Atrial fibrillation basically involves a chaotic movement of electrical impulses across the atria and leads to a loss of synchrony between the atria and the ventricles. Once an episode has begun the atria may quiver or fibrillate at a rate as high as 300 to 600 times per minute. This causes a very inefficient filling and emptying of the atria; the chaos is transferred to the ventricles causing them to lose their regular rhythm and begin to contract fast and in a totally irregular manner. This is what gives rise to the fast and irregular pulse rate felt during an AF episode (90-160 beats/minute).

Atrial fibrillation in itself is not a disease, but rather a symptom of some other disorder of the body. Atherosclerosis, angina, heart attack, heart surgery, valvular heart disease, hypoglycemia, hypertension, electrolyte imbalances, hyperthyroidism, anemia, pheochromocytoma, strenuous exercise, binge drinking, consumption of tyramine-containing foods, and exposure to mental or physical stress can all trigger atrial fibrillation. Very recent research has found that an inflammation of the heart lining (myocardium) is often involved in atrial fibrillation.

If none of the above conditions are causing the atrial fibrillation then it is diagnosed as primary or idiopathic (of no known cause).

Nevertheless, it is generally accepted that lone atrial fibrillation (LAF) is characterized by the absence of heart abnormalities or heart disease. This means that LAF is not life-threatening and is less likely to precipitate a stroke than is atrial fibrillation involving heart problems.

Medical intervention in lone atrial fibrillation is aimed at preventing episodes, ameliorating the symptoms of episodes, converting the fibrillation to normal sinus rhythm (NSR), and reducing the risk of stroke. With the exception of surgery (the maze procedure) and catheterization (radio frequency and ultrasound ablation) medical intervention is not meant to eliminate (cure) the disorder, but rather to control (manage) it over the long term.

It is possible, but probably rare, to have just one episode of LAF. Far more common is the paroxysmal (intermittent) form of LAF. The frequency and duration of episodes vary greatly, but generally increase with age and the number of years the disorder has been present. In some cases LAF becomes permanent, that is, the irregular, rapid heartbeat becomes a constant companion.

Violent palpitations, breathlessness, dizziness and frequent urination are common features of LAF episodes. Many LAF patients suffer greatly during their episodes while others have no symptoms at all and are diagnosed only by chance through a routine electrocardiogram.

Dr. Philippe Coumel of the Lariboisiere Hospital in Paris proposed in 1989 that a dysfunction of the autonomic nervous system plays a major role in LAF. He found that there are two varieties of paroxysmal LAF, an adrenergic form and vagal form.

Adrenergic type LAF is intimately connected with an over-active sympathetic (adrenergic) nervous system and is primarily found in older people. Episodes occur almost exclusively during daytime and is often preceded by exercise or emotional stress. This type of LAF can also be a symptom of hyperthyroidism or pheochromocytoma. Some cardiologists feel that adrenergic type LAF may involve some sort of unrecognized heart abnormality.

Vagal type LAF is associated with an overactive parasympathetic (vagal) nervous system and is often observed in athletes and people with digestive problems. It is most common among men aged 40 to 50 years. The commonest feature is that of weekly episodes, lasting from a few minutes to several hours. The essential feature is the occurrence of attacks at night, often ending in the morning. Rest, digestive periods (particularly after dinner), and alcohol consumption are also predisposing factors. Exercise or emotional stress does not trigger the arrhythmia. On the contrary, on feeling the sensation of an oncoming episode (repeated atrial premature beats), many patients have observed that they can prevent an attack by exercising, but the relaxation period that follows an effort or an emotional stress frequently coincides with the onset of vagal LAF. There is no indication that vagal LAF involves any heart abnormality and vagal LAF rarely if ever develops into a permanent condition.

Some LAF patients experience both vagal and adrenergic episodes and are classified as having a mixed variety of LAF.

Frequent urination (every 20 minutes or so) often occurs during the early phase of an episode and is due to the release of atrial natriuretic peptide from the fibrillating atria.

The triggers of subsequent episodes follow in the footsteps of the first one. The overwhelming favourite for the title of most important trigger is emotional or work-related stress. A full 50% of all respondents listed stress as a trigger. Physical overexertion was next at 24% closely followed by alcohol (including wine) and rest at 22% each. The digestive period following a heavy meal was a trigger for 18%, caffeine was mentioned by 16%, and an ice-cold drink by 12%. Ten per cent reported that MSG (monosodium glutamate) was a trigger for them and 6% said that lying on the left side would set off an episode. Aspartame (NutraSweet) was mentioned as a trigger by two respondents (4%) as was chocolate, coughing and burping, and flying (at high altitudes). Three men over 30 years of age (6%) felt that their episodes were cyclical in nature and not related to any specific trigger. Other triggers mentioned were aged cheese, sugar, food additives, acid indigestion, a hot bath, NyQuil (a cold remedy), electromagnetic radiation, toxic chemicals, hypoglycemia, high blood pressure, and changes in weather patterns. Please note that the percentages do not add up to 100 because many respondents listed more than one trigger.

It is clear that the triggers for LAF are many and varied and highly specific to each individual except for excessive emotional and physical stress which are pretty well universal.

Pharmaceutical drugs are prescribed in an attempt to prevent or terminate episodes or to slow the heart rate during an episode.

Prevention of adrenergic type LAF
Beta-blockers like atenolol, propranolol and metoprolol are usually prescribed as the first line of defense against repeated episodes of adrenergic type LAF. The surveys reported in the September 2001 and June 2002 issues of THE AFIB REPORT found no evidence that they are actually useful for this purpose. The second line of defense involves antiarrhythmic drugs like sotalol, propafenone and amiodarone. Again there was no evidence in the survey that they actually do any good. As a matter of fact there was some indication that adrenergic afibbers on drugs have more episodes than those not on drugs. In addition, amiodarone and to a lesser extent sotalol and propafenone have some very serious potential adverse effects. So, in a nutshell, pharmaceutical drugs would seem to be of little use in preventing LAF of the adrenergic variety.

Prevention of vagal type LAF
Flecainide and disopyramide can be quite effective in preventing vagal LAF episodes. They are both powerful drugs and can have very serious adverse effects so they should only be used by afibbers with structurally sound hearts. Beta-blockers and sotalol have strong beta-blocking properties and are contra-indicated for vagal afibbers as they are likely to worsen their condition by further increasing vagal dominance of the autonomic nervous system. Propafenone also has beta-blocking properties, but is likely to be OK for most vagal afibbers unless they have a genetic predisposition to metabolizing the drug slowly. Some afibbers have found the time-release version of propafenone (Rythmol SR) to be significantly more effective than the standard version taken two or three times a day.

Prevention of mixed LAF
Our survey found no evidence that any drugs were effective in preventing LAF of the mixed variety. As a matter of fact, it seems that mixed afibbers on drugs had substantially more and longer episodes than those not taking any drugs at all.

Termination of episodes
LAF episodes can be successfully terminated in a hospital setting by injection of flecainide, dofetilide or ibutilide provided the injection is carried out very soon after the start of an episode. It is also possible to terminate an episode at home by using the on-demand (pill-in-the-pocket) approach. Several afibbers have found this approach very effective in keeping the duration of their episodes to two hours or less. This approach involves swallowing propafenone or flecainide tablets with warm water as soon as possible after the start of an episode. The recommended dosage is 200 mg of flecainide or 450 mg of propafenone (for people weighing 70 kg (155 lbs)or less) or 600 mg of propafenone for people weighing more than 70 kg. I have found that lying down on my back (supine position) after swallowing the pills results in quicker conversion, perhaps because being in this position would give the heart rate-slowing parasymphatetic arm of the ANS a bit of a boost.

Slowing of heart rate
Heart rates of 100 bpm or higher can be very uncomfortable and, if continued for long periods, can also damage the heart and circulatory system. The calcium channel blockers verapamil and diltiazem are quite effective in slowing the heart rate although they are of no help in speeding up the conversion to sinus rhythm. Diltiazem in particular would seem to be the drug of choice for permanent afibbers.

Special note on digoxin
Digoxin (Lanoxin) is frequently prescribed for patients with lone atrial fibrillation. This is indeed unfortunate as there is ample clinical evidence that digoxin not only increases the number of episodes, especially in the case of vagal LAF, but also is very likely to turn intermittent (paroxysmal) LAF into permanent LAF. There is no justification for someone with LAF to be given digoxin on an ongoing basis (it can be used on an intermittent, short-term basis to slow down the heart rate) and many afibbers report a substantial improvement in their condition after discontinuing this drug.

Safe removal of amalgam fillings should be done by a holistic or "mercury-free" dentist. The procedure must be followed by effective detoxification as outlined in the July 2001 issue of THE AFIB REPORT.

The following links will assist you in locating a dentist and holistic physician or naturopath in your area who can help you with safe amalgam replacement.