Because of the inconvenience, relative lack of effectiveness, and the safety concerns associated with trying to restore and maintain a normal heart rhythm, for many patients with chronic or persistent atrial fibrillation, effective therapy requires another approach.
Instead of trying to abolish the atrial fibrillation, a patient's doctor may treat the symptoms caused by the arrhythmia. This treatment approach requires two things: preventing blood clots, and controlling the heart rate.
Preventing Blood Clots
Anticoagulation ("thinning" the blood to prevent blood clots) is necessary in these patients in order to reduce the risk of stroke caused by the formation of blood clots in the fibrillating atria.
Coumadin is the most effective "blood thinner" for preventing stroke in atrial fibrillation. Coumadin works by inhibiting the "clotting factors" - proteins made in the liver that circulate in the blood and facilitate blood clotting. The amount of inhibition of clotting factors achieved by coumadin is measured with a blood test called the "INR," and the proper dose of coumadin needs to be carefully adjusted by monitoring the INR.
Aspiring works by making platelets (tiny cells that circulate in the bloodstream and promote blood clotting) less "sticky," and less able to clump together.
In general, coumadin is more effective than aspirin for preventing stroke in atrial fibrillation.
Controlling the Heart Rate
In the large majority of patients, most of the symptoms of atrial fibrillation are directly caused by the resulting rapid heart rate. So, if the heart rate can be controlled, these patients can lead essentially normal lives despite the persistence of the atrial fibrillation. Generally, control of the heart rate can be obtained by giving digitalis and beta blockers, and sometimes calcium channel blockers.
All three of these classes of drugs work by slowing the conduction of the electrical impulse through the AV node, thus reducing the heart rate in atrial fibrillation. Read about the heart's electrical system here. Digitalis works by increasing the "vagal tone" in the AV node. Beta blockers work by blocking the effect of adrenaline on the AV node. Calcium blockers work by blocking the calcium channels responsible for most of the electrical activity in the AV node. Often, combinations of these drugs are required to achieve sufficient rate control.
In some instances, the heart rate cannot be controlled with drugs. For these patients, the heart rate can be controlled by ablating the AV node. In AV node ablation, radiofrequency energy is applied to the AV node via a catheter (during an EP study,) essentially cauterizing the AV node. ( Review the normal electrical system of the heart here.)
Ablating the AV node prevents the rapid, chaotic electrical impulses in the atria from reaching the ventricles, and thus keeps the heart rate slow. However, AV node ablation usually results in a heart rate that is too slow - and thus, the procedure almost always requires the insertion of a permanent pacemaker. While it is a somewhat drastic procedure, AV node ablation and pacemaker insertion often results in a remarkable improvement in symptoms for patients with persistent atrial fibrillation in whom other measures to control the heart rate have failed.
For the vast majority of patients with chronic atrial fibrillation, however, excellent control of the heart rate - and of symptoms - can be obtained by the use of medication.
Summary
While occasionally it may prove to be a challenge, in the large majority of patients with chronic atrial fibrillation it is possible to sufficiently slow the heart rate and to sufficiently reduce the risk of stroke to enable these individuals to live nearly symptom-free.
Sources:
Fogoros, RN. Treatment of Supraventricular Arrhythmias. In: Fogoros, RN. Antiarrhythmic Drugs - A Practical Guide. Blackwell Publishing, Malden, MA: 2007.
