Atrial fibrillation is a rapid, irregular heart rhythm in
the upper chambers of the heart (the atria).
Instead of having a regular, coordinated beat, the atria are rapid and
disorganized. When the atria are not beating in a coordinated fashion, the
blood in these chambers does not drain effectively into the lower chambers of
the heart (the ventricles). When blood is not draining well, it sits in the
atria and can form a blood clot. A clot, or a small part of a clot, can break
loose, go to the brain and cause a stroke.
Atrial fibrillation is the most common heart rhythm
disturbance with about 5.6 million diagnosed cases in the United States. If left untreated, atrial fibrillation leads
to stroke in 5 out of 100 people per year. Atrial fibrillation is treated with
medications such as beta blockers, calcium channel blockers or digoxin to
control the rapid heart rate. If doctors want to return a patient to a normal,
regular rhythm then antiarrhythmic agents are used, often with cardioversion
(shocking the heart back to normal rhythm). To prevent blood clots and strokes, Coumadin
(warfarin) has been prescribed for many decades. Coumadin will decrease the
risk for stroke to less than 1 in 100 patients per year. Coumadin however is
difficult to take, requiring frequent blood drawing to ensure that the blood is
not “too thin” (leading to bleeding) or “too thick” (leading to stroke). In
addition, eating green leafy foods will interfere with the level of blood
thinning provided by Coumadin (green leafy foods have Vitamin K which reverses
the effect of Coumadin). Many common medications interfere with Coumadin’s
effect as well. Lastly, there is a significant risk for major bleeding on
Coumadin, especially bleeding in the brain.
One recent break through in the management of atrial
fibrillation came with the introduction of novel oral anticoagulants
(NOACs). These agents include Dabigatran
(Pradaxa), Rivaroxaban (Xarelto) and Apixaban (Eliquis). The NOACs are easier to take than Coumadin
since there are no dietary restrictions. Their blood thinning effect is
consistent, so blood drawing to test levels is not needed. In addition, they
have been shown to reduce the risk of stroke to a greater degree than Coumadin
and they are generally safer with lower risk for major bleeding and bleeding
into the brain. The major down side to
the NOACs is that, to date, there is no antidote which can reverse the effect
of these medications if a patient comes to the hospital with bleeding (there is
an antidote for Coumadin). Until a reversing
agent becomes available, patents with bleeding on a NOAC are supported with
blood transfusions, surgery and time (letting the medication wash out of the
system).
Another recent innovation in the treatment of atrial
fibrillation is catheter ablation. It is felt that atrial fibrillation is
caused when tiny electrical wavelets are conducted from the pulmonary veins to
the atria (pulmonary veins are vessels that carry oxygenated blood from the lungs
to the heart). Once in the atria, these
wavelets perpetuate and cause the rapid chaotic rhythm. Catheter ablation entails threading an
electrical probe from the leg artery into the heart. The catheter is positioned
at the inlet of the pulmonary veins into the atria and small areas of the heart
tissue are burned, effectively causing a “circuit breaker”, the burned tissue
stops the wavelets from reaching the atria. Catheter ablation has been
successful in 84% of patients, allowing them to stop many of the medications,
including blood thinners, they were taking to control atrial fibrillation. Catheter ablation is generally recommended
for symptomatic atrial fibrillation patients, especially if they have failed
one or more antiarrhythmic agents.
Recently an association has been made between atrial
fibrillation and obstructive sleep apnea.
Sleep apnea is a condition where patients stop breathing during the
sleep cycle. When they stop breathing
the blood oxygen level decreases. When the oxygen level is low, patients are
then aroused and gasp for breath. This cycle continues throughout the night.
With frequent arousals, patients can’t enter the deepest phase of sleep, so the
body does not get its proper rest. When the body can’t rest, it is perpetually
aroused, there are excess catecholamines (adrenaline) and that may predispose
to atrial fibrillation. When sleep apnea is successfully treated with a CPAP
mask (to keep the airway open, stopping the drop in blood oxygen) episodes of
atrial fibrillation are reduced.
It is becoming more apparent that atrial fibrillation is a
disease related to life style and systemic disease. It has been known for years
that atrial fibrillation can occur with binge drinking of alcohol (the
so-called “holiday heart syndrome”). Reducing
alcohol intake can reduce episodes of atrial fibrillation. More recently, it
has been shown that obesity is related to atrial fibrillation. Obesity can lead
to diabetes, hypertension and sleep apnea, all factors in causing atrial
fibrillation. Now, for the first time, it has been shown that obese patients
who lost 10 per cent of their body weight achieved freedom from atrial
fibrillation without the use of any medication or ablation. The more weight
that was lost, the greater the freedom from atrial fibrillation.
Atrial fibrillation used to be thought of as a disease. Now
we are beginning to see that the atria are a window on overall health and that
atrial fibrillation is an exposure to an excess. Medications and procedures for
atrial fibrillation can help manage the acute episode, but then the real work
begins, as patients then must address life style issues such as alcohol intake
and treating obesity and sleep apnea. Despite the new advances in pharmacology
and surgery to treat atrial fibrillation, the future cure of atrial
fibrillation will more likely come from identifying the life style causes and
treating these causes.
