Atrial fibrillation

Presentation is similar to other forms of rapid heart rate and may be asymptomatic.[22] Palpitations and chest discomfort are common complaints.[22] The rapid uncoordinated heart rate may result in reduced output of blood pumped by the heart (cardiac output) resulting in inadequate blood flow and therefore oxygen delivery to the rest of the body. Common symptoms of uncontrolled atrial fibrillation may include shortness of breath,[22] shortness of breath when lying flat, dizziness, and sudden onset of shortness of breath during the night. This may progress to swelling of the lower extremities, a manifestation of congestive heart failure. Due to inadequate cardiac output, individuals with AF may also complain of light-headedness,[22] may feel like they are about to faint, or may actually lose consciousness.

AF can cause respiratory distress due to congestion in the lungs. By definition, the heart rate will be greater than 100 beats per minute. Blood pressure may be variable, and often difficult to measure as the beat-by-beat variability causes problems for most digital (oscillometric) non-invasive blood pressure monitors. For this reason, when determining heart rate in AF, direct cardiac auscultation is recommended. Low blood pressure is most concerning and a sign that immediate treatment is required. Many of the symptoms associated with uncontrolled atrial fibrillation are a manifestation of congestive heart failure due to the reduced cardiac output. Respiratory rate will be increased in the presence of respiratory distress. Pulse oximetry may confirm the presence of too little oxygen reaching the body's tissues related to any precipitating factors such as pneumonia. Examination of the jugular veins may reveal elevated pressure (jugular venous distention). Examination of the lungs may reveal crackles, which are suggestive of pulmonary edema. Examination of the heart will reveal a rapid irregular rhythm.

A family history of AF may increase the risk of AF. A study of more than 2,200 people found an increased risk factor for AF of 1.85 for those that had at least one parent with AF.[33][34][35] Various genetic mutations may be responsible.[36][37]

Four types of genetic disorder are associated with atrial fibrillation:[38]

• 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

Family history in a first degree relative is associated with a 40% increase in risk of AF. This finding led to the mapping of different loci such as 10q22-24, 6q14-16 and 11p15-5.3 and discover mutations associated with the loci. Fifteen mutations of gain and loss of function have been found in the genes of K⁺ channels, including mutations in KCNE1-5, KCNH2, KCNJ5 or ABCC9 among others. Six variations in genes of Na⁺ channels that include SNC1-4B, SNC5A and SNC10A have also been found. All of these mutations affect the processes of polarization-depolarization of the myocardium, cellular hyper-excitability, shortening of effective refractory period favouring re-entries.[39] Other mutations in genes, such as GJA5, affect Gap junctions, generating a cellular uncoupling that promotes re-entries and a slow conduction velocity.[40] Using genome-wide association study, which screen the entire genome for single nucleotide polymorphism (SNP), three susceptibility loci have been found for AF (4q25, 1q21 and 16q22).[41] In these loci there are SNPs associated with a 30% increase in risk of recurrent atrial tachycardia after ablation. There is also SNPs associated with loss of function of the Pitx2c gene (involved in cellular development of pulmonary valves), responsible for re-entries. There are also SNPs close to ZFHX3 genes involved in the regulation of Ca²⁺.[39] A GWAS meta-analysis study conducted in 2018 revealed the discovery of 70 new loci associated with AF. Different variants have been identified. They are associated with genes that encode transcription factors, such as TBX3 and TBX5, NKX2-5 or PITX2, involved in the regulation of cardiac conduction, modulation of ion channels and in cardiac development. Have been also identified new genes involved in tachycardia (CASQ2) or associated with an alteration in cardiomyocyte communication (PKP2).[42]

A sedentary lifestyle increases the risk factors associated with AF such as obesity, hypertension or diabetes mellitus. This favors remodeling processes of the atrium due to inflammation or alterations in the depolarization of cardiomyocytes by elevation of sympathetic nervous system activity.[39][43] A sedentary lifestyle is associated with an increased risk of AF compared to physical activity. In both men and women, the practice of moderate exercise reduces the risk of AF progressively,[44] but intense sports may increase the risk of developing AF, as seen in athletes.[45] It is due to a remodeling of cardiac tissue,[46] and an increase in vagal tone, which shortens the effective refractory period (ERP) favoring re-entries from the pulmonary veins.[44]

According to the CHARGE Consortium both systolic and diastolic blood pressure are predictors of the risk of AF. Systolic blood pressure values close to normal limit the increase in the risk associated with AF. Diastolic dysfunction is also associated with AF, which increased pressure, left atrial volume, size, and left ventricular hypertrophy, characteristic of chronic hypertension. All atrial remodeling is related to a heterogeneous conduction and the formation of re-entrant electric conduction from the pulmonary veins.[39][47]

The rate of AF in smokers is 1.4 times higher than in non-smokers.[47] Tobacco use increases susceptibility to AF through different processes. Exposure to tobacco products increases the release of catecholamines (e.g., epinephrine or norepinephrine) and promotes narrowing of the coronary arteries, leading to inadequate blood flow and oxygen delivery to the heart. In addition, it accelerates atherosclerosis, due to its effect of oxidative stress on lipids and inflammation, which leads to the formation of blood clots. Finally, nicotine induces the formation of patterns of collagen type III in the atrium and has profibrotic effects. All this modifies the atrial tissue, favoring the re-entry.[48][49]

There is a relationship between risk factors such as obesity and hypertension, with the appearance of diseases such as diabetes mellitus and sleep apnea-hypopnea syndrome, specifically, obstructive sleep apnea (OSA). These diseases are associated with an increased risk of AF due to their remodeling effects on the left atrium.[39]

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 be factors in some individuals. 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–angiotensin–aldosterone 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 occurs gradually, 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,[20] suggesting that dysfunction of the SA node is progressive with prolonged episodes of atrial fibrillation.

Conduction
Sinus rhythm	Atrial fibrillation

There are multiple theories about the cause 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 a re-entrant leading circle, or electrical spiral waves (rotors); 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. There are three fundamental components that favor the establishment of a leading circle or a rotor: slow conduction velocity of cardiac action potential, short refractory period, and small wavelength. Meanwhile, wavelength is the product of velocity and refractory period. If the action potential has fast conduction, with a long refractory period and/or conduction pathway shorter than the wavelength, an AF focus would not be established. In multiple wavelet theory, a wavefront will break into smaller daughter wavelets when encountering an obstacle, through a process called vortex shedding; but under proper conditions, such wavelets can reform and spin around a centre, forming an AF focus.[50]

In a heart with AF, the increased calcium release from sarcoplasmic reticulum and increased calcium sensitivity can lead to accumulation of intra-cellular calcium and causes down regulation of L-type calcium channels. This reduces the duration of action potential and refractory period, thus favorable for the conduction of re-entrant waves. Increased expression of inward-rectifier potassium ion channels can cause a reduced atrial refractory period and wavelength. The abnormal distribution of gap junction proteins such as GJA1 (also known as Connexin 43), and GJA5 (Connexin 40) causes non-uniformity of electrical conduction, thus causing arrhythmia.[51]

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 AF and atrial flutter are distinct arrhythmias, atrial flutter may degenerate into AF and an individual may experience both arrhythmias at different times.[12]

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 a 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.[52]

The USPSTF found insufficient evidence to determine the usefulness of screening in 2018.[53] Limited studies have suggested that screening for atrial fibrillation in those 65 years and older increases the number of cases of atrial fibrillation detected.[54]

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.

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.[20]

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.[20]

ECG of atrial fibrillation (top) and normal sinus rhythm (bottom). The purple arrow indicates a P wave, which is lost in atrial fibrillation.

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.[20] At very fast heart rates, atrial fibrillation may look more regular, which may make it more difficult to separate from other supraventricular tachycardias or ventricular tachycardia.[55]

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 a 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 person can be monitored for longer periods (e.g., a month) with an ambulatory event monitor.[20]

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 person's clinical state. This ultrasound-based scan of the heart may help identify valvular heart disease (which may greatly increase the risk of stroke and alter recommendations for the appropriate type of anticoagulation), 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 sensitivity), presence of left ventricular hypertrophy and pericardial disease.[20]

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 for 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.[20] In particular, if an underlying pneumonia is suggested, then treatment of the pneumonia may cause the atrial fibrillation to terminate on its own.

A regular echocardiogram (transthoracic echo/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.[20]

The TEE has much better visualization of the left atrial appendage than transthoracic echocardiography.[56] 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.[57][58] 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.[56]

If a blood clot is seen on TEE, then cardioversion is contraindicated due to the risk of stroke and anticoagulation is recommended.

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.

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.

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.[20]

All people with AF are initially in the category called first detected AF. These people 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 people 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 person's AF is then known as permanent.[59]

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.

About half of people with AF have permanent AF, while a quarter have paroxysmal AF, and a quarter have persistent AF.[4]

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 person.[20]

• 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

Lastly, atrial fibrillation is also classified by whether or not it is caused by valvular heart disease. Valvular atrial fibrillation refers to atrial fibrillation attributable to moderate to severe mitral valve stenosis or atrial fibrillation in the presence of a mechanical artificial heart valve.[60] This distinction is necessary since it has implications on appropriate treatment including differing recommendations for anticoagulation.

Anticoagulation can be used to reduce the risk of stroke from AF. Anticoagulation is recommended in most people other than those at low risk of stroke[63] or those at high risk of bleeding. The risk of falls and consequent bleeding in frail elderly people should not be considered a barrier to initiating or continuing anticoagulation since the risk of fall-related brain bleeding is low and the benefit of stroke prevention often outweighs the risk of bleeding.[64][65] Oral anticoagulation is underused in atrial fibrillation while aspirin is overused in many who should be treated with a direct oral anticoagulants (DOACs) or warfarin.[66][67][68] In 2019, DOACs were often recommended over warfarin by the American Heart Association.[69]

The risk of stroke from non-valvular AF can be estimated using the CHA₂DS₂-VASc score. In the 2019 AHA/ACC/HRS guidelines anticoagulation is recommended in non-valvular AF if there is a score of 2 or more in men and 3 or more in women, and may be considered if there is a score of 1 in men or 2 in women, and not using anticoagulation is reasonable if there is a score of 0 in men or 1 in women.[69] Guidelines from the American College of Chest Physicians, Asia-Pacific Heart Rhythm Society, Canadian Cardiovascular Society, European Society of Cardiology, Japanese Circulation Society, Korean Heart Rhythm Society, and the National Institute for Health and Care Excellence recommend the use of novel oral anticoagulants or warfarin with a CHADS2VASC score of 1 over aspirin and some directly recommend against aspirin.[68][70][71][72][73][74][75][76] Experts generally advocate for most people with atrial fibrillation with CHA₂DS₂-VASc score scores of 1 or more receiving anticoagulation though aspirin is sometimes used for people with a score of 1 (moderate risk for stroke).[66] There is little evidence to support the idea that the use of aspirin significantly reduces the risk of stroke in people with atrial fibrillation.[66] Furthermore, aspirin's major bleeding risk (including bleeding in the brain) is similar to that of warfarin and DOACs despite its inferior efficacy.[67][74]

Anticoagulation can be achieved through a number of means including warfarin,[77] heparin, dabigatran, rivaroxaban,[78] edoxaban,[79] and apixaban.[80] A number of issues should be considered, including the cost of DOACs, risk of stroke, risk of falls, comorbidities (such as chronic liver or kidney disease), the presence of significant mitral stenosis or mechanical heart valves, compliance, and speed of desired onset of anticoagulation.[60][81]

For those with non-valvular atrial fibrillation, DOACs (rivaroxaban, dabigatran, apixaban) are at least as effective as warfarin for preventing strokes and blood clots embolizing to the systemic circulation (if not more so) and are generally preferred over warfarin.[60][82][83][84] DOACs carry a lower risk of bleeding in the brain compared to warfarin,[65] although dabigatran is associated with a higher risk of intestinal bleeding.[82][83] Dual antiplatelet therapy with aspirin and clopidogrel is inferior to warfarin for preventing strokes and has comparable bleeding risk in people with atrial fibrillation.[85] In those who are also on aspirin, however, DOACs appear to be better than warfarin.[86]

Warfarin is the recommended anticoagulant choice for persons with valvular atrial fibrillation (atrial fibrillation in the presence of a mechanical heart valve and/or moderate-severe mitral valve stenosis).[60] The exception to this recommendation is in people with valvular atrial fibrillation who are unable to maintain a therapeutic INR on warfarin therapy; in such cases, treatment with a DOAC is then recommended.[60]

There are two ways to approach atrial fibrillation using medications: rate control and rhythm control. Both methods have similar outcomes.[87] Rate control lowers the heart rate closer to normal, usually 60 to 100 bpm, without trying to convert to a regular rhythm. Rhythm control tries to restore a normal heart rhythm in a process called cardioversion and maintains the normal rhythm with medications. Studies suggest that rhythm control is more important in the acute setting AF, whereas rate control is more important in the chronic phase.

The risk of stroke appears to be lower with rate control versus attempted rhythm control, at least in those with heart failure.[88] 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.[89]

Neither rate nor rhythm control is superior in people with heart failure when they are compared in various clinical trials. However, rate control is recommended as the first line treatment regimen for people with heart failure. On the other hand, rhythm control is only recommended when people experience persistent symptoms despite adequate rate control therapy.[90]

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.[91] A person with poor vital signs, mental status changes, preexcitation, or chest pain often will go to immediate treatment with synchronized DC cardioversion.[20] 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 to a target heart rate of less than 110 beats per minute is recommended in most people.[92] Lower heart rates may be recommended in those with left ventricular hypertrophy or reduced left ventricular function.[93] Rate control is achieved with medications that work by increasing the degree of block at the level of the AV node, decreasing the number of impulses that conduct into the ventricles. This can be done with:[20][94]

• Beta blockers (preferably the "cardioselective" beta blockers such as metoprolol, bisoprolol, or nebivolol)
• Non-dihydropyridine calcium channel blockers (e.g., diltiazem or verapamil)
• Cardiac glycosides (e.g., digoxin) – have less use, apart from in older people who are sedentary. They are not as effective as either beta blockers or calcium channel blockers.[5]

In those with chronic disease either beta blockers or calcium channel blockers are recommended.[92]

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).

Cardioversion is the attempt to switch an irregular heartbeat to a normal heartbeat using electrical or chemical means.[20]

• Electrical cardioversion involves the restoration of normal heart rhythm through the application of a DC electrical shock. Exact placement of the pads does not appear to be important.[95]
• Chemical cardioversion is performed with medications, such as amiodarone, dronedarone,[96] procainamide (especially in pre-excited atrial fibrillation), 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.[97]

In young people with little-to-no structural heart disease where rhythm control is desired and cannot be maintained by medication or cardioversion, then radiofrequency catheter ablation or cryoablation may be attempted and is preferred over years of drug therapy.[20][98] Although radiofrequency ablation is becoming an accepted intervention in selected younger people, there is currently a lack of evidence that ablation reduces all-cause mortality, stroke, or heart failure.[99] 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.[100]

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.[101] People with AF often undergo cardiac surgery for other underlying reasons and are frequently offered concomitant AF surgery to reduce the frequency of short- and long-term AF. Concomitant AF surgery are more likely to be free from atrial fibrillation and off medications three months after surgery, but these same people are more likely to need a pacemaker following the procedure.[102]

AF often occurs after cardiac surgery and is usually self-limiting. It is strongly associated with age, preoperative hypertension, and the number of vessels grafted. Measures should be taken to control hypertension preoperatively to reduce the risk of AF. Also, people with a higher risk of AF, e.g., people 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 postoperative rate and rhythm management. Some authors perform posterior pericardiotomy to reduce the incidence of postoperative AF.[103] When AF occurs, management should primarily be rate and rhythm control. However, cardioversion may be employed if the person is hemodynamically unstable, highly symptomatic, or persists for 6 weeks after discharge. In persistent cases, anticoagulation should be used.

There is tentative evidence that left atrial appendage occlusion therapy may reduce the risk of stroke in people with non-valvular AF as much as warfarin.[104]

After catheter ablation, people are moved to a cardiac recovery unit, intensive care unit, or cardiovascular intensive care unit where they are not allowed to move for 4–6 hours. Minimizing movement helps prevent bleeding from the site of the catheter insertion. The length of time people stay in hospital varies from hours to days. This depends on the problem, the length of the operation and whether or not general anaesthetic was used. Additionally, people should not engage in strenuous physical activity – to maintain a low heart rate and low blood pressure – for around six weeks.[100]

Determining the risk of an embolism causing a stroke is important for guiding the use of anticoagulants. The most accurate clinical prediction rules are:[108]

• CHADS2
• CHA2DS2-VASc

Both the CHADS2 and the CHA2DS2-VASc score predict future stroke risk in people with A-fib with CHA2DS2-VASc being more accurate. Some that had a CHADS2 score of 0 had a CHA2DS2-VASc score of 3, with a 3.2% annual risk of stroke. Thus a CHA2DS2-VASc score of 0 is considered very low risk.[109]

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.[57] 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.[110]

Atrial fibrillation has been independently associated with a higher risk of dementia.[107] Several mechanisms for this association have been proposed including silent small blood clots (subclinical microthrombi) traveling to the brain resulting in small ischemic strokes without symptoms, altered blood flow to the brain, inflammation, and genetic factors.[107] Effective anticoagulation with direct oral anticoagulants or warfarin appears to be protective against AF-associated dementia and evidence of silent ischemic strokes on MRI.[107]

It is more common in men than in women, in European and North American populations.[115] In Asian populations and in both developed and developing countries, there is also a higher rate in men than in women. The risk factors associated with AF are also distributed differently according to sex. In men, coronary disease is more frequent, while in women, high systolic blood pressure or valvular heart disease are more prevalent.[39]

Rates of AF are lower in populations of African descent than in populations of European descent. The African descent is associated with a protective effect of AF, due to the low presence of SNPs with guanine alleles, in comparison with the European ancestry. European ancestry has more frequent mutations.[39] The variant rs4611994 for the gene PITX2 is associated with risk of AF in African and European populations.[39][42] Other studies reveal that Hispanic and Asian populations have a lower risk of AF compared to populations of European descent. In addition, they demonstrate that the risk of AF in non-European populations is associated with characteristic risk factors of these populations, such as hypertension.[116]