Atrial Fibrillation

Atrial fibrillation is an abnormal rhythm of the heart. It is relatively common, affecting 2.3 million adults in the United States. Increasing age is an important predictor of risk, as most patients are more than 65 years of age. Atrial fibrillation is more frequent in men than women, and in whites than blacks.
There are two forms of this abnormal heart rhythm:
Intermittent (paroxysmal) atrial fibrillation, which is characterized by episodes that occur with varying frequency and last for a variable period of time before spontaneously stopping.
Chronic or persistent atrial fibrillation, which is sustained and does not usually stop spontaneously.
The purpose of this review is to describe the symptoms of atrial fibrillation, its risks, and to review current treatments.

HEART ANATOMY AND PHYSIOLOGY
To understand the importance of atrial fibrillation, it is necessary to briefly review the anatomy of the heart.
The heart is made up of four chambers: right atrium, right ventricle, left atrium, and left ventricle (show figure 1). Blood returning to the heart flows into the right atrium, and then the right ventricle. Blood is pumped out of the right ventricle into the lungs, where oxygen is added, and then returns to the heart in the left atrium. Blood in the left atrium flows into the left ventricle, which pumps the blood to the rest of the body through the aorta.
The heart primarily consists of muscle cells, which are stimulated by rhythmic electrical impulses that cause them to contract in a uniform and regular way. Normally, the electrical impulses arise from an area of specialized cells called the sinus node or normal pacemaker, located in the right atrium or upper right chamber of the heart. The normal sinus rate is 60 to 100 beats per minute. After leaving the sinus node, the impulse moves through and activates the right atrium and then left atrium (show figure 2). The impulse then travels slowly through the atrioventricular (AV) node, located between the atria and ventricles. After emerging from the AV node, the impulse travels through specialized heart fibers that rapidly transfer it to various parts of the right and left ventricles to produce uniform activation and contraction.
The atrioventricular (AV) node provides protection from too many impulses reaching the ventricles. It contains specialized cells that are capable of only slow conduction of the impulse. As a result, the AV node limits the number of impulses that can pass from the atria to the ventricles.
Atrial fibrillation — In atrial fibrillation (also called AF or a-fib), the normal orderly activation in the atria is “short-circuited” and replaced by many rapidly firing and disorganized impulses. These rapid impulses result in chaotic contractions of the atrial muscle, described as “quivering” or “worm-like.” Thus, instead of a forceful single contraction of the atria seen in normal sinus rhythm, the rapid contractions of atrial fibrillation are weak, resulting in the ejection of only a small amount of blood. The blood that remains in the atria becomes “sluggish” or static, which encourages the formation of blood clots (see “Risk of stroke” below).
During atrial fibrillation, the atria are stimulated 350 to 600 beats per minute or even more, much faster than the normal sinus rate of 60 to 100 beats per minute. Fortunately, the AV node cannot conduct all of these impulses. It allows up to approximately 170 impulses per minute to get through, though in an irregular fashion. As a result, the response of the ventricles to atrial fibrillation is rapid and irregular. If the ventricles beat too fast to fill completely with blood between beats, an inadequate amount of blood is pumped out of the heart to the rest of the body.

CAUSES
Atrial fibrillation increases in frequency with aging and typically occurs in people who have underlying heart disease. Almost any heart disease can increase the risk of this abnormal rhythm, but the most common causes are:
Hypertensive heart disease due to chronic high blood pressure.
A heart attack (myocardial infarction, or MI); episodes of atrial fibrillation associated with a heart attack are usually brief, although it may become persistent.
Heart failure of almost any cause.
Heart valve disease, such as mitral regurgitation or mitral stenosis; historically rheumatic fever was among the most common causes of valve disease, but this is now rare in developed countries. Up to 70 percent of patients who have rheumatic heart disease develop atrial fibrillation.
After heart surgery and, less often, after other types of surgery; atrial fibrillation in these settings is typically temporary.
A variety of chronic lung diseases, particularly emphysema.
Atrial fibrillation can also be induced by external events. These include:
Alcohol and binge drinking — Binge drinkers can develop atrial fibrillation that is usually transient. This often occurs over weekends or holidays when alcohol intake is excessive. It is called “holiday heart syndrome.”
Hyperthyroidism — Atrial fibrillation occurs in about 13 percent of all patients with an overactive thyroid gland (called hyperthyroidism) and in 20 to 25 percent of older patients with this disorder. It has been estimated that hyperthyroidism accounts for 5 percent of cases of atrial fibrillation. Thus, blood testing for this disorder should be performed in all patients with AF since it is easily treatable. (See “Patient information: Hyperthyroidism”).
Medications — Drugs that stimulate the heart can contribute to the development of atrial fibrillation. These include theophylline (used in the treatment of asthma or chronic lung disease), and caffeine.
Sleep Apnea - Atrial fibrillation can be caused by sleep apnea, a condition where patients stop breathing for prolonged periods of time while sleeping. Patients with atrial fibrillation who are overweight, or have a history snoring or excessive sleepiness during the daytime, should be evaluated with a sleep study. Treatment for sleep apnea can eliminate atrial fibrillation in some patients.
Some patients with atrial fibrillation have no apparent cause. When this occurs in patients under age 60 to 65, it is called lone atrial fibrillation. The cause is not well understood, but the risk of blood clots is much lower in these patients.

DIAGNOSIS
Atrial fibrillation is diagnosed by obtaining an electrocardiogram (ECG or EKG), which records the heart’s electrical activity. Other tests are performed to establish a cause for the atrial fibrillation, including measuring blood pressure to evaluate for hypertension and measuring thyroid stimulating hormone (TSH) in order to rule out an overactive thyroid gland. Other tests, such as an echocardiogram (ultrasound), may be performed to look for other causes of atrial fibrillation such as heart failure or heart valve problems, while lung function tests are sometimes used to look for underlying lung disease.
Patients who have symptoms suggesting atrial fibrillation, but who cannot be diagnosed with AF or other rhythm disorders based upon an office electrocardiogram, may need further monitoring. Continuous monitoring (eg, Holter monitor, show figure 3) or a recording device (eg, event monitor, show figure 4) that can be turned on by the patient when they feel palpitations are often used

SYMPTOMS AND RISKS
Three main factors determine the symptoms and risks of atrial fibrillation: how fast the ventricles are beating; the presence or absence of underlying heart disease; and the formation of blood clots, particularly in the left atrium, that can break off and enter the blood stream, possibly leading to a stroke or blockage of arteries going to other important organs.
Symptoms — Patient awareness of atrial fibrillation is highly variable; some patients have no symptoms while others may have debilitating shortness of breath. Most patients who are well controlled on medical therapy have no or mild symptoms; more severe symptoms occur when the ventricular rate is not well controlled. Mild symptoms include:
Unpleasant palpitations or irregularity of the heart beat
Mild chest discomfort (sensation of tightness) or pain
A sense of the heart racing
Lightheadedness
Mild shortness of breath and fatigue that limit the ability to exercise
As the ventricles beat more rapidly or irregularly, symptoms may be more severe and include:
Difficulty breathing
Shortness of breath with exertion
Fainting, or near fainting, due to a reduction in blood flow to the brain
Confusion, due to a reduction in blood supply to the brain
Chest discomfort
Fatigue

Chest discomfort generally results from inadequate blood flow to meet the needs of the heart (called angina); this can be due to an increase in the heart’s need for oxygen and/or a decrease in the heart’s supply of blood and oxygen. In some cases, chest pain is due to the rapid heart rate itself or perhaps to stretching of the heart’s chambers.
If the heart rate is very rapid, or if the patient has underlying heart disease, more serious symptoms of heart failure can develop:
Shortness of breath at rest or at night
Swelling of the legs
Rapid weight gain due to fluid accumulation
Angina or even a heart attack, primarily in patients with underlying coronary disease
Worsening heart failure or the development of angina may also produce other types of serious and potentially life-threatening arrhythmias.

Risk of stroke
A serious complication associated with atrial fibrillation is stroke, which can lead to permanent brain damage. A stroke can occur if a blood clot forms in the left atrium because of sluggish blood flow and a piece of the clot (also called an embolus) breaks off. The embolus enters the blood circulation and can obstruct a small blood vessel. The most dangerous place for this to occur is the brain, resulting in a stroke, but the embolus may also go to the eye, kidneys, spine, or important arteries of the arms or legs.
Like atrial fibrillation, the risk of stroke increases with age. Without preventive treatment (eg, blood thinners), stroke occurs in approximately 1.3 percent of patients aged 50 to 59 years and increases gradually to 5.1 percent each year for those aged 80 to 89 years. These percentages are average rates; for each patient the risk is also influenced by a number of other factors, including the presence of hypertension and additional heart disease. In some patients with multiple underlying medical conditions, the annual risk of a stroke can be as high as 8 to 10 percent.
The administration of a blood thinner (usually warfarin [Coumadin®]) lowers the risk of stroke by 50 to 65 percent in intermediate to high risk patients. Warfarin therapy is typically referred to as anticoagulation (see “Warfarin therapy” below). In patients at intermediate to high risk for stroke, no other therapy lowers the risk of a stroke as much as warfarin.
Low-risk patients have a stroke rate of less than 1 percent per year (usually patients under 60 to 65 years of age with one or no additional risk factors). Patients with this low-risk profile may be treated with aspirin instead of warfarin.

TREATMENT
There are four main issues that must be addressed in the treatment of atrial fibrillation: the need for hospitalization; conversion to and maintenance of normal sinus rhythm; rhythm versus rate control; and prevention of embolus formation and stroke.
Hospitalization — Most patients who have atrial fibrillation do not need to be admitted to the hospital. Situations in which hospitalization might be indicated include:
Symptoms of chest pain or pressure associated with electrocardiogram (ECG) changes that suggest the person is having a heart attack or angina due to a reduction in blood supply to the heart.
Patients who have other serious complications of atrial fibrillation, including low blood pressure, trouble breathing, heart failure, or stroke.
An underlying medical condition that caused the atrial fibrillation and that needs treatment itself.
When patients are cardioverted from atrial fibrillation to a normal sinus rhythm.
Patients who may be safer in a hospital while medications are started.
Patients who are at a particularly high risk of developing a thrombus in the atrium or who should be observed for potential bleeding problems while anticoagulation is started.
Conversion to normal rhythm — Patients with paroxysmal (intermittent) atrial fibrillation have episodes of varying duration that resolve spontaneously. Careful monitoring has shown that up to 90 percent of recurrent episodes are not recognized by the patient, including some that last more than two days.
Spontaneous conversion to normal sinus rhythm is much less likely in patients with chronic (persistent) atrial fibrillation. In these patients, atrial fibrillation is converted to sinus rhythm using either electrical cardioversion or medications.
Electrical cardioversion — Electrical cardioversion involves the use of an electrical shock from a cardioverter, delivered by paddles placed on the chest, to “reset” the heart rhythm. Urgent cardioversion is recommended if atrial fibrillation is interfering with heart’s ability to supply blood and oxygen to vital organs. Signs of this include a fall in blood pressure, angina (chest pain), shortness of breath, and/or heart failure.
Some patients with newly diagnosed atrial fibrillation can undergo electrical or medical cardioversion (using an antiarrhythmic drug) immediately. However, due to the risk of stroke from left atrial blood clots, doctors frequently recommend waiting to cardiovert until the patient has been treated with a blood thinner. This medication, (usually warfarin [Coumadin®]) is given for three to four weeks, which allows 85 percent of preexisting blood clots in the left atrium to resolve.
Even though normal electrical activity is restored with the cardioversion, the atria may not resume normal muscle contraction for several days or weeks. Thus, there is still a risk of clot formation in the period immediately after cardioversion. For this reason, a blood thinner is recommended for at least four weeks after cardioversion.
Repeat cardioversion is a reasonable treatment for patients with atrial fibrillation that has recurred after a long duration of normal heart rhythm; it is most likely to be successful in younger patients with a short history of atrial fibrillation.
Transesophageal echocardiogram — An alternative to waiting involves a procedure called transesophageal echocardiogram (TEE). TEE uses a small ultrasound device that is swallowed to visualize the left atria, looking for evidence of clots or slowed blood flow. If the atria appear to be without clots or slowed blood flow, cardioversion can be performed safely without warfarin pretreatment. Although there is still a risk that cardioversion may dislodge a clot that was not seen on the TEE, the risk is quite small.

Other treatment options — For patients with intermittent or chronic atrial fibrillation, there are two long-term treatment options: rhythm control and rate control. Two large clinical trials have addressed the effectiveness and safety of these two approaches. Before discussing these trials, it is useful to review the meaning of rhythm control and rate control and both the benefits and risks of long-term warfarin therapy.
Rhythm control — Rhythm control refers to electrical or medical cardioversion followed by an antiarrhythmic drug to lower the risk of recurrence of atrial fibrillation. After successful conversion to normal sinus rhythm, only 20 to 30 percent of patients are in sinus rhythm after one year. This can be increased to between 40 and 80 percent by adding an antiarrhythmic drug.
The advantages to rhythm control are improved cardiac function and, for some patients, reduced symptoms. Selected patients who are effectively maintained in normal rhythm may be allowed to stop chronic anticoagulation. However, rhythm control is more likely to reduce the frequency of AF than eliminate it entirely. Thus most patients treated with antiarrhythmic medications should continue anticoagulation therapy indefinitely.
The disadvantages of rhythm control are the high rate of recurrent atrial fibrillation and side effects associated with antiarrhythmic drugs, including the development of new abnormal heart rhythms.

Rate control — In patients who are treated with rate control, atrial fibrillation is allowed to continue; the patient uses a medication (a beta blocker, a calcium channel blocker, or digoxin) to slow conduction through the AV node, thereby slowing the ventricular rate into the normal range. All patients require chronic therapy with a blood thinner since there is a continued risk of blood clot formation and possible stroke.
There are two major disadvantages with the rate control strategy: it is sometimes difficult to adequately control the rate and relieve symptoms; and chronic anticoagulation, which carries a risk of bleeding, is mandatory, .
Nonpharmacologic treatments — There are alternatives to medicines to achieve rhythm or rate control. Nonpharmacologic treatments include radiofrequency catheter ablation, use of a pacemaker or implantable atrial defibrillator, and several surgical treatments. Radiofrequency ablation can result in a cure when performed by an experienced physician in carefully selected patients. (See “Patient information: Radiofrequency catheter ablation” and see “Patient information: Pacemakers” and see “Patient information: Implantable cardioverter-defibrillators”).

Surgical procedures, including the maze procedure and the corridor operation, may be considered in some patients with atrial fibrillation, especially those who must undergo open-heart surgery for other reasons.
Warfarin therapy — Chronic warfarin therapy reduces the rate of stroke by approximately 50 to 70 percent in patients with atrial fibrillation who are at intermediate to high risk. The potential benefit is actually greater since as many as one-half of strokes in treated patients are due to a less than optimal degree of blood thinning. (See “Patient information: Warfarin (Coumadin®)”). My opinion.. only use BRAND COUMADIN

The major problem with warfarin therapy is that anticoagulation can lead to bleeding. In a large review of studies of patients with atrial fibrillation, the incidence of major bleeding events with warfarin was increased by 0.9 percent per year compared to aspirin (2.2 versus 1.3 percent per year). The major concern is bleeding into the brain.
The major risk factors for bleeding into the brain are:
Age greater than 70 years
Uncontrolled high blood pressure
History of prior stroke
Excessive anticoagulation.
However, the risk of bleeding into the brain is substantially smaller than the benefit of preventing strokes in patients who use warfarin.

Patients taking warfarin must be carefully and continuously monitored with periodic blood tests to make certain that the degree of blood thinning is sufficient to protect against stroke but not too great to promote bleeding.
Clinical trials — In the past, most physicians preferred rhythm control because of the presumed advantages of better heart function and a much lower risk of stroke in patients in normal sinus rhythm. However, two major trials directly compared rhythm control and rate control. There were two major conclusions:
The outcomes were generally similar, but both studies showed a trend toward a better outcome with rate control compared to rhythm control (show figure 4 and show figure 5).
Contrary to expectations, rhythm control was associated with a trend toward a higher risk of stroke compared to rate control. However, the majority of strokes occurred in patients receiving no or suboptimal warfarin therapy. This finding suggests that patients treated with rhythm control should usually continue anticoagulation. In other words, choosing rhythm control should be based upon the desire to improve symptoms, not an effort to avoid chronic anticoagulation.
Patients should talk to their healthcare provider about which approach is best. A 2003 guideline from two major medical societies recommends rate control with chronic anticoagulation for the majority of patients. The type of blood thinner therapy (warfarin or aspirin) recommended depends upon a patient’s risk of stroke, which can be determined with a healthcare provider.

Newer therapies — There are limitations to current medical therapy of atrial fibrillation: normal sinus rhythm cannot be maintained in most patients with antiarrhythmic drugs, which also have side effects; rate control that control symptoms cannot be attained in all patients; and all patients except those at low risk require chronic warfarin therapy, which has a risk of bleeding.
Surgery and radiofrequency catheter ablation have been used for rate control and cure of atrial fibrillation. Patients with symptomatic atrial fibrillation that cannot be adequately controlled with medicines may be candidates for catheter ablation to cure the atrial fibrillation.