Atrial fibrillation is a condition in which the regular pumping function of the atria is replaced by a disorganized, ineffective
quivering caused by chaotic conduction of electrical signals through the upper chambers of the heart. Atrial fibrillation is often
associated with other forms of cardiovascular disease, including one or more of the following: congestive heart failure,
rheumatic heart disease, coronary artery disease, left ventricular hypertrophy, cardiomyopathy and hypertension.
The progression of atrial fibrillation varies among individuals. Initial episodes of atrial fibrillation are generally symptomatic,
intermittent paroxysmal episodes. Some people experience recurring episodes of atrial fibrillation that progress to a chronic
state of continuous fibrillation.
Although not immediately life threatening, atrial fibrillation may cause up to a 30% reduction in cardiac output resulting in
shortness of breath, fatigue and reduced exercise capacity and a reduction in cerebral blood flow during the fibrillation
episode, resulting in fainting and fatigue. Ventricular rates can also rise dangerously high when the chaotic signals of the atria
are conducted to these lower chambers of the heart. More seriously, since the atria provide minimal pumping function during
atrial fibrillation, blood pools in the chambers, which can lead to the formation of blood clots. Blood clots in the left atrium
can dislodge and travel to the brain resulting in stroke.
No longer considered a benign disorder, atrial fibrillation is now recognized as placing affected patients at a significantly
increased risk for stroke. The American Heart Association estimates that 1/4, or 75,000 strokes per year in the United
States are related to atrial fibrillation, with up to 23% of such patients dying and 43 % suffering significant neurologic deficit.
The mortality rate from other causes of stroke is only 8 %. Atrial fibrillation affects up to 4% of the U.S. population over the
age of 60 years.
Currently, the only curative treatment for atrial fibrillation is a rarely performed open heart surgical procedure (the surgical
maze procedure) in which the surgeon makes several incisions in the right and left atria, creating scar tissue to electrically
isolate portions of the atria. This open heart surgical procedure is complex, costly and associated with high morbidity and
mortality and therefore only used in extreme cases.
There are a small percentage of patients for whom a reversible cause for atrial fibrillation can be readily identified, for
example patients with hyperthyroidism, alcoholism or diabetes, and in whom atrial fibrillation does not recur once the cause
has been alleviated. Goals for managing patients with atrial fibrillation are to restore and maintain the normal atrial rhythm and
pumping function, control the ventricular rate and prevent stroke.
None of the commonly prescribed medical therapeutic options is curative and most have undesirable side effects.
Antiarrhythmic drugs, which control the ventricular rate during atrial fibrillation, increase the risk of the patient developing
life-threatening ventricular arrhythmias. In addition, the rate of recurrence of atrial fibrillation in patients using antiarrhythmic
drugs is high, with trials reporting as many as 60% of the patients failing to sustain normal heart rhythm for one year. Side
effects can include nausea, diarrhea, difficulty in urinating, thyroid dysfunction, pulmonary fibrosis and liver dysfunction.
Anticoagulation drugs are generally recommended for use in concert with antiarrhythmic drugs to reduce the risk of stroke.
Anticoagulation therapy requires frequent patient follow-up, generally including monthly prothrombin time testing (an
indicator of the blood’s ability to form clots) and dose adjustments to prevent hemorrhage complications.
Internal electrical cardioversion, in which an implantable atrial defibrillator automatically detects the onset of atrial fibrillation
and delivers low-energy shocks, has recently been introduced as a method to convert atrial fibrillation to normal heart
rhythm. Clinical trials of this proposed treatment are in their early stages. A recent study indicated that initial conversion rates
are near 85%. However, reversion rates to atrial fibrillation are high, and the automatic implantable atrial defibrillator is not a
curative therapy. In addition, the level of patient comfort is often unacceptable.
Less invasive treatments of atrial fibrillation include permanent destruction of the AV node by catheter ablation accompanied
by implantation of a pacemaker, a procedure generally reserved for symptomatic individuals experiencing prolonged or
chronic episodes of atrial fibrillation where control of the ventricular rate is the primary objective. The procedure ensures a
regular, controlled ventricular rate and improved cardiac output, but the risks of stroke remain, and the atrial contribution to
cardiac output is not restored since the atria continue to fibrillate. In addition, the patient becomes dependent upon the
pacemaker to maintain an adequate heart rate, and failure of the pacemaker can result in sudden loss of consciousness or
Several institutions in Europe and the United States have undertaken procedures in which conventional radio-frequency
ablation catheters are dragged along the inside surface of the right and/or left atrium, applying radio-frequency energy to
electrically isolate portions of the atria with scar tissue, a kind of surgery without the knife. However, it has been difficult to
create a continuous line of block to electrically isolate portions of the atria using conventional radio-frequency catheters. In
addition, the mean time of this center’s ablation procedures has been approximately 10 hours.
The primary goal, of course, is to decrease the risk of complications of AF. The most important complication is stasis of
blood in the left atrium with clot formation and then stroke by virtue of movement of clotted blood from the left atrium to the
left ventricle and then to the brain. That is the reason for anticoagulation of patients with AF. However, standard
anticoagulation itself presents serious risks, one of which is stoke, although by a different mechanism. The agents usually used
is coumadin, which is also the major ingredient in rat poison. It induces hemorrhagic strokes (that is to say, they bleed into
their little brains) in rats and that is how it works.
Of course there should be no consumption of alcohol, coffee, tobacco, or unnecessary drugs as these items can aggravate
the condition. A safer, nutritional, alternative to coumadin is high dose vitamin E in the range of at least 2000 IU per day.
This provides anticoagulation, but in a fashion safer than coumadin. However if a person is already anti-coagulated, there
must be a transition phase supervised by a physician and the proper lab tests to be sure that clotting ability is not too far
compromised while both the coumadin and vitamin E are on board at the same time.
AF is usually present with other cardiac problems and its very presence is probably the tip of an iceberg, so to speak. It is
reasonable to think that other heart problems are on the way when AF appears. To strengthen the heart AF patients should
be on a full range of heart supporting nutrients such as minerals and trace minerals, co-Q10, L-carnitine, taurine, magnesium,
vitamin C, fish oil, and thiamine. In addition, EDTA chelation therapy, in my experience, strengthens the heart and provides
an anti-coagulant action of its own. These should be alternated with intravenous mineral drips and this sometimes stops AF.
This is the course I myself would follow if I had AF, before I would consider the more radical solutions such as ablation of
parts of the conducting system of the heart.