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 five 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 one 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 downside 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 percent 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.
Bridgewater resident Steve Georgeson is a cardiologist who works for Medicor Cardiology. Here, he writes about topics and events pertaining to cardiology
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