Vagally Mediated Paroxysmal Fibrillation - A Patient's View

A good overview of AF available on the web 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. 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?

Victor Thuronyi - July 2000