimes work to stem an attack.  See what works for you, knowing that it may make things worse.

In contrast to vagal manoeuvres which are unlikely to help with vagal AF, I recently found evidence (Ref 22) that a Yoga breathing technique, kapalabhati, could reduce vagal activity and increase sympathetic activity.  If this could be harnessed well enough to help vagal AF sufferers, this would be useful.  If anyone knows of this technique and application to vagal AF, please contact us.

The difference in the speed at which the two nerves affect the heart's rate provides the key here: the heart's response to the vagus nerve occurs in a matter of milliseconds, whereas the response to the cardiac nerve takes several seconds.  In vagally-mediated AF, the heart rate can therefore vary from beat to beat.  You may even be sensitive enough to feel this - consecutive beats are not exactly the same, even when you are not in AF.  In the adrenergically mediated form, the rate of change is slower, over a number of seconds or minutes.  From an ECG or Holter monitor, by calculating beat-to-beat rate-of-change and using averaging techniques over longer periods, it is possible to detect which influence is predominant.  For details, see Reference 1.

Ask your Cardiologist to perform a "Heart Rate Variability" (HRV)Analysis.

However, having said this, it is not always easy to diagnose vagal vs. adrenergic modes by this method - Ref. 1. indicates certain difficulties - but at least in the cases where the cause is clear, then this method will be helpful.  Note that Flecainide has a noticeable effect on the results of these tests (Ref. 1).  Presumably other drugs such as Beta-Blockers will also have effects on the vagosympathetic balance. Try and perform the tests when off any drugs.

Finally, and importantly, many people may have a mixed or indeterminate pattern of AF, displaying at different times different characteristics.

There are machines which could, if designed to, monitor the state of the vago-sympathetic balance from a heart rate analysis. The machine is of the type called an interpretive ECG - i.e. it has the ability to analyse and interpret the traces according to predetermined rules.

The particular test required to assist diagnosis of vagal AF is an "R-R Trend Analysis", which is conventionally used to detect other more serious conditions.  It would appear however that it could also be used for indicating vagal AF.  It is not clear whether the same heart rate trend algorithms are used in such machines as Coumel recommends in his papers.  Initial information suggests that the algorithms available as standard analyses are not the same as required for AF type determination.  Therefore in requesting a heart rate variability analysis, some difficulty may still be experienced in getting the correct analysis done.

The lack of adrenergic drive and predominance of vagal drive will allow the heart to slow down under these situations.  This "extra" stimulation can start an attack.  Vagal AF classically (but not always) starts during sleep and ends in the morning.  Another way of looking at it is that if resting does not stop or seem to help your AF at all, vagal AF should be suspected.

In general, exercise will tend to reduce the likelihood of a vagal AF attack.  In fact, Coumel states, and the author of this FAQ can confirm, that exercise is useful to stave off an impending attack that is indicated by a start of, or increase in, ectopic beats.  Immediately running up 2 or 3 flights of stairs (in a reasonably fit individual) will raise the heart rate just enough to offset the vagal influence.  Note that the amount of exercise should not be too much.  Too much exercise can upset the vagal/cardiac balance and cause the vagus to overcompensate - this is known as "vagal rebound" and can equally cause an attack.

In general, stress is much like exercise - stress raises the heart rate and in the classical categorisation of vagal AF will not usually set it off.  However, a number of factors mean that stress is unlikely to help with vagal AF. 
         Think of the two branches of the nervous system as being in a delicate equilibrium, such that it is not always easy to know which is the predominant influence at any one time.  Short-term stress classically should not set off vagal AF - but calming down afterwards often will.  This is when the adrenalin has finished flowing and the heart rate can reduce to the resting rate again. 
         There is also the phenomenon of vagal rebound - an adrenalin rush may be over-compensated for by the body trying to re-balance things, and the consequent vagal stimulation can set off the AF.
        If your AF is of a mixed vagal/adrenergic pattern (which is quite common), stress is overall likely to adversely affect it. 
        Finally, with vagal or adrenergic AF, chronic stress should not be underestimated as a factor - suffering long term stress will generally disturb the body's equilibrium and make it less likely that it will be able to cope with the short-term responses necessary without risking an AF trigger event.

The vagus nerve (means "wandering") is one of the most extensive in the body.  As well as feeding the heart it is also the nerve which stimulates digestion.  Thus eating or drinking, particularly large quantities, will cause vagal stimulation.  This often has a side-effect of bringing on a vagal AF attack.

One point is that a great deal of the population have, sometimes unknown to them, a digestive problem to some degree - such as the incidence of constipation, wind or bloating, or of irritable bowel syndrome testifies.  These situations can be chronic and cause AF.  An Italian paper (Ref. 3.) examined 516 patients hospitalised for acute abdominal problems.  After excluding inappropriate groups of patients, ECGs were performed on the remaining patients.  Arrhythmia were found including atrial extrasystoles (extra atrial beats - probably similar to the ectopic beats an AF patient will experience), and PAF.  These changes were benign and disappeared after resolution of the abdominal disease. 

The author of this FAQ had no luck with traditional drug treatments for AF, and though with hindsight there were early indications of vagal AF, it was not until an underlying constipation and wind problem was identified that the persistent AF disappeared virtually overnight, reducing attacks to times when the digestive problems returned.

Monitor your bowel frequency, eat well - 5 pieces of fruit a day (though some sources recommend not to eat fruit except on an empty stomach), and drink plenty (2 litres water/day).  Avoid large meals in the evening (the body is not set up for the modern predeliction for evening restaurant eating).  If you have to have large meals, make them easily digestible, eat them slowly and chew well.  In bad cases you may need to get some extra digestive help, but do so under medical supervision and do not stay on them permanently.  Preferably use a bulking agent (psyllium or ispaghula husk). If necessary consider laxatives of the osmotic type such as lactose syrups (Lactulose) in preference to senna-based irritants or Epsom salts.  Be aware of possible lactose intolerance, also some can react to psyllium husk.) Avoid staying on the same agent for too long as it may stop working.

Some AF sufferers get effective relief from wind and bloating, and hence can often avoid AF attacks, using tablets based on calcium and magnesium carbonate and including simethicone, a silicone-based "antifoam" - many proprietary preparations are available.

If you have a digestive problem, though - get to its root as soon as you can.  Food intolerances can exacerbate or even cause AF - wheat and dairy intolerances are the most common, and getting more common. Do not allow the digestive upset to continue - the incessant vagal stimulation could in time convert a lone or paroxysmal AF to persistent or permanent. It is becoming far more recognised these days that pro-active treatment for AF is important to prevent this progression. It is also recognised that vagal stimulation is an important mechanism in converting healthy heart tissue to fibrillatory tissue.

However, (and not to negate what is said above), bear in mind that even a normal vagal drive could be enough to set off a vagally-mediated AF if the heart tissue is sensitive enough.  My own AF started off as vagally-mediated due to excessive vagal stimulation, but because the gastric problem was never fully resolved, the long-term vagal stimulation eventually seems to have tipped the AF into being a persistent AF now triggered by even a normal vagal drive.

Personal correspondence resulting from newsgroups and mailing lists suggest that some GI (gastrointestinal) specialists may be familiar with AF (and other arrhythmia such as tachycardia) caused in relation to other GI "dismotility" problems (lack of proper peristaltic action). Reference 3 describes one study where a relationship occurred between AF and GI problems. 

A search of Medline also showed other cases, e.g. Ref. 4.  Gastric endoscopy (of the stomach) was found to induce premature atrial beats and atrial fibrillation, amongst other things.  Two cases of AF continued even after the end of the examination.  It is quite clear, therefore, that GI problems including motility issues, can directly induce AF, almost certainly vagal AF.

This is an area that would benefit from more research focused at lone AF as a side-effect.

In an effort to understand better what is going on in these situations, the rest of section 13 is offered as a possible framework for understanding - some content is speculative, but hopefully with time it can be confirmed or refined.

What probably happens under conditions of gastric discomfort is as follows.  When food is eaten, sensors within the gut detect the food entering - including the "stretch receptors" in the stomach and intestine, and pH receptors which detect reduction in acidity. In addition, it appears that the oesophagus can respond in similar ways, also to physical stimulation of the food pipe, such as with "rough" foods. Wind and bloating is another common cause of stretching or irritation of the GI tract, and hard knots in the intestines can easily be mistaken for food when they can in fact be trapped wind.

The sensors send messages to the brain's control centres which then stimulate the vagus nerve to increase digestive secretions and increase contractions of the stomach and intestines.  It is under this increased vagal stimulation that the heart's vagal drive can be over stimulated, setting off the AF.

It is possible that normal digestion would not cause AF, but if a gastric upset is chronic or severe, the persistent vagal stimulation could well lead to an increased risk of AF. It seems that achieving a generally comfortable digestive tract is one way to minimise vagal AF attacks from this source, rather than there necessarily being any particular trigger food, though there can certainly be different trigger foods for different individuals.

The occasional report that vinegar can reduce the severity of an attack could also have a basis in the above theory, by reduction of stimulation to the pH receptor cells.  The receptors are stimulated by a reduction in acidity (higher pH) - and vinegar is of course acidic (low pH).

In addition to the purely digestive aspects of the abdomen,  the oesophagus passes through the diaphragm between the  chest and abdominal cavities right next to the vagus nerve, so it is possible that direct stimulation of the vagus could occur in the same way as pressing on the carotid artery in the neck.  Also, the oesophagus runs right next to the pulmonary veins which are often the source of ectopic beats which can initiate AF. These factors could be the reason for occurrences such as unchewed, irritant foods, or endoscopies, setting AF off.

Certainly vagal AF suffers may be familiar with certain postures that risk setting off AF - bending forward and down, or leaning over, or on all fours.  The risk of setting off AF by these moves can be reduced by keeping the abdomen taut.  However - be aware that when doing this, normal breathing should be maintained otherwise the diaphragm could be misused leading to direct stimulation of the vagus nerve where it passes through.

"Mesenteric Arterial / Intestinal Ischaemia" is reported in some GP literature, and in the research literature, as a condition where AF is a main symptom in around 43% of cases of a different condition.  Although I am not expert here, this appears to be a condition where for one reason or another the blood flow to the intestinal area is reduced (this is what ischaemia means - mesenteric means the internal abdominal area), which in turn causes abdominal pain and AF.  The references would tend to suggest that the pain is sudden.  The blood flow can be restricted due to an embolism (blood clot) or other reason.  See references 17 to 21 for more information.
      Ref 18 suggests a case where a woman had a 5 year history of "rheumatic heart disease and atrial fibrillation"  It is not clear from the abstract whether the AF also took place over 5 years.
      What is clear is that when Mesenteric Ischaemia strikes there is (or should be!) no mistaking it, (though only 35% may be correctly diagnosed prior to operating).  What is not clear to me is whether it might be preceded by a period where the ischaemia could be much more minor in nature, and maybe might never develop into the full-blown emergency.  Ref.  19 refers to the creation of "reflex mesenteric vasoconstriction" as a result of (artificially-) induced AF, which I speculate could then perpetuate the AF.
       I would strongly suspect that AF induced due to such a condition would be vagal in nature.  Maybe a professional reading this could contribute and let me/us know (at the contact e-mail address) what the truth of this is.

Firstly, as explained, the vagal drive is the predominant mode in the normal heart. Secondly, fit people such as athletes often have a very efficient cardio-vascular system.  This means the heart does not need to beat as fast as in less fit people.  Slow heart rates can predispose people to vagal AF, as the vagal "tone" is high.  Hakeem Olajuwon, the American basketball player, is reputed to suffer from AF after drinking cold water at half-time - this is probably vagal.  The case described in Ref. 25 is a classic!

But don't give up exercise or sport - fitness still helps!

As vagal (and adrenergic) AF respond to heart rate changes, you can become familiar with your own particular physiological responses by monitoring your heart rate.  Take a rate count at various times of day, such as just after you wake up, during normal activity, before and after meals, after exercise, just before sleep, and so forth.  (Monitor the rate over at least 30 seconds).  This will help you to understand your own patterns, which can help you to further understand your personal tendencies to AF.  I find, for example, that if I am in a period of proneness to an attack, my heart rate drops unnaturally fast immediately after vigorous exercise.  If I am currently not prone to an attack, it stays high much longer.  Also, if my heart rate drops much below 60 at any time, I know I am at risk of an attack.

A couple of words of warning, though.  Don't get too focused on heart rate and cause yourself anxiety.  Heart rate is additional information which, if you can determine a pattern, can help you to understand how you respond.  Also, and in particular, you may find that your heart rate is high just as you go into an attack - this does not mean that you do not have vagal AF - this might be vagal rebound.  See Ref. 1 for discussion on this.
 

An encouraging factor for those suffering from vagal AF is that, in Coumel's words "A remarkable pattern of the syndrome is the lack of tendency towards permanent AF" (Ref. 1).  Similarly, Ref 3 includes the words "The Authors have underlined the benignity of these ECG changes", (this note referred to arrhythmia brought on by gastric difficulties).

However, Ref. 2 states: "there is no evidence that autonomic nervous system function is fundamentally abnormal in these patients...." but Coumel then states: "....in the long term, a permanent 'lone' AF may appear: at this stage the electrophysiological disease is not in doubt" and "...(various electrical changes in the heart) are probably potentiated by vagosympathetic changes before becoming permanent".  Coumel's warning may well refer to re-modelling ("AF begets AF"). 

What I believe this means is : 

If you have vagal AF and can understand it and control it adequately through this understanding, then:

(a) you are immediately likely to achieve a radically improved quality of life, (I was able to control my AF better than the drugs were)
(b) you may delay any progression to permanent AF, and 
(c) possibly you may escape permanent AF.

It is, however, extremely important to take a pro-active approach to identify any means of reducing or eliminating the base cause/triggers.  This is because (i) if the vagal stimulation continues, it can possibly turn healthy heart tissue into fibrillatory tissue, and (ii) once AF starts, if allowed to continue it is likely to cause re-modelling of the atrial tissues* and make the AF become more likely to continue and develop.  If your pro-active approach includes drugs, it is extremely important to avoid medications such as beta-blockers and digoxin which can make vagal AF worse, also others which might be pro-arrhythmic (as a general side-effect).  These options could achieve the very result you are trying to avoid. 

(*A NASPE paper (Ref 24) recently suggested that vitamin C could help to delay early-stage remodelling)

The range of opinion about the significance of vagal AF ranges from it being unimportant as a subtype and of no clinical significance to the other extreme that it is merely a symptom of a neurological manifestation and not a heart problem at all.  The truth is probably somewhere between these extremes.  As stated before, in spite of increasing recognition (Refs. 25, 26, 27, 28), I personally believe that vagal AF is still a significantly  under-recognised condition.  If it were better recognised, perhaps an initial occasional bout of vagal AF would not be allowed to develop into a more serious AF, at which point the differentiation between vagal and adrenergic AF certainly becomes less important. Also, if it were postulated and recognised earlier, before it becomes more pathological, early-onset lone AF might turn out to be far more commonly vagal than is presently recognised - as Einstein said, "The theory determines what is observed".

Further research is still needed to verify the full situation.
 

So "take heart"! 

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