Atrial fibrillation

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}} Atrial fibrillation (AF or afib) is an abnormal heart rhythm (cardiac arrhythmia) which involves the two small, upper heart chambers (the atria). Heart beats in a normal heart begin after electricity generated in the atria by the sinoatrial node spread through the heart and cause contraction of the heart muscle and pumping of blood. In AF, the regular electrical impulses of the sinoatrial node are replaced by disorganized, rapid electrical impulses which result in irregular heart beats.

Atrial fibrillation is one of the most common cardiac arrhythmias. The risk of developing atrial fibrillation increases with age — AF affects four percent of individuals in their 80s. An individual may spontaneously alternate between AF and a normal rhythm (paroxysmal atrial fibrillation) or may continue with AF as the dominant cardiac rhythm without reversion to the normal rhythm (chronic atrial fibrillation). Atrial fibrillation is often asymptomatic, but may result in symptoms of palpitations, fainting, chest pain, or even heart failure. These symptoms are especially common when atrial fibrillation results in a heart rate which is either too fast or too slow. In addition, the erratic motion of the atria leads to blood stasis which predisposes to blood clots which may travel from the heart to the brain and other areas. Thus, AF is an important risk factor for stroke, the most feared complication of atrial fibrillation.

The symptoms of atrial fibrillation may be treated with medications which slow the heart rate. Several medications as well as electrical cardioversion may be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent atrial fibrillation in certain individuals. People with AF are often given blood thinners such as warfarin to protect them from strokes.

Contents 1 Classification 1.1 First Detected 1.2 Recurrent 1.2.1 Paroxysmal 1.2.2 Persistent 1.3 Lone atrial fibrillation 2 Signs and symptoms 3 Diagnosis 3.1 Electrocardiogram 3.2 Other investigations 4 Causes 5 Pathophysiology 6 Treatment 6.1 Rate control 6.1.1 AV nodal ablation 6.2 Rhythm control 6.2.1 Radiofrequency ablation 6.2.2 Cox maze Procedure 6.2.3 Minimaze surgical procedures 6.3 Anticoagulation 7 Prognosis 8 Epidemiology 9 History 10 References 11 See also 12 External links

Classification

The American Heart Association, American College of Cardiology, and the European Society of Cardiology have proposed the following classification system based on simplicity and clinical relevance.Template:Ref

First Detected

Any patient newly diagnosed with atrial fibrillation fits in this category, as the exact onset and chronicity of the disease is often uncertain.

Recurrent

Any patient with 2 or more identified episodes of atrial fibrillation is said to have recurrent atrial fibrillation. This is further classified into paroxysmal and persistent based on when the episode terminates without therapy.

Paroxysmal

Atrial fibrillation is said to be paroxysmal when it terminates spontaneously within 7 days, most commonly within 24 hours.

Persistent

Persistent or chronic atrial fibrillation is AF established for more than seven days. Differentiation of paroxysmal from chronic or established AF is based on the history of recurrent episodes and the duration of the current episode of AF.Template:RefTemplate:Ref

Lone atrial fibrillation

Lone atrial fibrillation (LAF) is defined as atrial fibrillation in the absence of clinical or echocardiographic findings of cardiopulmonary disease. [1] Patients with LAF who are under 65 have the best prognosis.

Signs and symptoms

Atrial fibrillation is usually accompanied by symptoms related to either the rapid heart rate or embolization. Rapid and irregular heart rates may be perceived as palpitations, exercise intolerance, and occasionally produce angina and congestive symptoms of shortness of breath or edema. Sometimes the arrhythmia will be identified with the onset of a stroke or a TIA. It is not uncommon to identify atrial fibrillation on a routine physical examination or electrocardiogram, as it may be asymptomatic in some cases.

Paroxysmal atrial fibrillation is the episodic occurrence of the arrhythmia and may be difficult to diagnose. Episodes may occur with sleep or with exercise, and their episodic nature may require prolonged ECG monitoring (e.g. a Holter monitor) for diagnosis.

Diagnosis

Electrocardiogram

Atrial fibrillation is diagnosed on an electrocardiogram, an investigation performed routinely whenever irregular heart beat is suspected. Characteristic findings are (a "rhythm strip" of lead II is shown):

• absence of P waves
• unorganized electrical activity in their place
• irregularity of R-R interval due to irregular conduction of impulses to the ventricles

If paroxysmal AF is suspected, episodes may be documented with the use of Holter monitoring (continuous ECG recording for 24 hours or longer).

Other investigations

While many cases of AF have no definite cause, it may be the result of various other problems (see below). Hence, renal function and electrolytes are routinely determined, as well as thyroid-stimulating hormone (commonly suppressed in hyperthyroidism and of relevance if amiodarone is administered for treatment) and a blood count. A chest X-ray is generally performed. In acute-onset AF associated with chest pain, cardiac troponins or other markers of damage to the heart muscle may be ordered. Coagulation studies (INR/aPTT) are usually performed, as anticoagulant medication may be commenced. An transesophageal echocardiogram may be indicated to identify any intracardiac thrombus. [2]

Causes

AF is linked to several cardiac causes, but may occur in otherwise normal hearts. Known associations include:

• High blood pressure
• Mitral stenosis (e.g. due to rheumatic heart disease or mitral valve prolapse)
• Mitral regurgitation
• Heart surgery
• Coronary artery disease
• Hypertrophic cardiomyopathy
• Excessive alcohol consumption ("binge drinking" or "holiday heart")
• Hyperthyroidism
• Hyperstimulation of the vagus nerve, usually by having large meals ("binge eating")
• Lung pathology (such as pneumonia, lung cancer, pulmonary embolism, Sarcoidosis)
• Pericarditis
• Intense emotional turmoil
• Congenital heart disease

Pathophysiology

The normal electrical conduction system of the heart allows the impulse that is generated by the sinoatrial node (SA node) of the heart to be propagated to and stimulate the myocardium (muscle of the heart). When the myocardium is stimulated, it contracts. It is the ordered stimulation of the myocardium that allows efficient contraction of the heart, thereby allowing blood to be pumped to the body.

In atrial fibrillation, the regular impulses produced by the sinus node to provide rhythmic contraction of the heart are overwhelmed by the rapid randomly generated discharges produced by larger areas of atrial tissue. It can be distinguished from atrial flutter, which is a more organized electrical circuit usually in the right atrium that produces characteristic saw toothed waves on the electrocardiogram.

Often, the rhythm produced is more rapid than normal, but the difficulty is in obtaining control of the heart rate both at rest and with exercise. Good rate control will usually require two drugs, and can only be checked by observing heart rate response to exercise.

An organized electrical impulse in the atrium produces atrial contraction; the lack of such an impulse, as in atrial fibrillation, produces stagnant blood flow, especially in the atrial appendage and predisposes to clotting. The dislodgement of a clot from the atrium results in an embolus, and the damage produced is related to where the circulation takes it. An embolus to the brain produces the most feared complication of atrial fibrillation, stroke, while an embolus may also lodge in the mesenteric circulation (the circulation supplying the abdominal organs) or digit, producing organ-specific damage.

Treatment

The main goals of treatment of atrial fibrillation are to prevent temporary circulatory instability and to prevent stroke. Rate and rhythm control are principally used to achieve the former, while anticoagulation may be required to decrease the risk of the latter.Template:Ref

AF can cause disabling and annoying symptoms. Palpitations, angina, lassitude (weariness), and decreased exercise tolerance are related to rapid heart rate and inefficient cardiac output caused by AF. There are two ways to approach these symptoms: rate control and rhythm control. Rate control treatments seek to reduce the heart rate to normal, usually 60 to 100 beats per minute. Rhythm control seeks to restore the normal heart rhythm, called normal sinus rhythm. Studies suggest that rhythm control is mainly a concern in newly diagnosed AF, while rate control is more important in the chronic phase. Rate control with anticoagulation is as effective a treatment as rhythm control in long term mortality studies, the AFFIRM Trial (Wyse et al., 2002).

AF with a persistent rapid rate can cause a form of heart failure called chronotropic cardiomyopathy. This can significantly increase mortality and morbidity. The early treatment of AF through either rate-control or rhythm-control can prevent this condition and thereby improve mortality and morbidity.

Rate control

Rate control methods include:

• Beta blockers (e.g. metoprolol)
• Cardiac glycosides (e.g. digoxin)
• Calcium channel blockers (e.g. verapamil)

These medications work by slowing the generation of impulses from the atria and the conduction of those impulse from the atria to the ventricles.

In refractory cases where none of the above drugs are sufficient, a variety of other antiarrhythmic drugs, most commonly including quinidine, flecainide, propafenone, disopyramide, sotalol, or amiodarone may be used. Of these, only propafenone, sotalol, and amiodarone (which possess some beta blocking activity) control the ventricular rate; the others may maintain sinus rhythm, but may actually increase the ventricular rate. Many of these drugs are less frequently used today than in the past. All (with the possible exception of amiodarone) increase the risk of ventricular tachycardia, which can be fatal. In symptomatic patients with normal heart function, however, the small increase in risk is usually felt to be acceptable. In the presence of heart failure, the only antiarrhythmic drugs thought to be safe are amiodarone and dofetilide. It should be noted that many of these agents are not approved by the FDA for this use.

In emergencies, when circulatory collapse is imminent due to uncontrolled tachycardia, immediate cardioversion may be indicated. [3]

AV nodal ablation

In patients with AF where rate control drugs are ineffective and it is not possible to restore sinus rhythm using cardioversion, non-pharmacological alternatives are available. For example, to control rate it is possible to destroy the bundle of cells connecting the upper and lower chambers of the heart - the atrioventricular node - which regulates heart rate, and to implant a pacemaker instead. A more complex technique involves ablating groups of cells near the pulmonary arteries where atrial fibrillation is thought to originate, or creating more extensive lesions in an attempt to prevent atrial fibrillation from establishing itself.[4]

Rhythm control

Rhythm control methods include electrical and chemical cardioversion:

• Electrical cardioversion involves the restoration of normal heart rhythm either through the application of a DC electrical shock (electrical cardioversion)
• Chemical cardioversion is performed with drugs, such as amiodarone, propafenone or flecainide.

The anti-arrhythmic medications often used in either pharmacological cardioversion or in the prevention of relapse to AF alter the flux of ions in heart tissue, making them less excitable, setting the stage for spontaneous and durable cardioversion. These medications are often used in concert with electrical cardioversion. However, the AFFIRM study showed no difference in risk of stroke in patients who have converted to a normal rhythm with anti-arrhythmic treatment, compared to those who have only rate control.Template:Ref

The main risk of cardioversion is systemic embolization by a bloodclot from the previously fibrillating left atrium. It should not be performed without adequate anticoagulation in patients who have been in atrial fibrillation for more than 48 hours.

Whichever method of cardioversion is used, approximately 50% of patient relapse within one year, although the continued daily use of oral antiarrhythmic drugs may extend this period. The key risk factor for relapse is duration of AF, although other risk factors that have been identified include the presence of structural heart disease, and increasing age.

Radiofrequency ablation

Radiofrequency ablation (RFA) uses radiofrequency energy to destroy abnormal electrical pathways in heart tissue. It is used in recurrent AF. The energy emitting probe (electrode) is placed into the heart through a catheter. The practitioner first "maps" an area of the heart to locate the abnormal electrical activity before the responsible tissue is eliminated. Ablation is a newer technique and has shown some promise for cases unresponsive to conventional treatments. New techniques include the use of cryoablation (tissue freezing using a coolant which flows through the catheter), and microwave ablation, where tissue is ablated by the microwave energy "cooking" the adjacent tissue. The abnormal electrophysiology can also be modified in a similar way surgically, and this procedure referred to as the Cox maze procedure, is commonly performed concomitantly with cardiac surgery. More recently, minimally invasive surgical variations on the Cox Maze procedure ("minimaze" procedures) have also been developed.

This is an area of active research, especially with respect to the RF ablation technique and emphasis on isolating the pulmonary veins that enter into the left atrium.

Cox maze Procedure

James Cox, MD, and associates developed the Cox maze procedure, an open-heart surgical procedure intended to eliminate atrial fibrillation, and performed the first one in 1987. "Maze" refers to the series of incisions made in the atria (upper chambers of the heart), which are arranged in a maze-like pattern. The intention was to eliminate AF by using incisional scars to block abnormal electrical circuits (atrial macroreentry) that AF requires. This procedure required an extensive series of endocardial (from the inside of the heart) incisions through both atria, a median sternotomy (vertical incision through the breastbone) and cardiopulmonary bypass (heart-lung machine). A series of improvements were made, culminating in 1992 in the Cox maze III procedure, which is now considered to be the "gold standard” for effective surgical cure of AF. The Cox maze III is sometimes referred to as the “traditional maze”, the “cut and sew maze”, or simply the "maze".

Minimaze surgical procedures

Minimaze surgery is minimally invasive cardiac surgery intended to cure atrial fibrillation. Minimaze refers to "mini" versions of the original maze procedure. These procedures are less invasive than the Cox maze procedure and do not require a median sternotomy (vertical incision in the breastbone) or cardiopulmonary bypass (heart-lung machine). These procedures use microwave, radiofrequency, or acoustic energy to ablate atrial tissue near the pulmonary veins.

Anticoagulation

In confirmed AF, anticoagulant treatment is a crucial way to prevent stroke. Treatment of AF patients over age 60 with warfarin (also known as Coumadin® or Marevan®) results in a significant reduction in the subsequent risk of stroke. Patients under age 65 who have any structural heart disease (i.e. valvular heart disease, ejection fraction <= 35%, history of heart attack) also benefit from warfarin.

The use of warfarin is associated with a delayed clinical effect. It typically takes three to five days to achieve a demonstrable anticoagulant effect, and in this time, physicians commonly use heparin or other heparinoids such as enoxaparin to provide early anticoagulation.

Patients under age 65 who do not have structural heart disease (i.e. with LAF) do not require warfarin, and can be treated with aspirin Template:Ref or clopidogrel. Other guidelines are also used. The new anticoagulant ximelagatran has been shown to prevent stroke with equal efficacy as warfarin, without the difficult monitoring process associated with warfarin and with possibly fewer adverse haemorrhagic events. Unfortunately, ximegalatran and other similar anticoagulant drugs (commonly referred to as direct thrombin inhibitors), have yet to be widely licensed. License applications for ximelegatran (made by AstraZeneca) have been rejected by both American and European licensing authorities, and its evaluation has been suspended in the UK. This is primarily due to concerns over possible liver toxicity.

Prognosis

Atrial fibrillation can usually be controlled with treatment. The natural tendency of atrial fibrillation, however, is to become a chronic condition. Chronic AF leads to an increased risk of death.Template:Ref Patients with atrial fibrillation are at significantly increased chance of stroke (about 2 to 7 times the regular population) [5]

Epidemiology

Atrial fibrillation is common among older adults. In developed countries, the number of patients with atrial fibrillation is likely to increase during the next 50 years, due to the growing proportion of elderly individuals.Template:Ref

History

Because the diagnosis of atrial fibrillation requires measurement of the electrical activity of the heart, atrial fibrillation was not truly described until 1874, when Edmé Félix Alfred Vulpian observed the irregular atrial electrical behavior that he termed "fremissement fibrillaire" in dog hearts.Template:Ref However, the irregular pulse and its association with disease have been recognized since antiquity. Direct visualization of cardiac fibrillation was first described in 1628 by William Harvey in dying animals. In the mid-eighteenth century, Jean Baptiste de Sénac made note of dilated, irritated atria in people with mitral stenosis.Template:Ref The irregular pulse associated with AF was first recorded in 1876 by Carl Wilhelm Hermann Nothnagel and termed "delirium cordis" stating, "In this form of arrhythmia the heartbeats follow each other in complete irregularity. At the same time, the height and tension of the individual pulse waves are continuously changing."Template:Ref Correlation of delirium cordis with the loss of atrial contraction as reflected in the loss of a waves in the jugular venous pulse was made by Sir James MacKenzie in 1904.Template:Ref Willem Einthoven published the first electrocardiogram showing AF in 1906.Template:Ref The connection between the anatomic and electrical manifestations of AF and the irregular pulse of delirium cordis was made in 1909 by Carl Julius Rothberger, Heinrich Winterberg, and Sir Thomas Lewis.Template:RefTemplate:RefTemplate:Ref

References

1. Template:Note AHA Consensus for classification
2. Template:Note Template:Cite journal PMID 9727680
3. Template:Note Template:Cite journal PMID 10666661
4. Template:Note Template:Cite journal PMID 10822035
5. Template:Note Template:Cite journal PMID 12466506
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9. Template:Note Vulpian A. Note sur les effets de la faradisation directe des ventricules du coeur chez le chien. Archives de Physiologie Normale et Pathologique. 1874; 6:975
10. Template:Note Nothnagel H. Ueber arythmische Herzthatigkeit. Deutsches Archiv fur Klinische Medizin. 1876; 17:190-220
11. Template:Note MacKenzie J. The inception of the rhythm of the heart by the ventricle. Br Med J. 1904; 1:529-36
12. Template:Note McMichael J. History of atrial fibrillation 1628-1819 Harvey-de Senac-Laennec. Br Heart J. 1982; 48:193-7 PMID 7049202
13. Template:Note Einthoven W. Le telecardiogramme. Archives Internationales de Physiologie. 1906; 4:132-64
14. Template:Note Rothberger CJ, Winterberg H. Vorhofflimmern und Arhythmia perpetua. Wiener Klinische Wochenschrift. 1909; 22:839-44
15. Template:Note Lewis T. Auricular fibrillation: a common clinical condition. Br Med J. 1909; 2:1528
16. Template:Note Flegel KM.From delirium cordis to atrial fibrillation: historical development of a disease concept. Ann Intern Med. 1995 Jun 1;122(11):867-73. PMID 7741373

• Template:Cite journal PMID 9792255
• Template:Cite journal PMID 15596953

See also

• Atrial flutter
• Ashman phenomenon

External links

• Atrial Fibrillation Resources for Patients
• Hybrid therapy of Atrial Fibrillation
• Atrial Fibrillation Center at the University of Virginia
• Minimally Invasive Treatment for Atrial Fibrillation at Robert Wood Johnson University Hospital
• Cardiovillagede:Vorhofflimmern

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