A steady, inconspicuous heartbeat is usually taken for granted so when an attack of atrial fibrillation strikes it is a very frightening experience. The heart beats wildly with a pulse rate as high as 200 beats/minute, dizziness and breathlessness and even fainting may follow and chest pain, extreme fatigue and the need for frequent urination are common symptoms. Fibrillation attack victims usually experience one or more of these symptoms, but a few patients are not aware of any symptoms at all until an electrocardiogram exposes their irregular heart rhythm(1-4).

Atrial fibrillation is the most common cardiac arrhythmia and affects more than 1.5 million Americans. Its primary characteristic is a rapid and irregular heartbeat. The incidence of atrial fibrillation shows a significant increase beyond the age of 50 years and the condition is considerably more common among men than among women. Atrial fibrillation may be chronic or intermittent (paroxysmal) and may be triggered by an underlying heart disease such as mitral valve prolapse or stenosis, coronary artery disease, hypertensive heart disease, a heart attack or an inflammation of the membrane surrounding the heart (pericarditis). Atrial fibrillation is also a common complication of heart surgery(1-3,5-7).

Lone Atrial Fibrillation.
Many cases of atrial fibrillation are not connected with heart disease or hypertension at all and not too long ago were described as "idiopathic", that is, with no known cause. In recent years however, intensive research has uncovered many conditions, which may trigger atrial fibrillation, and the diagnosis "idiopathic atrial fibrillation" is now much less common. Atrial fibrillation not caused by an underlying heart disease is referred to as primary or lone atrial fibrillation(3).

Lone atrial fibrillation (LAF) may be an isolated event or it may recur on an intermittent basis; it is rarely chronic. It is significantly more prevalent among men than among women. An attack may last a few hours or several days, but rarely longer than a week. The frequency of attacks in intermittent LAF may vary from less than one a year to three per year or more(4,8).

Lone atrial fibrillation caused by an overactive thyroid gland (hyperthyroidism) is fairly common and can usually be eliminated by dealing with the underlying disease(1,2,5,6,7,9).

LAF may also be triggered by hypoglycemia, surgery, chronic infections, alcohol abuse (especially binge drinking), nicotine and caffeine (coffee and cola drinks)(1,2,7,9,10). An allergic reaction may also act as a trigger. Thyramine-containing foods such as cheese, red wine, yogurt, bananas, and chocolate have been known to trigger LAF attacks(11). Serious electrolyte imbalances, such as between sodium and potassium and between calcium and magnesium are other potent triggers for arrhythmias(5,9,12).

Many drugs, chief among them digitalis (digoxin, Lanoxin) and other antiarrhythmic drugs, may trigger atrial fibrillation as may excessive physical and emotional stress(1-3,5,10,13).

The rhythm of the heart is controlled through a fine balance of input from the parasympathetic (vagal nerve) and sympathetic nervous system. Thus events, which disturb either of these systems, may trigger LAF. Dr. Philippe Coumel, MD, a French cardiologist, has done extensive work on the link between the nervous system and LAF. He has identified a vagal form of LAF which is most common among men aged 40 to 50, occurs during the night, at rest, after eating or following intake of alcohol. This type of LAF may be triggered by sudden stimulation of the vagal nerve through, for example, vomiting or violent sneezing. Dr. Coumel also describes an adrenergic (adrenal hormone linked) form of LAF which occurs exclusively during daytime and which is often preceded by exercise or emotional stress. Frequent urination is a common feature of this type of LAF(3,13).

Dr. Abram Hoffer, MD, a prominent Canadian physician, also believes that many LAF attacks are caused by excessive physical or emotional stress. He postulates that adrenochrome, a metabolite of adrenaline (epinephrine) is the culprit that initiates LAF attacks. Dr. Hoffer also believes that adrenochrome's negative effects can be negated by certain antioxidants(14).

It is clear that there are many types and potential triggers for LAF and this, of course, makes treatment and prevention extremely complicated and difficult.

Electric cardioversion is used in serious cases to re-establish regular heart rhythm once the pulse rate has been lowered(2,7,17). However, in many cases, sinus rhythm is re-established spontaneously. Cardioversion is not very effective when it comes to LAF and is not recommended for this condition(18).

Many clinical trials have shown magnesium injections to be very effective in stopping fibrillation attacks and some doctors now advocate its routine use in the emergency department. Unfortunately, no studies have been made yet to evaluate the benefits of oral magnesium supplementation in the prevention of LAF(19-24).

Drugs such as procainamide, quinidine, flecainide, sotalol and amiodarone may also be successful in many cases in restoring sinus rhythm. However, these drugs are dangerous and their effect often transient(5,17,25). There is no clear consensus that they are of any value in treating LAF, especially not in cases where symptoms are relatively mild(25).

Atrial fibrillation patients usually also receive aspirin when treated in the emergency ward. The rapid irregular beating of the heart may dislodge small pieces of atherosclerotic plaque in people with heart disease and if these pieces of plaque get stuck in the narrow blood vessels in the brain a stroke may result. There is now compelling evidence that heart disease patients with atrial fibrillation can lessen their risk of a stroke significantly by taking an anticoagulant such as aspirin or warfarin on a regular basis(2,3,5,7,17).

There is however, considerable controversy as to the benefits of anticoagulation therapy in the case of LAF patients, that is, patients with no underlying heart disease, hypertension or other specific risk factors for ischemic stroke (stroke caused by a blood clot). Several studies have found that LAF sufferers do not seem to have a higher risk of stroke than does the general public and therefore may not benefit from taking warfarin or aspirin on a regular basis(5,7,9,15). Researchers at the Mayo Clinic believe that routine anticoagulation is unwarranted for LAF patients under the age of 60 years and that the dangers (internal bleeding, stomach ulcers) of such therapy significantly outweigh the benefits(10). Italian researchers found no difference in the incidence of stroke among LAF patients under 70 years of age regardless of whether they received anticoagulation therapy or not(8).

Prevention of recurrence of LAF
Digoxin has long been prescribed as the drug of choice for preventing LAF(2). However, it is now clear that it does not do so and undoubtedly does more harm than good(3,6,15-17). Digoxin does not prevent intermittent atrial fibrillation and its prolonged use may actually convert the intermittent form to the chronic form(2,7,16,17). It is ineffective in preventing or halting the adrenergic form of LAF and may aggravate LAF of vagal origin(3,13). Recent studies concluded that almost 50% of all patients prescribed digoxin should not be taking it at all and can safely be weaned from it(26,27). Another study found that tens of thousands of patients end up in emergency wards every year with potentially life-threatening digitalis poisoning(28). In short, digitalis is not recommended for the prevention of intermittent LAF attacks(7,15,26).

Other antiarrhythmic drugs such as quinidine, amiodarone, propranolol, sotalol and flecainide may be effective in preventing some types of LAF, but may have no effect on others or may actually aggravate the situation. All antiarrhythmic drugs have very serious side effects and may cause life-threatening arrhythmias themselves. Several clinical trials have shown that patients treated with quinidine and other antiarrhythmic drugs have a higher mortality rate than do patients who are left untreated(3,5,7,15-17,25,29).

Although there is no clear consensus regarding antiarrhythmic drugs in the treatment of LAF many experts believe that their use should be limited to cases where symptoms are severe and persistent(17,25,29).

Fortunately, there are several alternative approaches that show promise in preventing LAF.

Dr. Matthias Rath, MD, a leading American expert on cardiovascular disease, believes that arrhythmias are primarily caused by nutritional deficiencies and can be prevented by optimizing the intake of such nutrients as vitamin-C, l-carnitine, coenzyme Q10, magnesium and vitamin B complex(30). Magnesium is of particular importance as it is highly concentrated in the heart muscle and counteracts excessive calcium, which tends to excite the heart. L-carnitine has been found to have excellent antiarrhythmic properties and is also useful in the treatment of heart attack patients and patients with intermittent claudication(31- 33).

Dr. Abram Hoffer, MD reports excellent results in the prevention of LAF through the use of mega-doses of niacin and folic acid(14).

Japanese researchers have found coenzyme Q10 to be effective in the management of arrhythmias(34-36).

Hawthorn (Crataegus oxyacantha) is widely used in the management of arrhythmias in Europe. It is non-toxic and has been found to improve the overall performance of the heart(37-39).

The bottom line
Although an acute atrial fibrillation attack is very frightening it is rarely life threatening. Several recent studies have concluded that the mortality rate among people who have intermittent atrial fibrillation attacks, but no underlying heart disease, is no greater than that of the general population(8,10).

The first step in preventing LAF attacks is, of course, to avoid the trigger factors. Staying away from alcohol, caffeine and antiarrhythmic drugs such as digoxin is extremely important. Foods that may cause an allergic reaction should be avoided, as should excessive physical and emotional stress.

If you have been diagnosed with true LONE atrial fibrillation, are not on antiarrhythmic drugs and are familiar with the symptoms of an attack you might want to try some or all of these techniques before you head for the emergency department:

Stop what you are doing, take a deep breath and relax

Plunge your face into a basin with ice water

Apply a cold compress to your neck

Do the Valsalva Maneuver (Sit down and bend forward at the waist - hold your breath and strain as if blowing up a balloon)

Take three pellets of Aconite (30cc) homeopathic remedy (sublingually)

Have a warm bath with 6-8 drops of pure orange flower oil (neroli oil) in it

Ask your doctor about carotid sinus massage or your acupuncturist about acupuncture to stop the attack. It is also a good idea to take an aspirin if you are not already on anticoagulants (Take 30 minutes before or after taking a homeopathic remedy)

REFERENCES

1. Mandel, William J., ed. Cardiac Arrhythmias: Their Mechanisms, Diagnosis & Management. Philadelphia, PA, J.B. Lippincott Company, 2nd edition, 1987, pp. 186-234
2. Cheitlin, Melvin D., et al. Clinical Cardiology. Norwalk, CT, Appleton & Lange, 6th edition, 1993, pp. 527-34
3. Prystowsky, Eric N., et al. Management of patients with atrial fibrillation. Circulation, Vol. 93, No. 6, March 15, 1996, pp. 1262-77
4. Davidson, Ehud, et al. Diagnosis and characteristics of lone atrial fibrillation. Chest, Vol. 95, May 1989, pp. 1048-50
5. Alpert, Martin A., et al. Management of atrial fibrillation. Comprehensive Therapy, Vol. 22, No. 8, August 1996, pp. 501-08
6. Baer, Margaret and Goldschlager, Nora. Atrial fibrillation: an update on new management strategies. Geriatrics, Vol. 50, No. 4, April 1995, pp. 22-29
7. Havranek, Edward P. The management of atrial fibrillation: current perspectives. American Family Physician, Vol. 50, No. 5, October 1994, pp. 959-68
8. Rostagno, Carlo, et al. Clinical course of lone atrial fibrillation since first symptomatic arrhythmic episode. American Journal of Cardiology, Vol. 76, October 15, 1995, pp. 837-39
9. Aboaf, Alan P. and Wolf, Phillip S. Paroxysmal atrial fibrillation. Archives of Internal Medicine, Vol. 156, February 26, 1996, pp. 362-67
10. Kopecky, Stephen L., et al. The natural history of lone atrial fibrillation. New England Journal of Medicine, Vol. 317, No. 11, September 10, 1987, pp. 669-74
11. Jacob, Leonard H. and Carron, D.B. Atrial fibrillation precipitated by tyramine containing foods. British Heart Journal, Vol. 57, 1987, pp. 205-06
12. Mandel, William J., ed. Cardiac Arrhythmias: Their Mechanisms, Diagnosis & Management. Philadelphia, PA, J.B. Lippincott Company, 2nd edition, 1987, pp. 81-100
13. Attuel, Patrick, et al., eds. The Atrium in Health and Disease. Mount Kisco, NY, Futura Publishing Company, 1989, pp. 213-32
14. Hoffer, A. Schizophrenia: an evolutionary defence against severe stress. Journal of Orthomolecular Medicine, Vol. 9, No. 4, 1994, pp. 205-21
15. Pritchett, Edward L.C. Management of atrial fibrillation. New England Journal of Medicine, Vol. 326, No. 19, May 7, 1992, pp. 1264-71
16. Falk, Rodney H. Proarrhythmia in patients treated for atrial fibrillation or flutter. Annals of Internal Medicine, Vol. 117, No. 2, July 15, 1992, pp. 141-50
17. Golzari, Houtan, et al. Atrial fibrillation: restoration and maintenance of sinus rhythm and indications for anticoagulation therapy. Annals of Internal Medicine, Vol. 125, No. 4, August 15, 1996, pp. 311-23
18. Mandel, William J., ed. Cardiac Arrhythmias: Their Mechanisms, Diagnosis & Management. Philadelphia, PA, J.B. Lippincott Company, 2nd edition, 1987, p. 745
19. Dietch, Daniel, et al. Magnesium is underused in acute atrial fibrillation. British Medical Journal, Vol. 312, April 27, 1996, p. 1101
20. Wesley, Robert C., et al. Effect of intravenous magnesium sulfate on supraventricular tachycardia. American Journal of Cardiology, Vol. 63, May 1, 1989, pp. 1129-31
21. Hays, Janet V., et al. Effect of magnesium sulfate on ventricular rate control in atrial fibrillation. Annals of Emergency Medicine, Vol. 24, July 1994, pp. 61-64
22. Iseri, Lloyd T. Role of magnesium in cardiac tachyarrhythmias. American Journal of Cardiology, Vol. 65, June 19, 1990, pp. 47K-50K
23. DeCarli, Charles, et al. Serum magnesium levels in symptomatic atrial fibrillation and their relation to rhythm control by intravenous digoxin. American Journal of Cardiology, Vol. 57, April 15, 1986, pp. 956-59
24. Iseri, Lloyd T., et al. Magnesium therapy of cardiac arrhythmias in critical-care medicine. Magnesium, Vol. 8, 1989, pp. 299-306
25. Roden, Dan M. Risks and benefits of antiarrhythmic therapy. New England Journal of Medicine, Vol. 331, No. 12, September 22, 1994, pp. 785-91
26. Aronow, Wilbert S. Prevalence of appropriate and inappropriate indications for use of digoxin in older patients at the time of admission to a nursing home. Journal of the American Geriatrics Society, Vol. 44, No. 5, May 1996, pp. 588-90
27. Fair, James F. Supervised withdrawal of long-term digoxin therapy. Family Practice, Vol. 7, No. 1, 1990, pp. 56-59
28. Warren, Joan L., et al. Hospitalizations with adverse events caused by digitalis therapy among elderly medicare beneficiaries. Archives of Internal Medicine, Vol. 154, July 11, 1994, pp. 1482-87
29. Coumel, Philippe, et al. Drug therapy for prevention of atrial fibrillation. American Journal of Cardiology, Vol. 77, January 25, 1996, pp. 3A-9A
30. Rath, Matthias. Eradicating Heart Disease. San Francisco, CA, Health Now, 1993, pp. 144-50
31. DiPalma, J.R., et al. Cardiovascular and antiarrhythmic effects of carnitine. Archives Internationales de Pharmacodynamie et de Therapie, Vol. 217, No. 2, October 1975, pp. 246-50
32. Iliceto, Sabino, et al. Effects of L-carnitine administration on left ventricular remodeling after acute anterior myocardial infarction. Journal of the American College of Cardiology, Vol. 26, No. 2, August 1995, pp. 380-87
33. Brevetti, Gregorio, et al. Carnitine-related alterations in patients with intermittent claudication. Circulation, Vol. 93, No. 9, May 1, 1996, pp. 1685-89
34. Oda, T., et al. Stress echocardiography for pediatric patients with symptomatic mitral valve prolapse. Jpn. Circ. J., Vol. 47, 1983, p. 1335
35. Oda, T. and Hamamoto, K. Effect of coenzyme Q10 on the stress- induced decrease in cardiac performance in pediatric patients with mitral valve prolapse. Jpn. Circ. J., Vol. 48, 1984, p. 1387
36. Folkers, K. and Yamamura, Y., eds. Biomedical and Clinical Aspects of Coenzyme Q, Vol. 5. Amsterdam, Elsevier Scientific Publications B.V., 1986, pp. 269-80
37. Ammon, H.P.T. and Handel, M. Crataegus, toxicology and pharmacology, Pt. 1: Toxicology. Planta Medica - Journal of Medicinal Plant Research, Vol. 43, No. 2, October 1981, pp. 105- 20 (in German)
38. Ammon, H.P.T. and Handel, M. Crataegus, toxicology and pharmacology, Pt. 2: Pharmacodynamics. Planta Medica - Journal of Medicinal Plant Research, Vol. 43, No. 3, November 1981, pp. 209-39 (in German)
39. O'Conolly, Von M., et al. Behandlung der nachlassenden herzleistung. Fortschr. Med., Vol. 104, No. 42, November 13, 1986, pp. 805-08