Research has yet to uncover the definitive cause of AF. A number of other health conditions including thyroid disorders, valve disease, hypertension, sick sinus syndrome, pericarditis, lung disease, and congenital heart defects are also associated with AF. This type of arrhythmia can occur at any age, but its prevalence tends to increase with age and affects men slightly more often than women.

How things are supposed to work

To better understand the mechanism and characteristics of AF, it is best to begin by describing the normal mechanical and electrical activity of the heart. The heart is a muscle and functions primarily as a double-sided pump. The left side of the heart pumps blood rich in oxygen to supply all parts of the body, while the right side of the heart pumps blood back to the lungs to pick up more oxygen.

There are four chambers, two upper chambers called the left and the right atria and two lower chambers known as the right and left ventricles. Separating these upper and lower chambers there are valves that passively open and close to direct the flow of blood. The left ventricle performs the most work and is the strongest of the chambers because it ejects blood into the aorta (the main pipeline that supplies oxygenated blood to the entire body).
In order for the heart to pump, it must first receive some sort of electrical stimulation that will cause the muscle to contract. During a normal heart beat, an electrical impulse originates in the right atrium in the sinoatrial node (SA node) and travels simultaneously to the left atrium and down the interatrial septum to the atrioventricular node (AV node). The impulse slows briefly at the AV node and then continues to travel down a common pathway splitting off into the left and right bundle branches located in both ventricles. This cycle of electrical stimulation is known as normal sinus rhythm (NSR), which describes a form of orchestrated synchrony between the atria and the ventricles of the heart, producing the familiar (lub-dub) heart sounds.

In the broadest sense, AF represents the loss of synchrony between the atria and the ventricles. Typically, AF is characterized as a storm of electrical energy that travels in spinning wavelets across both atria, causing these upper chambers to quiver or to fibrillate at 300 to 600 times per minute.

For many years, AF was believed to be a completely chaotic event with unorganized electrical impulses bouncing around the atria randomly. However, research and computerized mapping techniques have provided greater insight into the mechanism of AF. Typically, there are at least six different locations in the left and right atria where relatively large circular waves can occur, creating a pattern of continuous electrical activity that is characteristic of complex AF. This important discovery paved the way for the development of the Maze procedure, a surgical intervention that extinguishes atrial fibrillation.

Atrial fibrillation can also occur as a secondary event. Other arrhythmias such as atrial tachycardia and atrial flutter may be initiated from a single region of either atrium and subsequently degenerate into AF.

The many faces of atrial fibrillation

Several different terms are used to describe AF. "Lone" or primary atrial fibrillation is a form of AF with no identifiable cause or associated abnormalities of the heart.

Paroxysmal AF occurs intermittently and varies in frequency and duration from a few seconds to more protracted episodes lasting several hours or even days.

Both lone and paroxysmal AF tend to be seen more often in younger people aged 30-50 years.

Chronic AF on the other hand, is persistent, becoming the primary heart rhythm and it is usually unresponsive to medical therapy or other non-pharmacologic interventions such as electrical cardioversion. This form of AF is typically seen in an older population.

Early genetic research on familial AF, a relatively uncommon type of AF often affecting younger people (<20 years of age) has identified a specific chromosomal defect that is responsible for this form of arrhythmia.

Neurogenic AF indicates an imbalance in the nervous system regulation of the heart. One type of neurogenic atrial fibrillation, vagal AF, occurs in conjunction with enhanced parasympathetic response from the vagus nerve. Stimulation of the vagus nerve (or increased vagal tone) causes the heart rate to slow down and the refractory period (rest period) of the atria to shorten. Typically, vagal AF occurs more frequently at rest or following a meal, and is usually in seen men who are between 30 and 50 years of age. Often times, patients note the onset of this type of AF is preceded by a period of progressive bradycardia (slow heart rate) and in this case, medications such as beta blockers or digitalis may actually worsen the AF.

Adrenergic AF is another type of neurogenic atrial fibrillation that occurs as a result of excessive adrenaline that comes from stimulation of the sympathetic portion ("fight or flight"response) of the nervous system. Sympathetic effects on the heart include increased rate and force of contraction. This type of AF is most likely to occur during the day and may be associated with emotional stress or physical exertion. Unlike the case of vagal AF, medical therapy with beta blockers may be quite helpful in controlling this form of atrial fibrillation.

The impact of AF on daily life:  Why it makes you feel the way you do

A broad range of physical symptoms may be associated with AF. Some people have absolutely no awareness of being in atrial fibrillation, while others know precisely the moment when their heart rhythm destabilizes from normal sinus rhythm to AF. Many patients describe the irregular, often rapid pulsations of the heart in AF as an uncomfortable flopping sensation inside of the chest with a sudden and keen awareness of every heartbeat. This may be accompanied by shortness of breath, profuse sweating, chest pain, presyncope (dizziness), syncope (passing out), exercise intolerance and extreme fatigue.

Others describe anxiety and a feeling of impending doom, especially when AF is first discovered. For some patients, the pattern of atrial fibrillation may progress from a paroxysmal and infrequent event to become a chronic condition. Often, there is a worsening or progression of the symptoms such that many patients feel incapable of carrying out normal daily activities.

It is difficult for those who have not experienced AF to understand the impact that it can have on one's daily life. Battling the physical and emotional effects of AF is debilitating, yet no one knows that the battle exists because there are few outward physical symptoms. Employers, family members and yes, even treating physicians may be unaware of the decrease in functional capacity that AF causes. As a result, patients with AF often feel that others think that they are "exaggerating" their symptoms.

Because AF is so unpredictable, patients are often reluctant to travel and may even avoid committing to social engagements. Frequent trips to the hospital for repeated episodes of atrial fibrillation can completely disrupt one's life, causing significant emotional and physical distress to victims and families alike.

How is atrial fibrillation treated?

There are three major goals of medical treatment of AF: the restoration of normal sinus rhythm, control of the ventricular rate during AF, and prevention of blood clot formation. Other current treatment options include medications, electrical cardioversion, ablations, pacemakers, and surgery. Early research on atrial defibrillators is ongoing for certain types of AF. The choice of therapy is quite individualized and is usually based on the degree of disability and symptoms associated with the AF.

Pharmacological Therapy: Medicine's First Line of Defense

Restoration of Sinus Rhythm

Sinus rhythm is often restored with medications by slowing the conduction of electrical impulses, decreasing the excitability and automaticity of cardiac cells, or prolonging the refractory period (rest period) of cardiac tissue. Several medications may be used to terminate atrial fibrillation including procainimide (Pronestyl), quinidine, disopyramide (Norpace), and amiodarone (Cordarone). The effectiveness of pharmacological cardioversion and one's tolerance of drug therapy is quite individualized. Medications may often be changed in order to achieve the desired outcome of reducing symptomatic episodes of AF. Unfortunately, some of these drugs can have pro-arrhythmic effects, causing the heart to become even more irritable and setting the stage for new arrhythmias to occur.

Control of Ventricular Rate

To effectively reduce the symptoms associated with AF, it is important that the ventricular rate be controlled. The irregular, flopping sensation in the chest that is so uncomfortable and worrisome to patients with AF is not from the irregular atrial beat, but rather is from the irregular ventricular beat in response to the AF.  In fact, patients are not capable of feeling their atria beating, only the ventricles. So, the faster the ventricles go, the more symptomatic patients usually become. The goal of medications such as beta blockers, calcium channel blockers, and digoxin is to slow down the heart rate by decreasing the excitability of the cardiac cells and by slowing the conduction of the electrical impulses through the AV node.

Remember, the AV node is located between the atria and the ventricles and has a protective "gatekeeper" mechanism that only allows so many impulses to travel through to the ventricles. Therefore, the goal is to reduce the ventricular rate to 70-90 beats per minute via the AV node during an episode of AF. The idea here is that even though the heartbeat is irregular, it is better to be irregular at 70-80 beats per minute than to be irregular at 140-150 beats per minute. This rate control in turn, decreases the workload of the heart and the symptoms of discomfort associated with a fast irregular heart beat. Some of the medications used to produce this effect include sotalol (Sotacor), amiodarone (Cordarone), propranolol (Inderal), diltiazem (Cardizem), verapamil (Isoptin), and digoxin (Lanoxin).

Prevention of Blood Clot Formation

During atrial fibrillation, the atria lose their organized pumping action and fibrillate (quiver) in response to the continuous electrical stimulation. In normal sinus rhythm, the atria contract, the valves open and blood fills the ventricles (the lower chambers). The ventricles then contract to complete the organized cycle of contraction that occurs with each heartbeat. Since the atria don't contract during AF, the blood is not able to empty efficiently from the atria into the ventricles with each heartbeat. Blood can then pool and become stagnant in the atria, creating a site for blood clot formation. Since the left side of the heart pumps the oxygenated blood to all parts of the body, clot formation in the left atrium can become a primary source of stroke in patients with AF.

One type of stroke (thromboembolic cerebral vascular accident, or CVA) occurs when a blood clot travels to the brain and lodges in a vessel causing the normal blood flow to stop and the brain tissue to die from lack of oxygen. This serious complication of AF occurs approximately six times more often in the elderly. Since atrial fibrillation is the most common arrhythmia in this group, it poses a substantial and potentially devastating risk.

Research has demonstrated that anticoagulation with warfarin (Coumadin) is effective in reducing the risk of blood clot formation and stroke but it does not totally eliminate the risk.  An anticoagulant or blood thinner such as Coumadin interferes with the body's normal clotting mechanism. The dose of Coumadin is highly individualized and must be carefully monitored with blood tests to ensure safety. The blood test used to determine the level of anticoagulation is called the INR (International Normalized Ratio). The therapeutic range is usually between 2.0 and 3.0 for the prevention of stroke.

Aspirin is an antiplatelet drug that is also used for stroke prevention. Aspirin decreases the stickiness of circulating platelets (small blood cells that initiate the normal clotting process), so they will not adhere to one another and thus reduces the likelihood of forming blood clots. Aspirin is much safer than Coumadin or warfarin because it is less likely to cause abnormal bleeding, including even strokes from bleeding due to the Coumadin itself.

However, current research indicates that aspirin is not as effective in preventing blood clots (and therefore, strokes) as Coumadin. Patients who are otherwise considered to be at low risk may be advised by their physician to take aspirin for stroke prevention. Patients with atrial fibrillation should discuss the risk of stroke with their physician in order to make appropriate decisions regarding the choice of therapy.

Non-pharmacological Therapy:  The Next Step in AF Treatment 

Electrical Cardioversion

Electrical cardioversion is used to terminate atrial fibrillation but in and of itself has no long-term effect on the recurrence of AF. Patients are generally admitted as an outpatient to the hospital, placed on a heart monitor, an intravenous form of anesthetic is given and patches are placed on the chest.

Once the patient is completely anesthetized, a small electrical charge over the heart is delivered. This electrical charge causes a momentary electrical discharge of all the cardiac cells and allows the primary pacemaker, the SA node, to take control of the rhythm, thus stopping the atrial fibrillation and resetting the heart.

Sometimes, cardioversion is done in conjunction with antiarrhythmic medications to reduce the likelihood of recurrence of the AF.

Ablations for Specific Arrhythmias

Ablation procedures are used to terminate arrhythmias by introducing catheters into the heart and directing energy at specific areas of heart tissue found to be the source of the irregular rhythms. An electrophysiology (EP) study  is performed to discover the location and the characteristics of the arrhythmia. Once the specific location is mapped, then special catheters are precisely placed, radio frequency (RF) energy is passed down the catheter to the heart tissue and the tissue is destroyed. The tissue is no longer able to initiate or to conduct any type of electrical impulse.

Several types of arrhythmias are amenable to ablation therapy including: Wolff-Parkinson-White syndrome (WPW), AV nodal reentrant tachycardia (AVNRT), certain types of atrial flutter, and some cases of ventricular tachycardia.

Secondary “Treatment” of AF

Catheter ablation of the AV node may be performed to modify the ventricular response to atrial tachycardias and atrial fibrillation. This therapy is usually reserved for patients with rapid heart rates that are not well-controlled with medications and present with symptoms related to the uncontrolled heart rate. The procedure destroys the tissue at the AV node and His bundle and stops the conduction of all electrical impulses from the atria to the ventricles. In other words, it disconnects the electrical pathway that drives the bottom of the heart.

Ablation of the AV node requires the placement of a permanent pacemaker at the time of the procedure. The pacemaker then provides a steady and regular heart beat (ie. ventricular beat) that often diminishes the symptoms associated with atrial fibrillation, even though the atria continue to fibrillate. This procedure does not cure atrial fibrillation nor does it diminish the risk of stroke and therefore, anticoagulation will be continued after the procedure. However, some patients are able to reduce or discontinue medications such as beta blockers or anti-arrhythmics following an AV nodal ablation because the ventricular rate is now controlled by the pacemaker.

Pacemakers

The various types of pacemakers in use today are far more sophisticated and better capable of responding to the changing needs of our bodies than those of a generation ago . The first pacemaker inserted nearly forty years ago was limited to pacing only one chamber at a fixed rate. Today's pacemakers consist of two major parts: a generator that houses a battery and electronic sensors, and the leads that connect into the heart. The generator provides a small electrical current that stimulates the heart to pump via the leads. (Remember the heart requires an electrical impulse to cause it to pump, or contract.) Sophisticated onboard electronic sensors provide continuous feedback and information from the heart , instructing the pacemaker to compensate according to the body's requirements. This allows for maximal fine-tuning of the pacemaker to meet the needs of the patient.

Pacemakers are inserted for a variety of heart conditions including sick sinus syndrome, supraventricular tachycardia, heart block and ventricular tachycardia. Although AF is usually not an indication for a pacemaker, some underlying conditions such as sick sinus syndrome could necessitate the placement of a pacemaker. This is something that your cardiologist will discuss with you in great detail prior to recommending this procedure.

Atrial Defibrillators

Atrial defibrillators are investigational devices that are currently being studied at several centers in the US.  Early reports from the European trials and initial US trials with small numbers of patients are being evaluated at this time. The device utilizes specialized technology to accurately recognize AF and electrically converts the arrhythmia by delivering a small electrical shock via leads placed in the heart. The device is also equipped with an additional lead that provides backup pacing of the ventricle if needed. Atrial defibrillators are about the size of a conventional pacemaker and consist of a small battery pack, a generator, and three leads. The device is inserted under x-ray guidance in the cardiac catheterization laboratory by interventional cardiologists.

It is still too early in the research process to predict the reliability and efficacy of this device. It may yet offer another choice of therapy for selected patients with AF.

Beyond Prescription: Surgical Treatment of AF

The Maze Procedure

The Maze procedure is a surgical intervention that cures atrial fibrillation (AF) by interrupting the circular electrical patterns or wavelets that are responsible for this arrhythmia. Strategic placement of incisions in both atria stops the formation and the conduction of errant electrical impulses and channels the normal electrical impulse in one direction from the top of the heart to the bottom. Scar tissue generated by the incisions permanently blocks the abnormal paths of the electrical impulses that cause AF, thus eradicating the arrhythmia. The major advantage that this surgical intervention to cure AF offers over other less-invasive forms of therapy is that it corrects all three problems associated with AF. The Maze procedure

A further in-depth discussion of the Maze procedure is presented in a question and answer format found in the Maze FAQ section of this web site.

What else is on the horizon for treatment of atrial fibrillation?

Several research centers are currently developing specialized catheters to attempt a less invasive maze-type of procedure with ablation catheters instead of an open-heart surgical approach. There have been some early trials with the “catheter maze” but the results were not optimal and development is ongoing. Technology advances and continued research have recently provided for the development of a less-invasive surgical approach for atrial fibrillation that we are now routinely employing in selective patients. In