|Classification and external resources|
Schematic diagram of normal sinus rhythm for a human heart as seen on ECG. In atrial fibrillation, however, the P waves, which represent depolarization of the atria, are absent.
Atrial fibrillation (AF or A-fib) is the most common abnormal heart rhythm. It may cause no symptoms, but is often associated with palpitations, fainting, chest pain, or congestive heart failure. The cause of an individual's AF may not be identified.
In AF, the normal regular electrical impulses generated by the sinoatrial node in the right atrium of the heart are overwhelmed by disorganized electrical impulses usually originating in the roots of the pulmonary veins. This leads to irregular conduction of ventricular impulses that generate the heartbeat. AF may occur in episodes lasting from minutes to days (paroxysmal AF) or may be permanent in nature. Many medical conditions increase the risk of AF, in particular mitral stenosis (narrowing of the mitral valve of the heart).
The risk of stroke is increased fivefold in individuals with AF. The degree of increased risk may be substantial, depending on the presence of additional risk factors (such as high blood pressure). AF is often treated with medications to slow the heart rate to a normal range (known as rate control) or to correct the heart rhythm to normal sinus rhythm (known as rhythm control). Synchronized electrical cardioversion can also be used to convert AF to a normal heart rhythm. Surgical and catheter-based ablation may be used to prevent recurrence of AF in some individuals.
Depending on the risk of stroke and blood clot formation, people with AF may use anti-clotting medications such as warfarin, which substantially reduces these risks but may increase the risk of major bleeding, mainly in older patients. The prevalence of AF in a population increases with age; 8% of people over the age of 80 have AF. Chronic AF leads to a small increase in the risk of death.
- 1 Signs and symptoms
- 2 Causes
- 3 Pathophysiology
- 4 Diagnosis
- 5 Management
- 6 Prognosis
- 7 Epidemiology
- 8 History
- 9 References
- 10 External links
Signs and symptoms
AF is usually accompanied by symptoms related to a rapid heart rate. Rapid and irregular heart rates may be perceived as palpitations or exercise intolerance and occasionally may produce anginal chest pain (if the high heart rate causes ischemia). Other possible symptoms include congestive symptoms such as shortness of breath or swelling. The arrhythmia is sometimes only identified with the onset of a stroke or a transient ischemic attack (TIA). It is not uncommon for a patient to first become aware of AF from a routine physical examination or ECG, as it is often does not cause symptoms.
Since most cases of AF are secondary to other medical problems, the presence of chest pain or angina, signs and symptoms of hyperthyroidism (an overactive thyroid gland) such as weight loss and diarrhea, and symptoms suggestive of lung disease can indicate an underlying cause. A history of stroke or TIA, as well as high blood pressure), diabetes, heart failure, or rheumatic fever may indicate whether someone with AF is at a higher risk of complications. The risk of a blood clot forming in the left atrium, breaking off, and then traveling in the bloodstream can be assessed using the CHADS2 score.
Rapid heart rate
Presentation is similar to other forms of rapid heart rate and may be asymptomatic. Palpitations and chest discomfort are common complaints. The rapid uncoordinated heart rate may result in the heart being unable to provide adequate blood flow and oxygen delivery to the rest of the body. Therefore, common symptoms may include shortness of breath, shortness of breath when lying flat, and sudden onset of shortness of breath during the night. This may progress to swelling of the lower extremities. Due to inadequate blood flow, individuals with AF may also complain of light-headedness, may feel like they are about to faint, or may actually lose consciousness.
AF can cause significant respiratory distress. Inadequate oxygen delivery may cause a blue appearance. By definition, the heart rate will be greater than 100 beats per minute. Blood pressure will be variable, and often difficult to measure as the beat-by-beat variability causes problems for most digital (oscillometric) non-invasive blood pressure monitors. Low blood pressure is most concerning. Respiratory rate will be increased in the presence of respiratory distress. Pulse oximetry may confirm the presence of hypoxia related to any precipitating factors such as pneumonia. Examination of the jugular veins may reveal elevated pressure (jugular venous distention). Lung exam may reveal crackles, which are suggestive of pulmonary edema. Heart exam will reveal a rapid irregular rhythm.
- Central sleep apnea (CSA)- Possible explanations for the association between CSA and AF are a causal relationship between the two conditions, or an abnormality of central cardiorespiratory regulation.
- Left atrial enlargement
- Mitral stenosis
AF is linked to several cardiac causes, but may occur in otherwise-normal hearts. Known associations include the following:
- Hypertension (High blood pressure)
- Primary heart diseases including coronary artery disease, mitral stenosis (e.g., due to rheumatic heart disease or mitral valve prolapse), mitral regurgitation, hypertrophic cardiomyopathy (HCM), pericarditis, congenital heart disease, previous heart surgery
- Lung diseases (such as pneumonia, lung cancer, pulmonary embolism, sarcoidosis)
- Excessive alcohol consumption ("binge drinking" or "holiday heart syndrome"). Even otherwise-healthy middle-age women having consumed more than 2 drinks daily were 60% more likely to develop AF.
- Dual-chamber pacemakers in the presence of normal atrioventricular conduction.
- A family history of AF may increase the risk of AF. A study of more than 2,200 AF patients found that 30 percent had parents with AF. Various genetic mutations may be responsible.
Four types of genetic disorder are associated with atrial fibrillation:
- familial AF as a monogenic disease
- familial AF presenting in the setting of another inherited cardiac disease (hypertrophic cardiomyopathy, dilated cardiomyopathy, familial amyloidosis)
- inherited arrhythmic syndromes (congenital long QT syndrome, short QT syndrome, Brugada syndrome)
- non-familial AF associated with genetic backgrounds (polymorphism in the ACE gene) that may predispose to atrial fibrillation
The primary pathologic change seen in atrial fibrillation is the progressive fibrosis of the atria. This fibrosis is due primarily to atrial dilation, however genetic causes and inflammation may have a cause in some individuals. One study found that atrial dilation can occur as a consequence of AF, although another study found that AF by itself does not cause it.
Dilation of the atria can be due to almost any structural abnormality of the heart that can cause a rise in the pressure within the heart. This includes valvular heart disease (such as mitral stenosis, mitral regurgitation, and tricuspid regurgitation), hypertension, and congestive heart failure. Any inflammatory state that affects the heart can cause fibrosis of the atria. This is typically due to sarcoidosis but may also be due to autoimmune disorders that create autoantibodies against myosin heavy chains. Mutation of the lamin AC gene is also associated with fibrosis of the atria that can lead to atrial fibrillation.
Once dilation of the atria has occurred, this begins a chain of events that leads to the activation of the renin aldosterone angiotensin system (RAAS) and subsequent increase in matrix metalloproteinases and disintegrin, which leads to atrial remodeling and fibrosis, with loss of atrial muscle mass. This process is not immediate, and experimental studies have revealed patchy atrial fibrosis may precede the occurrence of atrial fibrillation and may progress with prolonged durations of atrial fibrillation.
Fibrosis is not limited to the muscle mass of the atria, and may occur in the sinus node (SA node) and atrioventricular node (AV node), correlating with sick sinus syndrome. Prolonged episodes of atrial fibrillation have been shown to correlate with prolongation of the sinus node recovery time, suggesting that dysfunction of the SA node is progressive with prolonged episodes of atrial fibrillation.
|Sinus rhythm||Atrial fibrillation|
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 (muscular layer 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.
There are multiple theories about the etiology of atrial fibrillation. An important theory is that, in atrial fibrillation, the regular impulses produced by the sinus node for a normal heartbeat are overwhelmed by rapid electrical discharges produced in the atria and adjacent parts of the pulmonary veins. Sources of these disturbances are either automatic foci, often localized at one of the pulmonary veins, or a small number of localized sources in the form of either reentrant electrical spiral waves (rotors) or repetitive focal beats; these localized sources may be found in the left atrium near the pulmonary veins or in a variety of other locations through both the left or right atrium.
Because recovery of the atria from excitation is heterogeneous, the electrical waves generated by the AF sources undergo repetitive, spatially distributed breakup and fragmentation in a process known as "fibrillatory conduction".Another theory is the multiple wavelet theory first formulated by Moe, which was experimentally proven by Allessie et al.
AF can be distinguished from atrial flutter (AFL), which appears as an organized electrical circuit usually in the right atrium. AFL produces characteristic saw-toothed F-waves of constant amplitude and frequency on an ECG whereas AF does not. In AFL, the discharges circulate rapidly at a rate of 300 beats per minute (bpm) around the atrium. In AF, there is no regularity of this kind, except at the sources where the local activation rate can exceed 500 bpm.
Although the electrical impulses of AF occur at a high rate, most of them do not result in a heart beat. A heart beat results when an electrical impulse from the atria passes through the atrioventricular (AV) node to the ventricles and causes them to contract. During AF, if all of the impulses from the atria passed through the AV node, there would be severe ventricular tachycardia, resulting in severe reduction of cardiac output. This dangerous situation is prevented by the AV node since its limited conduction velocity reduces the rate at which impulses reach the ventricles during AF.
The evaluation of atrial fibrillation involves determination of the cause of the arrhythmia, and classification of the arrhythmia. Diagnostic investigation of AF typically includes a complete history and physical examination, ECG, transthoracic echocardiogram, complete blood count, and serum thyroid stimulating hormone level. Depending upon given resources, afflicted individuals may benefit from an in-depth evaluation that may include correlation of the heart rate response to exercise, exercise stress testing, chest X-ray, transesophageal echocardiography, and other studies.
If a patient presents with a sudden onset of severe symptoms, other forms of abnormal heart rhythm with high heart rate must be ruled-out, as some may be immediately life-threatening, such as ventricular tachycardia. While most patients will be placed on continuous cardiorespiratory monitoring, an ECG is essential for diagnosis. Provoking causes should be sought out. A common cause of any tachycardia is dehydration, as well as other forms of hypovolemia. Acute coronary syndrome should be ruled out. Intercurrent illness such as pneumonia may be present.
In general, screening for atrial fibrillation is not performed. Screening in those 65 years and older has been studied and been found to increase the number of cases of atrial fibrillation detected.
In general, the minimal evaluation of atrial fibrillation should be performed in all individuals with AF. The goal of this evaluation is to determine the general treatment regimen for the individual. If results of the general evaluation warrant it, further studies may then be performed.
History and physical examination
The history of the individual's atrial fibrillation episodes is probably the most important part of the evaluation. Distinctions should be made between those who are entirely asymptomatic when they are in AF (in which case the AF is found as an incidental finding on an ECG or physical examination) and those who have gross and obvious symptoms due to AF and can pinpoint whenever they go into AF or revert to sinus rhythm.
While many cases of AF have no definite cause, it may be the result of various other problems. Hence, kidney 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.
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.
Atrial fibrillation is diagnosed on an electrocardiogram (ECG), an investigation performed routinely whenever an irregular heart beat is suspected. Characteristic findings are the absence of P waves, with disorganized electrical activity in their place, and irregular R-R intervals due to irregular conduction of impulses to the ventricles. At very fast heart rates atrial fibrillation may look more regular, which may make it more difficult to separate from SVT or ventricular tachycardia.
QRS complexes should be narrow, signifying that they are initiated by normal conduction of atrial electrical activity through the intraventricular conduction system. Wide QRS complexes are worrisome for ventricular tachycardia, although in cases where there is disease of the conduction system, wide complexes may be present in A-Fib with rapid ventricular response.
If paroxysmal AF is suspected but an ECG during an office visit shows only a regular rhythm, AF episodes may be detected and documented with the use of ambulatory Holter monitoring (e.g., for a day). If the episodes are too infrequent to be detected by Holter monitoring with reasonable probability, then the patient can be monitored for longer periods (e.g., a month) with an ambulatory event monitor.
In general, a non-invasive transthoracic echocardiogram (TTE) is performed in newly diagnosed AF, as well as if there is a major change in the patient's clinical state. This ultrasound-based scan of the heart may help identify valvular heart disease (which may greatly increase the risk of stroke), left and right atrial size (which indicates likelihood that AF may become permanent), left ventricular size and function, peak right ventricular pressure (pulmonary hypertension), presence of left atrial thrombus (low sensivity), presence of left ventricular hypertrophy and pericardial disease.
Significant enlargement of both the left and right atria is associated with long-standing atrial fibrillation and, if noted at the initial presentation of atrial fibrillation, suggests that the atrial fibrillation is likely to be of a longer duration than the individual's symptoms.
In general, an extended evaluation is not necessary in most individuals with atrial fibrillation, and is performed only if abnormalities are noted in the limited evaluation, if a reversible cause of the atrial fibrillation is suggested, or if further evaluation may change the treatment course.
In general, a chest X-ray is performed only if a pulmonary cause of atrial fibrillation is suggested, or if other cardiac conditions are suspected (in particular congestive heart failure.) This may reveal an underlying problem in the lungs or the blood vessels in the chest. In particular, if an underlying pneumonia is suggested, then treatment of the pneumonia may cause the atrial fibrillation to terminate on its own.
A normal echocardiography (transthoracic or TTE) has a low sensitivity for identifying blood clots in the heart. If this is suspected (e.g., when planning urgent electrical cardioversion) a transesophageal echocardiogram (TEE or TOE where British spelling is used) is preferred.
The TEE has much better visualization of the left atrial appendage than transthoracic echocardiography. This structure, located in the left atrium, is the place where a blood clot forms in more than 90% of cases in non-valvular (or non-rheumatic) atrial fibrillation or flutter. TEE has a high sensitivity for locating thrombi in this area and can also detect sluggish bloodflow in this area that is suggestive of blood clot formation.
If no blood clot is seen on TEE, the incidence of stroke, (immediately after cardioversion is performed), is very low.
Ambulatory Holter monitoring
A Holter monitor is a wearable ambulatory heart monitor that continuously monitors the heart rate and heart rhythm for a short duration, typically 24 hours. In individuals with symptoms of significant shortness of breath with exertion or palpitations on a regular basis, a holter monitor may be of benefit to determine whether rapid heart rates (or unusually slow heart rates) during atrial fibrillation are the cause of the symptoms.
Exercise stress testing
Some individuals with atrial fibrillation do well with normal activity but develop shortness of breath with exertion. It may be unclear whether the shortness of breath is due to a blunted heart rate response to exertion caused by excessive atrioventricular node-blocking agents, a very rapid heart rate during exertion, or other underlying conditions such as chronic lung disease or coronary ischemia. An exercise stress test will evaluate the individual's heart rate response to exertion and determine if the AV node blocking agents are contributing to the symptoms.
|AF Category||Defining Characteristics|
|First detected||only one diagnosed episode|
|Paroxysmal||recurrent episodes that stop on their own in less than 7 days|
|Persistent||recurrent episodes that last more than 7 days|
|Permanent||an ongoing long-term episode|
The American College of Cardiology (ACC), American Heart Association (AHA), and the European Society of Cardiology (ESC) recommend in their guidelines the following classification system based on simplicity and clinical relevance.
All patients with AF are initially in the category called first detected AF. These patients may or may not have had previous undetected episodes. If a first detected episode stops on its own in less than 7 days and then another episode begins later on, the category changes to paroxysmal AF. Although patients in this category have episodes lasting up to 7 days, in most cases of paroxysmal AF the episodes will stop in less than 24 hours. If the episode lasts for more than 7 days, it is unlikely to stop on its own, and is then known as persistent AF. In this case, cardioversion can be used to stop the episode. If cardioversion is unsuccessful or not attempted and the episode continues for a long time (e.g., a year or more), the patient's AF is then known as permanent.
Episodes that last less than 30 seconds are not considered in this classification system. Also, this system does not apply to cases where the AF is a secondary condition that occurs in the setting of a primary condition that may be the cause of the AF.
Using this classification system, it is not always clear what an AF case should be called. For example, a case may fit into the paroxysmal AF category some of the time, while other times it may have the characteristics of persistent AF. One may be able to decide which category is more appropriate by determining which one occurs most often in the case under consideration.
In addition to the above four AF categories, which are mainly defined by episode timing and termination, the ACC/AHA/ESC guidelines describe additional AF categories in terms of other characteristics of the patient.
- Lone atrial fibrillation (LAF) – absence of clinical or echocardiographic findings of other cardiovascular disease (including hypertension), related pulmonary disease, or cardiac abnormalities such as enlargement of the left atrium, and age under 60 years
- Nonvalvular AF – absence of rheumatic mitral valve disease, a prosthetic heart valve, or mitral valve repair
- Secondary AF – occurs in the setting of a primary condition that may be the cause of the AF, such as acute myocardial infarction, cardiac surgery, pericarditis, myocarditis, hyperthyroidism, pulmonary embolism, pneumonia, or other acute pulmonary disease
The main goals of treatment are to prevent circulatory instability and stroke. Rate or rhythm control are used to achieve the former, whereas anticoagulation is used to decrease the risk of the latter. If cardiovascularly unstable due to uncontrolled tachycardia, immediate cardioversion is indicated.
Anticoagulation can be achieved through a number of means including the use of heparin, warfarin, dabigatran, rivaroxaban and apixaban. Aspirin is somewhat effective in reducing the risk of stroke in AF patients, but is inferior to warfarin and is typically reserved for AF patients at lower risk for stroke. The method used depends on a number of issues, including: cost, risk of stroke, risk of falls, compliance, and speed of desired onset of anticoagulation. Some other anticoagulants were discussed in a 2012 state-of-the-art paper but were not generally approved at that time for stroke prevention in AF: apixaban, and edoxaban.
For those with non-valvular atrial fibrillation, the new oral anticoagulants (rivaroxaban, dabigatran, apixaban) are not superior to warfarin in preventing non-hemorrhagic stroke and systemic embolic events but they do have a lower risk of intracranial bleeding compared to warfarin.
Rate versus rhythm control
There are two ways to approach atrial fibrillation using medications: rate control and rhythm control. Both methods have similar outcomes. Rate control lowers the heart rate closer to normal, usually 60 to 100 bpm, without trying to convert to a regular rhythm. Rhythm control restores normal heart rhythm in a process called cardioversion and maintains the normal rhythm with drugs. Studies suggest that rhythm control is most important in the acute setting AF, whereas rate control is more important in the chronic phase.
There is no difference in risk of stroke in people having converted to a normal rhythm with anti-arrhythmic treatment compared to those with only rate control. AF is associated with a reduced quality of life, and, while some studies indicate that rhythm control leads to a higher quality of life, some did not find a difference.
A further study focused on rhythm control in patients with AF with concomitant heart failure, based on the hypothesis that AF confers a higher mortality risk in heart failure. In this setting, rhythm control offered no advantage compared to rate control. However, the diagnosis and progression of atrial fibrillation and other cardiovascular disease requires further investigation.
In those with a fast ventricular response, intravenous magnesium significantly increases the chances of successful rate and rhythm control in the urgent setting without major side-effects. A patient with fluctuating vital signs, mental status changes, preexcitation, or chest pain often will go to immediate treatment with synchronized DC cardioversion. Otherwise the decision of rate control versus rhythm control using drugs is made. This is based on a number of criteria that includes whether or not symptoms persist with rate control.
Rate control is achieved with medications that work by increasing the degree of block at the level of the AV node, in effect decreasing the number of impulses that conduct into the ventricles. This can be done with:
- Beta blockers (preferably the "cardioselective" beta blockers such as metoprolol, atenolol, bisoprolol, nebivolol)
- Non-dihydropyridine calcium channel blockers (e.g., diltiazem or verapamil)
- Cardiac glycosides (e.g., digoxin) – have limited use, apart from in the sedentary elderly patient
In addition to these agents, amiodarone has some AV node blocking effects (in particular when administered intravenously), and can be used in individuals when other agents are contraindicated or ineffective (particularly due to hypotension).
Diltiazem has been shown to be more effective than either digoxin or amiodarone.
- Electrical cardioversion involves the restoration of normal heart rhythm through the application of a DC electrical shock.
- Chemical cardioversion is performed with drugs, such as amiodarone, dronedarone, procainamide, dofetilide, ibutilide, propafenone, or flecainide.
After successful cardioversion the heart may be in a stunned state, which means that there is a normal rhythm but restoration of normal atrial contraction has not yet occurred.
In young patients with little-to-no structural heart disease where rhythm control is desired and cannot be maintained by medication or cardioversion, then radiofrequency ablation or cryoablation may be attempted and is preferred over years of drug therapy. Although radiofrequency ablation is becoming an accepted intervention in select younger patients, there is currently a lack of evidence that ablation reduces all-cause mortality, stroke, or heart failure. There are two ongoing clinical trials (CABANA [Catheter Ablation Versus Antiarrhythmic Drug Therapy for Atrial Fibrillation] and EAST [Early Therapy of Atrial Fibrillation for Stroke Prevention Trial]) that should provide new information for assessing whether AF catheter ablation is superior to more standard therapy.
The Maze procedure, first performed in 1987, is an effective invasive surgical treatment that is designed to create electrical blocks or barriers in the atria of the heart, forcing electrical impulses that stimulate the heartbeat to travel down to the ventricles. The idea is to force abnormal electrical signals to move along one, uniform path to the lower chambers of the heart (ventricles), thus restoring the normal heart rhythm.
AF often occurs after cardiac surgery and is usually self-limiting. It is strongly associated with age, pre-operative hypertension, and the number of vessels grafted. Measures should be taken to control hypertension pre-operatively to reduce the risk of AF. Also, patients with a higher risk of AF, e.g., patients with pre-operative hypertension, more than 3 vessels grafted, or greater than 70 years of age, should be considered for prophylactic treatment. Postoperative pericardial effusion is also suspected to be the cause of atrial fibrillation. Prophylaxis may include prophylactic post-operative rate and rhythm management. Some authors perform posterior pericardiotomy to reduce the incidence of postoperative AF. When AF occurs, management should primarily be rate and rhythm control. However, cardioversion may be employed if the patient is haemodynamically unstable, highly symptomatic, or persists for 6 weeks after discharge. In persistent cases anticoagulation should be used.
Prediction of embolism
Mechanism of thrombus formation
In atrial fibrillation, the lack of an organized atrial contraction can result in some stagnant blood in the left atrium (LA) or left atrial appendage (LAA). This lack of movement of blood can lead to thrombus formation (blood clotting). If the clot becomes mobile and is carried away by the blood circulation, it is called an embolus. An embolus proceeds through smaller and smaller arteries until it plugs one of them and prevents blood from flowing through the artery. This process results in end-organ damage due to loss of nutrients, oxygen, and removal of cellular waste products. Emboli in the brain may result in an ischemic stroke or a transient ischemic attack (TIA).
More than 90% of cases of thrombi associated with non-valvular atrial fibrillation evolve in the left atrial appendage. However, the LAA lies in close relation to the free wall of the left ventricle and thus the LAA's emptying and filling, which determines its degree of blood stagnation, may be helped by the motion of the wall of the left ventricle, if there is good ventricular function.
If the LA is enlarged, there is an increased risk of thrombi that originate in the LA. Moderate to severe, non-rheumatic, mitral regurgitation (MR) reduces this risk of stroke. This risk reduction may be due to a beneficial stirring effect of the MR blood flow into the LA.
Atrial fibrillation and a corresponding enlargement of the left atrium may cause an increase in the perimeter of the mitral valve. The somewhat circular perimeter of the mitral valve is defined by the mitral annulus.
With a sinus rhythm, the mitral annulus undergoes dynamic changes during the cardiac cycle. For example, at the end of diastole the annular area is smaller than at the end of systole. A possible reason for this dynamic size difference is that the coordinated contraction of the left atrium acts like a sphincter about the mitral annulus and reduces its size. This may be important for mitral valve competence so that it does not leak when the left ventricle pumps blood. However, when the left atrium fibrillates, this sphincter action is not possible and may contribute to, or result in, mitral regurgitation in some cases.
Atrial fibrillation is the most common arrhythmia affecting 0.4 to 1% of the population. It also accounts for 1/3 of hospital admissions for cardiac rhythm disturbances, and the rate of admissions for AF has risen in recent years. Strokes from AF account for 6-24% of all ischemic strokes. After a transient ischemic attack or stroke about 11% are found to have a new diagnosis of atrial fibrillation. Between 3–11% of those with AF have structurally normal hearts. Approximately 2.2 million individuals in the United States and 4.5 million in the European Union have AF.
The incidence of atrial fibrillation increases with age. In individuals over the age of 80 it affects about 8%. In developed countries, the number of patients with atrial fibrillation is likely to increase during the next 50 years, owing to the growing proportion of elderly individuals.
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. In the mid-eighteenth century, Jean-Baptiste de Sénac made note of dilated, irritated atria in people with mitral stenosis. The irregular pulse associated with AF was first recorded in 1876 by Carl Wilhelm Hermann Nothnagel and termed "delirium cordis", stating that "[I]n 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". 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. Willem Einthoven published the first ECG showing AF in 1906. 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.
- Ferguson C, Inglis SC, Newton PJ, Middleton S, Macdonald PS, Davidson PM (2013). "Atrial fibrillation: stroke prevention in focus". ACC 00 (00): IN PRESS. PMID 24054541. doi:10.1016/j.aucc.2013.08.002.
- Ciervo CA, Granger CB, Schaller FA (September 2012). "Stroke prevention in patients with atrial fibrillation: disease burden and unmet medical needs.". J Am Osteopath Assoc (Review) 112 (9 (Suppl 2)): eS2–8. PMID 23014814.
- Fuster V, Rydén LE, Cannom DS et al. (2006). "ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation 114 (7): e257–354. PMID 16908781. doi:10.1161/CIRCULATIONAHA.106.177292.
- Gutierrez C, Blanchard DG (January 2011). "Atrial Fibrillation: Diagnosis and Treatment". Am Fam Physician (Review) 83 (1): 61–68.
- Leung, RS; Huber MA; Rogge T; Maimon N; Chiu KL; Bradley TD (2005-12-01). "Association between atrial fibrillation and central sleep apnea". Sleep 28 (12): 1543–6. PMID 16408413. Retrieved 2014-08-06. See p.1545, second paragraph of Discussion section.
- Conen D, Tedrow UB, Cook NR, Moorthy MV, Buring JE, Albert CM (December 2008). "Alcohol Consumption and Risk of Incident Atrial Fibrillation in Women". JAMA 300 (21): 2489–96. PMC 2630715. PMID 19050192. doi:10.1001/jama.2008.755.
- Sweeney MO, Bank AJ, Nsah E et al. (2007). "Minimizing ventricular pacing to reduce atrial fibrillation in sinus-node disease". N. Engl. J. Med. 357 (10): 1000–8. PMID 17804844. doi:10.1056/NEJMoa071880.
- Fox CS, Parise H, D'Agostino RB et al. (2004). "Parental atrial fibrillation as a risk factor for atrial fibrillation in offspring". JAMA 291 (23): 2851–5. PMID 15199036. doi:10.1001/jama.291.23.2851.
- Saffitz JE (2006). "Connexins, conduction, and atrial fibrillation". N. Engl. J. Med. 354 (25): 2712–4. PMID 16790707. doi:10.1056/NEJMe068088.
- "OMIM Online Mendelian Inheritance of Man". The National Center for Biotechnology Information. Retrieved 2010-08-24.
- Shimizu W (2013) Atrial fibrillation and genetic abnormalities. Nihon Rinsho 71(1):161-1666
- Sanfilippo AJ, Abascal VM, Sheehan M, Oertel LB, Harrigan P, Hughes RA and Weyman AE (1990). "Atrial enlargement as a consequence of atrial fibrillation A prospective echocardiographic study". Circulation 82 (3): 792–7. PMID 2144217. doi:10.1161/01.CIR.82.3.792. Archived from the original on 1 December 2009. Retrieved 2009-12-02.
- Osranek M, Bursi F, Bailey KR, Grossardt BR, Brown RD Jr, Kopecky SL, Tsang TS, Seward JB. (December 2005). "Left atrial volume predicts cardiovascular events in patients originally diagnosed with lone atrial fibrillation: three-decade follow-up". European Heart Journal 26 (23): 2556–61. PMID 16141257. doi:10.1093/eurheartj/ehi483. Retrieved 2009-12-27.
- Elvan A, Wylie K, Zipes D (1 December 1996). "Pacing-induced chronic atrial fibrillation impairs sinus node function in dogs. Electrophysiological remodeling". Circulation 94 (11): 2953–60. PMID 8941126. doi:10.1161/01.CIR.94.11.2953.
- Manios EG, Kanoupakis EM, Mavrakis HE, Kallergis EM, Dermitzaki DN, Vardas PE (2001). "Sinus pacemaker function after cardioversion of chronic atrial fibrillation: is sinus node remodeling related with recurrence?". Journal of Cardiovascular Electrophysiology 12 (7): 800–6. PMID 11469431. doi:10.1046/j.1540-8167.2001.00800.x.
- Fuster V, Rydén LE, Asinger RW et al. (October 2001). "ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology". Circulation 104 (17): 2118–50. PMID 11673357.
- Klabunde, Richard (2005). Cardiovascular Physiology Concepts. Lippincott Williams & Wilkins. pp. 25, 28. ISBN 978-0-7817-5030-1.
- Moran, PS; Flattery, MJ; Teljeur, C; Ryan, M; Smith, SM (Apr 30, 2013). "Effectiveness of systematic screening for the detection of atrial fibrillation.". The Cochrane database of systematic reviews 4: CD009586. PMID 23633374. doi:10.1002/14651858.CD009586.pub2.
- Zipes, Ziad F. Issa, John M. Miller, Douglas P. (2009). Clinical arrhythmology and electrophysiology : a companion to Braunwald's heart disease. Philadelphia: Saunders. p. 221. ISBN 978-1-4160-5998-1.
- Blackshear JL, Odell JA (February 1996). "Appendage obliteration to reduce stroke in cardiac surgical patients with atrial fibrillation". Ann. Thorac. Surg. 61 (2): 755–9. PMID 8572814. doi:10.1016/0003-4975(95)00887-X.
- Acar J, Cormier B, Grimberg D et al. (1991). "Diagnosis of left atrial thrombi in mitral stenosis – usefulness of ultrasound techniques compared with other methods". European Heart Journal. 12 (Supplement B) (Jul): 70–6. PMID 1936030. doi:10.1093/eurheartj/12.suppl_B.70. Retrieved 2009-10-20.
- Fatkin D, Kelly RP, and Feneley MP (1994). "Relations between left atrial appendage blood flow velocity, spontaneous echocardiographic contrast and thromboembolic risk in vivo". Journal of the American College of Cardiology 23 (4): 961–9. PMID 8106703. doi:10.1016/0735-1097(94)90644-0. Retrieved 2009-10-21.
- Levy S (2000). "Classification system of atrial fibrillation". Current Opinion in Cardiology 15 (1): 54–7. PMID 10666661. doi:10.1097/00001573-200001000-00007.
- Prystowsky EN (2000). "Management of atrial fibrillation: therapeutic options and clinical decisions". Am J Cardiol 85 (10A): 3D–11D. PMID 10822035. doi:10.1016/S0002-9149(00)00908-5.
- "FDA approves Xarelto to prevent stroke in people with common type of abnormal heart rhythm". FDA. Retrieved Nov 4, 2011.
- Singer DE, Albers GW, Dalen JE, Go AS, Halperin JL, Manning WJ (Sep 2004). "Antithrombotic Therapy in Atrial Fibrillation : The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy". Chest 126 (3_suppl): 429S–456S. PMID 15383480. doi:10.1378/chest.126.3_suppl.429S. Retrieved 2012-10-02.
- De Caterina R, Husted S, Wallentin L, Andreotti F, et al. (17 Apr 2012). "New oral anticoagulants in atrial fibrillation and acute coronary syndromes: ESC Working Group on Thrombosis-Task Force on Anticoagulants in Heart Disease position paper". Journal of the American College of Cardiology 59 (16): 1413–25. PMID 22497820. doi:10.1016/j.jacc.2012.02.008. Retrieved 2012-10-02.
- Gómez-Outes, A; Terleira-Fernández, AI; Calvo-Rojas, G; Suárez-Gea, ML; Vargas-Castrillón, E (2013). "Dabigatran, Rivaroxaban, or Apixaban versus Warfarin in Patients with Nonvalvular Atrial Fibrillation: A Systematic Review and Meta-Analysis of Subgroups.". Thrombosis 2013: 640723. PMC 3885278. PMID 24455237. doi:10.1155/2013/640723.
- Al-Khatib, SM; Allen LaPointe, NM; Chatterjee, R; Crowley, MJ; Dupre, ME; Kong, DF; Lopes, RD; Povsic, TJ; Raju, SS; Shah, B; Kosinski, AS; McBroom, AJ; Sanders, GD (Jun 3, 2014). "Rate- and rhythm-control therapies in patients with atrial fibrillation: a systematic review.". Annals of internal medicine 160 (11): 760–73. PMID 24887617. doi:10.7326/M13-1467.
- Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, Corley SD (2002). "A comparison of rate control and rhythm control in patients with atrial fibrillation". N Engl J Med 347 (23): 1825–33. PMID 12466506. doi:10.1056/NEJMoa021328.
- Thrall G, Lane D, Carroll D, Lip GY (2006). "Quality of life in patients with atrial fibrillation: a systematic review". Am. J. Med. 119 (5): 448.e1–19. PMID 16651058. doi:10.1016/j.amjmed.2005.10.057.
- Roy D, Talajic M, Nattel S et al. (June 2008). "Rhythm control versus rate control for atrial fibrillation and heart failure". N Engl J Med 358 (25): 2667–2677. PMID 18565859. doi:10.1056/NEJMoa0708789.
- Onalan O, Crystal E, Daoulah A, Lau C, Crystal A, Lashevsky I (2007). "Meta-analysis of magnesium therapy for the acute management of rapid atrial fibrillation". Am. J. Cardiol. 99 (12): 1726–32. PMID 17560883. doi:10.1016/j.amjcard.2007.01.057.
- "Atrial fibrillation: national clinical guideline for management in primary and secondary care" (PDF). National Collaborating Centre for Chronic Conditions. London: Royal College of Physicians. 2006. Retrieved 2009-05-05.
- Siu CW, Lau CP, Lee WL, Lam KF, Tse HF (July 2009). "Intravenous diltiazem is superior to intravenous amiodarone or digoxin for achieving ventricular rate control in patients with acute uncomplicated atrial fibrillation". Crit. Care Med. 37 (7): 2174–9; quiz 2180. PMID 19487941. doi:10.1097/CCM.0b013e3181a02f56.
- Singh BN, Connolly SJ, Crijns HJ et al. (2007). "Dronedarone for maintenance of sinus rhythm in atrial fibrillation or flutter". N. Engl. J. Med. 357 (10): 987–99. PMID 17804843. doi:10.1056/NEJMoa054686.
- Finnin M (July 2010). "Vernakalant: A novel agent for the termination of atrial fibrillation". Am J Health Syst Pharm 67 (14): 1157–64. PMID 20592320. doi:10.2146/ajhp080501.
- Watson T, Shantsila E, Lip GY (10 Jan 2009). "Mechanisms of thrombogenesis in atrial fibrillation: Virchow's triad revisited". Lancet 373 (9658): 155–66. PMID 19135613. doi:10.1016/S0140-6736(09)60040-4.
- Leong-Sit P, Zado E, Callans DJ, et al. Efficacy and risk of atrial fibrillation ablation before 45 years of age. Circ Arrhythm Electrophysiol. 2010;3:452-7.
- Agency for Healthcare Research and Quality. Research Protocol: Treatment of Atrial Fibrillation. 2012; December 2012.
- January CT, Wann LS, Alpert JS, Calkins H, Cleveland Jr JC, Cigarroa JE, Conti JB, Ellinor PT, Ezekowitz MD, Field ME, Murray KT, Sacco RL, Stevenson WG, Tchou PJ, Tracy CM, Yancy CW, 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation, Journal of the American College of Cardiology (2014), doi:10.1016/j.jacc.2014.03.022
- Northwestern Surgery for Atrial Fibrillation. Atrial Fibrillation Surgery
- Kaleda VI, McCormack DJ, Shipolini AR (April 2012). "Does posterior pericardiotomy reduce the incidence of atrial fibrillation after coronary artery bypass grafting surgery?". Interact. Cardiovasc. Thorac. Surg. 14 (4): 384–9. PMC 3309809. PMID 22235005. doi:10.1093/icvts/ivr099.
- Lopes RD, Crowley MJ, Shah BR, et al . Stroke Prevention in Atrial Fibrillation. ComparativeEffectiveness Review No. 123. AHRQ Publication No. 13-EHC113-EF. Rockville, MD: Agency for Healthcare Research and Quality; August 2013. www.effectivehealthcare.ahrq.gov/ reports/final.cfm.
- Al-Saady, N. M.; O. A. Abel; A. J. Camm (1999). "Left atrial appendage: structure, function, and role in thromboembolism". Heart 82 (5): 547–55. PMC 1760793. PMID 10525506.
- Nakagami H, Yamamoto K, Ikeda U, Mitsuhashi T, Goto T, Shimada K (1998). "Mitral regurgitation reduces the risk of stroke in patients with nonrheumatic atrial fibrillation". Americal Heart Journal 136 (3): 528–32. PMID 9736148. doi:10.1016/S0002-8703(98)70231-5. Retrieved 2010-02-23.
- Cheng, TO (November 1999). "Reduced risk for thromboembolism in atrial fibrillation and mitral regurgitation". American Heart Journal 138 (5 Pt 1): 998–9. PMID 10539836. doi:10.1016/S0002-8703(99)70045-1.
- Pai, RG; Varadarajan, P; Tanimoto, M (January 2003). "Effect of Atrial Fibrillation on the Dynamics of Mitral Annular Area". The Journal of Heart Valve Disease 12 (1): 31–7. PMID 12578332. Retrieved 2009-12-20.
- Friberg J, Buch P, Scharling H, Gadsbphioll N, Jensen GB. (2003). "Rising rates of hospital admissions for atrial fibrillation". Epidemiology 14 (6): 666–72. PMID 14569181. doi:10.1097/01.ede.0000091649.26364.c0.
- Narumiya T, Sakamaki T, Sato Y, Kanmatsuse K (January 2003). "Relationship between left atrial appendage function and left atrial thrombus in patients with nonvalvular chronic atrial fibrillation and atrial flutter". Circulation Journal 67 (1): 68–72. PMID 12520155. doi:10.1253/circj.67.68.
- Kishore, A; Vail, A; Majid, A; Dawson, J; Lees, KR; Tyrrell, PJ; Smith, CJ (Feb 2014). "Detection of atrial fibrillation after ischemic stroke or transient ischemic attack: a systematic review and meta-analysis.". Stroke; a journal of cerebral circulation 45 (2): 520–6. PMID 24385275. doi:10.1161/STROKEAHA.113.003433.
- Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV, Singer DE (2001). "Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study". JAMA 285 (18): 2370–5. PMID 11343485. doi:10.1001/jama.285.18.2370.
- Vulpian, A. (1874). "Note sur les effets de la faradisation directe des ventricules du coeur chez le chien". Archives de Physiologie Normale et Pathologique 6: 975.
- McMichael, J. (1982). "History of atrial fibrillation 1628–1819 Harvey – de Senac – Laënnec". Br Heart J 48 (3): 193–7. PMC 481228. PMID 7049202. doi:10.1136/hrt.48.3.193.
- Nothnagel, H. (1876). "Ueber arythmische Herzthatigkeit". Deutsches Archiv fur Klinische Medizin 17: 190–220.
- MacKenzie, J. (1904). "Observations on the Inception of the Rhythm of the Heart by the Ventricle: As the cause of Continuous Irregularity of the Heart". Br Med J 1 (2253): 529–36. PMC 2353402. PMID 20761393. doi:10.1136/bmj.1.2253.529.
- Einthoven, W. (1906). "Le telecardiogramme". Archives Internationales de Physiologie 4: 132–64.
- Rothberger, CJ, Winterberg, H. (1909). "Vorhofflimmern und Arhythmia perpetua". Wiener Klinische Wochenschrift 22: 839–44.
- Lewis, T (1909). "Auricular fibrillation: a common clinical condition". Br Med J 2 (2552): 1528. doi:10.1136/bmj.2.2552.1528.
- Flegel KM (1995). "From delirium cordis to atrial fibrillation: historical development of a disease concept". Ann. Intern. Med. 122 (11): 867–73. PMID 7741373. doi:10.7326/0003-4819-122-11-199506010-00010.