Revised July 7, 2000

Vagally Mediated Paroxysmal Atrial Fibrillation -- A Patient's View

� 2000 by Victor Thuronyi

I.  In general

Atrial fibrillation has many causes and forms.  This note deals only with one type, atrial 
fibrillation that is (i) paroxysmal, i.e. occurring from time to time and converting 
spontaneously to normal sinus rhythm, and (ii) vagally mediated, i.e. triggered by the 
vagus nerve (hereinafter VMAF). The percentage of people with AF who will fall into 
this category is very small.  I am writing about it simply because I have this kind of AF 
and I would like to increase my understanding of this particular condition and share this 
information with others.  If you have comments you can email me at [email protected].   
An important caveat:  Nothing in this article should be considered as offering medical 
advice.  I have no medical training; therefore please do not act on anything written here 
without consulting your physician.  

A good overview of AF available on the web (www.americanheart.org) is "Management 
of Patients with Atrial Fibrillation" (hereinafter AHA Statement).  It goes over all types 
of AF, discusses treatment options, and contains extensive references.  

II.  Classification of AF Cases

AF can be classified according to different characteristics:

? Idiopathic vs. caused by a preexisting condition.  If you suffer from AF, the first 
thing that doctors will do is see whether some other disorder is causing the AF, for 
example thyroid disorder, heart disease, heavy alcohol ingestion, recent surgery, etc.  
If a cause is found, then possibly the AF will go away if the cause can be treated.  If 
no cause can be found, then the AF is classified as "idiopathic" or "lone".  VMAF is 
idiopathic.  For a useful general article on idiopathic AF from an alternative health 
perspective, See Larsen, Lone Atrial Fibrillation, available on the web at 
http://vvv.com/healthnews/lafforum.html.  However, even though the conventional 
classification is idiopathic, it appears that in some cases so-called idiopathic AF may 
in fact be caused by nutritional deficiencies.  See my separate article about this.  
Moreover, in other cases the AF is triggered by various factors (for example, 
ingesting food containing MSG (monosodium glutamate), drinking alcohol, or 
drinking caffeinated beverages), and can be avoided by avoiding these triggers.

? AF can also be broken down according to whether it is paroxysmal (spontaneously 
converting to normal sinus rhythm), persistent (staying in AF for over 48 hours or 
until a cardioversion is done), or permanent (persistent AF that is refractory to 
cardioversion; i.e. cardioversion does not work).  VMAF is paroxysmal.  However, 
there can be a lot of variation within paroxysmal AF in terms of the frequency and 
duration of episodes.

? Finally, paroxysmal AF can be broken down according to whether it is neurogenic 
(i.e. triggered by an anomaly in the control of heart rate by the autonomous nervous 
system) or not.  According to Sopher, Malik, and Camm, Neural Aspects of Atrial 
Fibrillation, in Atrial Fibrillation: Mechanisms and Management (Falk and Podrid 
ed. 1997): "the majority of patients with paroxysmal AF do not have a clear 
autonomic pattern".  Of the patients whose AF does have an autonomic pattern, there 
are two subgroups: vagally mediated and sympathetically mediated.   The former 
tend to have AF onset at night, during rest, or postprandially (i.e. after eating).  The 
latter experience onset during activity or stress and occurring more frequently during 
the morning.

III.  Characteristics of VMAF

Good statistics on the percentage of patients with VMAF have not been developed.  On 
the basis of the available data it seems safe to say that of the universe of persons with AF, 
only a very small percentage can be categorized as having VMAF (see AHA Statement 
and article by Sopher, Malik, and Camm cited above).

Only your doctor can confirm whether you have VMAF (although in some cases, like 
mine, it can be pretty obvious.  I had numerous episodes over a period of several months 
and each one fit into the classic VMAF pattern.  For those people with fewer episodes it 
may be harder to tell.).  Usually it will take some time to identify, by observing the 
pattern of onset of AF episodes.  The classic article on this condition was written by Dr. 
Philippe Coumel (Role of the Autonomic Nervous System in Paroxysmal Atrial 
Fibrillation, in Toubol ed., Atrial Arrythmias (1989)).  In this article, he describes the 
typical case:  

"The predominance of men over women is constant, with a ratio of about 4 
to 1.  The age when the first sympton appears is between 40 and 50, with 
extremes ranging from 25 to 60....A remarkable pattern of the syndrome is 
the lack of tendency towards permanent AF.  In all cases the arrhythmia is 
idiopathic and can be classified as a lone AF.  The number of the attacks is 
variable from patient to patient.  It may take from 2 to 15 years for episodic 
attacks to develop into daily attacks.  The commonest feature is that of 
weekly episodes, lasting from a few minutes to several hours.  The 
essential feature is the occurrence of the attacks at night, often ending in 
the morning.  Rest, digestive periods (particularly after dinner), and 
alcohol absorption also are favoring factors.  Exercise or emotional stress 
does not trigger the arrythmia.  On the contrary, on feeling the sensation of 
an incoming arrythmia (repeated atrial extrasystoles), many patients 
observed that they could prevent it by exercising.  But the relaxation period 
that follows an effort or an emotional stress frequently coincides with the 
onset of AF."

The heart rate is controlled by the autonomic nervous system, which is divided into 
sympathetic and parasympathetic.  It is the balance of the sympathetic and 
parasympathetic systems that results in the heart rate.  The parasympathetic system 
(vagus nerve) slows the heart down, while the sympathetic system accelerates the rate.  
Stimulation of the vagus nerve is known as a vagal maneuver.

IV.  Relevance of diagnosis of VMAF for management of this condition

A.  Vagal stimulation  

For patients with VMAF, vagal stimulation can bring on or terminate episodes of AF.  
This includes activities such as:

? bending down, sitting down, or lying down
? drinking cold water or eating cold food (e.g., popsicles, frozen yogurt)
? jumping into a cold swimming pool
? gas buildup in the stomach
? eating a heavy meal
? coughing hard
? alcohol ingestion
? straining with a bowel movement.

These activities are especially likely to bring on AF in late afternoon until early morning, 
when vagal tone is predominant.  So can vagal maneuvers (carotid sinus massage, 
particularly when lying down, Valsalva maneuver (sitting, bending forward, and trying to 
blow out), plunging face into a basin of ice water while holding breath for half a minute). 

In my experience, vagal maneuvers have worked sometimes to terminate my AF, but 
usually not on the first try.  Light exercise can also terminate AF, particularly when it has 
lasted into the morning or early afternoon.  Several posts to the atrial fibrillation message 
board have also reported that sleeping on the left side can trigger AF during the night 
(this has also been my experience), and I have found that I can avoid AF by sleeping on 
the right side or on the back.  It can also help to elevate the head and upper part of the 
body when sleeping, either by using several pillows or a bed that can be adjusted to do 
this.

Particularly in the late afternoon, I try to avoid the above activities that stimulate the 
vagus nerve.  For example, instead of bending over to pick something up, I bend at the 
knees keeping my back straight (this is also better for the back).

B.  Antiarrythmic Drugs  

According to Coumel,  "Patients with vagal AF not only have the number of their attacks 
clearly increased by beta-blockers (as well as by digoxin), but they also tolerate these 
drugs poorly when in sinus rhythm."  Further, "Type Ia drugs like disopyramide or 
quinidine have a well-known vagolytic effect that is probably, at least in part, the 
explanation of their activity in the treatment of paroxysmal AF.  As far as type Ic drugs 
are concerned, experience has shown that flecainide and propafenone have a clearly 
different preventive effect on paroxysmal AF.  Flecainide is much more active than 
propafenone every time a vagal mechanism is the cause, possibly because it seems to 
have some vagolytic effect in addition to its direct antiarrhythmic effect..... The same 
probably applies to amiodarone... Amiodarone is indeed active in vagally induced AF, for 
the simple reason that it prevents the dramatic shortening of the action potential, an 
action propafenone does not have."

(Note: personally I would stay away from amiodarone except if it is a last resort, the AF 
is debilitating, and there is very careful monitoring, since it has some pretty horrific side 
effects.)

According to an  article on Medscape (Safety of Antiarrythmic Agents), "current thinking 
recommends that:

Class Ia agents should only be used in patients who have successfully received the drugs 
for some years or have vagatonic atrial fibrillation that may respond to the anticholinergic 
component of the action of disopyramide or quinidine ...

Class Ic agents [includes flecainide, propafenone] are very effective in patients without 
myocardial ischemia or significant structural heart disease..."

My own experience is that flecanaide (also known as tambocor) works for me.  It may 
also be significant that the first time I went into the ER for AF, I was given digoxin, and 
stayed in AF for nearly 48 hours until I was cardioverted.  It seems quite possible that the 
digoxin actually made the AF worse in my case. 

My electrophysiologist has started me on a regime he calls "pulse therapy" under which I 
take flecainide (at a somewhat higher dosage than would usually be taken) only at the 
onset of an attack.  This way I am not on the drug all the time.  

C.  Nutrition; Minerals

I have been tested as having low levels of intracellular magnesium and high levels of 
mercury.  Both of these can apparently contribute to AF.  I am hopeful that adjusting this 
can either cure or substantially diminish AF episodes.  I have noticed that several posts 
on the AF page have reported twitching, which can also be caused by low magnesium 
and by high mercury.  According to Richard Firshein, The Nutraceutical Revolution, 
stress depletes magnesium, as does marathon running.  Perhaps this can help explain why 
a number of marathon runners seem to have developed AF.   I am writing a separate note 
about magnesium deficiency because this may have broader implications than just for 
VMAF.  Until clinical trials are done, it is hard to say precisely what the role of 
magnesium deficiency in various forms of AF might be.

V.  Questions for those with VMAF

? What is the experience of those with VMAF with caffeine and alcohol?  Since 
caffeine stimulates the heart, perhaps it is not a problem for those with VMAF?  
Coumel notes alcohol as a trigger, but my question is -- how much?  Have people 
found that one or two glasses of wine is ok?  A glass of wine once triggered AF for 
me and I have largely stayed away from it since then.  I also initially gave up coffee.  
However, when it became clear that I had VMAF, I figured that coffee was unlikely 
to trigger it and so went back to drinking coffee, but at about half the amounts I had 
previously ingested.  Occasionally I find that if I am drinking strong coffee I will get 
a skipped beat or two.

? How about decongestants?  They have pseudoephedrine, which stimulates the heart.  
Some with AF have complained about these, but perhaps they do not both those with 
VMAF?  Similar question for asthma inhaler (albuterol).  I haven't taken either since 
I have had AF but am assuming they are ok for VMAF.

? For those with VMAF, have supplements such as magnesium, Coenzyme Q10,  L-
carnitine, taurine, or hawthorne been effective?

? Is there anything to the idea (noted in one post) of taking a tablespoon of vinegar 
with  water?  Has anyone tried this?  

? Have people had trouble with air travel?

? What have been the experiences with progression of this condition?  Have any 
experienced it getting better over time, or does it just tend to get worse?  What 
antiarrythmic drugs have worked?  Has anyone had experience with pulse therapy as 
I described above?