| Atrial fibrillation | |
|---|---|
| Other names | Auricular fibrillation[1] |
 | |
| Electrocardiogram samples displaying atrial fibrillation in the upper recording with absence ofP waves (red arrow), an erratic baseline between QRS complexes, and elevated heart rate. Bottom recording shows normal sinus rhythm with P waves (purple arrow) | |
| Specialty | Cardiology |
| Symptoms | None, heartpalpitations,fainting,dizziness,decreased level ortotal loss of consciousness,shortness of breath[2][3] |
| Complications | Heart failure,dementia,stroke[3] |
| Usual onset | Age > 50[4] |
| Risk factors | High blood pressure,valvular heart disease,coronary artery disease,cardiomyopathy,congenital heart disease,COPD,obesity,smoking,sleep apnea[3][5][6][7] |
| Diagnostic method | Feeling thepulse,electrocardiogram[8] |
| Differential diagnosis | Irregular heartbeat[9] |
| Treatment | Lifestyle modifications, rate control, rhythm control, anticoagulation[5] |
| Frequency | 3.5% (developed world), 1.5% (developing world)[4] |
| Deaths | 315,000 withatrial flutter (2019)[10] |
Atrial fibrillation (AF,AFib orA-fib) is anabnormal heart rhythm (arrhythmia) characterized byrapid and irregular beating of theatrial chambers of the heart.[11] It often begins as short periods of abnormalbeating, which become longer or continuous over time.[4] It may also start as other forms of arrhythmia such asatrial flutter that then transform into AF.[12]
Episodes can be asymptomatic.[3] Symptomatic episodes may involve heartpalpitations,fainting,lightheadedness,loss of consciousness, orshortness of breath.[2] Atrial fibrillation is associated with an increased risk ofheart failure,dementia, andstroke.[3][13] It is a type ofsupraventricular tachycardia.[14]
Atrial fibrillation frequently results from bursts oftachycardia that originate in muscle bundles extending from theatrium to thepulmonary veins.[15] Pulmonary vein isolation bytranscatheter ablation can restoresinus rhythm.[15] Theganglionated plexi (autonomicganglia of the heartatrium andventricles) can also be a source of atrial fibrillation, and are sometimes also ablated for that reason.[16] Not only the pulmonary vein, but theleft atrial appendage andligament of Marshall can be a source of atrial fibrillation and are also ablated for that reason.[17][18] As atrial fibrillation becomes more persistent, the junction between the pulmonary veins and theleft atrium becomes less of an initiator and the left atrium becomes an independent source of arrhythmias.[19]
High blood pressure andvalvular heart disease are the most common modifiable risk factors for AF.[5][6] Other heart-related risk factors includeheart failure,coronary artery disease,cardiomyopathy, andcongenital heart disease.[5] In low- and middle-income countries, valvular heart disease is often attributable torheumatic fever.[20] Lung-related risk factors includeCOPD,obesity, andsleep apnea.[3] Cortisol and other stress biomarkers, as well as emotional stress, may play a role in the pathogenesis of atrial fibrillation.[21]
Other risk factors include excessalcohol intake,tobacco smoking,diabetes mellitus, subclinical hypothyroidism, andthyrotoxicosis.[3][7][22][20] However, about half of cases are not associated with any of these aforementioned risks.[3] Healthcare professionals might suspect AF after feeling thepulse and confirm the diagnosis by interpreting anelectrocardiogram (ECG).[8] A typical ECG in AF shows irregularly spacedQRS complexes withoutP waves.[8]
Healthy lifestyle changes, such as weight loss in people with obesity, increased physical activity, and drinking lessalcohol, can lower the risk for AF and reduce its burden if it occurs.[23] AF is often treated with medications to slow the heart rate to a near-normal range (known as rate control) or to convert the rhythm tonormal sinus rhythm (known as rhythm control).[5]Electrical cardioversion can convert AF to normal heart rhythm and is often necessary for emergency use if the person is unstable.[24]Ablation may prevent recurrence in some people.[25] For those at low risk of stroke, AF does not necessarily require blood-thinning though some healthcare providers may prescribe ananti-clotting medication.[26] Most people with AF are at higher risk of stroke.[27] For those at more than low risk, experts generally recommend an anti-clotting medication.[26] Anti-clotting medications includewarfarin anddirect oral anticoagulants.[26] While these medications reduce stroke risk, they increase rates ofmajor bleeding.[28]
Atrial fibrillation is the most common serious abnormal heart rhythm and, as of 2020, affects more than 33 million people worldwide.[3][23] As of 2014, it affected about 2 to 3% of the population of Europe and North America.[4] The incidence and prevalence of AF increases.[27] In thedeveloping world, about 0.6% of males and 0.4% of females are affected.[4] The percentage of people with AF increases with age with 0.1% under 50 years old, 4% between 60 and 70 years old, and 14% over 80 years old being affected.[4] The first known report of an irregular pulse was byJean-Baptiste de Sénac in 1749.[3]Thomas Lewis was the first doctor to document this by ECG in 1909.[3]
Atrial fibrillation is usually accompanied by symptoms related to arapid heart rate. Rapid and irregular heart rates may be perceived asthe sensation of the heart beating too fast, irregularly, or skipping beats (palpitations) orexercise intolerance.
Other possible symptoms includecongestive heart failure symptoms such as fatigue,shortness of breath, orswelling.Loss of consciousness can also occur on atrial fibrillations due to lack of oxygen and blood to the brain. Theabnormal heart rhythm (arrhythmia) is sometimes only identified with the onset of astroke or atransient ischemic attack (TIA). It is not uncommon for a person to first become aware of AF from a routine physical examination orelectrocardiogram, as it often does not cause symptoms.[29]
Since most cases of AF are secondary to other medical problems, the presence ofchest pain orangina, signs and symptoms ofhyperthyroidism (an overactivethyroid gland) such asweight loss anddiarrhea, and symptoms suggestive oflung disease can indicate an underlying cause. A history of stroke or TIA, as well ashigh blood pressure,diabetes,heart failure, orrheumatic fever, may indicate whether someone with AF is at a higher risk of complications.[29]
Presentation is similar to other forms ofrapid heart rate and may be asymptomatic.Palpitations and chest discomfort are common complaints. The rapid uncoordinated heart rate may result in reducedoutput 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 includeshortness of breath,shortness of breath when lying flat, dizziness, andsudden onset of shortness of breath during the night. This may progress toswelling of the lower extremities, a manifestation of congestive heart failure. Due to inadequate cardiac output, individuals with AF may also complain oflightheadedness.[30]
AF can causerespiratory distress due to congestion in the lungs. By definition, the heart rate will begreater 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 the heart rate in AF, direct cardiacauscultation 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. The affected person's respiratory rate often increases in the presence of respiratory distress. Pulse oximetry may confirm the presence oftoo little oxygen reaching the body's tissues, related to any precipitating factors such aspneumonia. Examination of thejugular veins may reveal elevatedpressure (jugular venous distention). Examination of the lungs may reveal crackles, which are suggestive ofpulmonary edema. Examination of the heart will reveal a rapid irregular rhythm.[citation needed]
AF is linked to several forms of cardiovascular disease but may occur in otherwise normal hearts. Cardiovascular factors known to be associated with the development of AF includehigh blood pressure,[31]coronary artery disease,mitral valve stenosis (e.g., due torheumatic heart disease ormitral valve prolapse),mitral regurgitation,left atrial enlargement,hypertrophic cardiomyopathy,pericarditis,congenital heart disease, and previousheart surgery.[32] People with congenital heart disease tend to develop atrial fibrillation at a younger age, that is more likely to be of right atrial origin (atypical) than of left origin, and have a greater risk of progressing to permanent atrial fibrillation.[33]
Additionally, lung diseases (such aspneumonia,lung cancer,pulmonary embolism, andsarcoidosis) may play a role in certain people.Sepsis also increases the risk of developing new-onset atrial fibrillation.[34][35] Disorders of breathing during sleep, such asobstructive sleep apnea (OSA), are also associated with AF.[36][37] OSA, specifically, was found to be a very strong predictor of atrial fibrillation. Patients with OSA were shown to have an increased incidence of atrial fibrillation and a study done byGami et al. demonstrated that increased nocturnal oxygen desaturation from OSA severity was correlated with higher incidences of atrial fibrillation.[38]Obesity is a risk factor for AF.[39]Hyperthyroidism andsubclinical hyperthyroidism are associated with AF development.[40]
Caffeine consumption does not appear to be associated with AF;[23][41] excessivealcohol consumption ("binge drinking" or "holiday heart syndrome") is linked to AF.[42] Low-to-moderate alcohol consumption also appears to be associated with an increased risk of developing atrial fibrillation, although the increase in risk associated with drinking less than two drinks daily appears to be small.[42][43]Tobacco smoking andsecondhand tobacco smoke exposure are associated with an increased risk of developing atrial fibrillation.[7][44] Long-term endurance exercise that far exceeds the recommended amount of exercise (e.g., long-distancecycling ormarathon running) appears to be associated with a modest increase in the risk of atrial fibrillation in middle-aged and elderly people.[27][45][46]
Major stress biomarkers (includingcortisol andheat shock proteins) indicate thatstress plays a significant role in causing atrial fibrillation.[21] There is some evidence that night shift working may be linked to a diagnosis of AF.[47]
Atrial fibrillation is associated with elevated levels ofinflammatory markers andclotting factors.[48]Mendelian randomization indicates a causal relationship of inflammation leading to atrial fibrillation.[49]
Family history in a first degree relative is associated with a 40% increase in risk of AF. This finding led to themapping of different loci such as 10q22-24, 6q14-16 and 11p15-5.3 and discovermutations associated with the loci. Mutations have been found in the genes of K+ channels and Na+ channels which affect the processes of polarization-depolarization of themyocardium, cellular hyper-excitability, shortening ofeffective refractory period favoring re-entries.[7]
Usinggenome-wide association study (GWAS), which screen the entire genome forsingle nucleotide polymorphism (SNP), three susceptibility loci have been found for AF (4q25, 1q21 and 16q22).[50] In these loci there are SNPs associated with a 30% increase in risk of recurrent atrialtachycardia afterablation. There are also SNPs associated with loss of function of thePitx2c gene (involved in cellular development ofpulmonary valves), responsible for re-entries. There are also SNPs close toZFHX3 genes involved in the regulation of Ca2+.[7] A 2018meta-analysis of GWAS studies identified 97 locis associated with AF, of which 70 were newly identified associations: they are associated with genes that encodetranscription factors, such asTBX3 andTBX5,NKX2-5 orPITX2, involved in the regulation of cardiac conduction, modulation ofion channels and in cardiac development.[51]
Asedentary lifestyle increases the risk factors associated with AF, such asobesity,hypertension, ordiabetes mellitus. This favors remodeling processes of the atrium due toinflammation or alterations in thedepolarization ofcardiomyocytes by elevation ofsympathetic nervous system activity.[7][52] A sedentary lifestyle is associated with an increased risk of AF compared tophysical activity. In both men and women, the practice of moderate exercise reduces the risk of AF progressively;[53] intense sports may increase the risk of developing AF, as seen inathletes.[54] It is due to a remodeling of cardiac tissue,[55] and an increase in vagal tone, which shortens theeffective refractory period (ERP) favoring re-entries from thepulmonary veins.[53]
The rate of AF in smokers is 1.4 times higher than in non-smokers.[56]Snus consumption, which delivers nicotine at a dose equivalent to that of cigarettes, is not correlated with AF.[57]
Acute alcohol consumption can directly trigger an episode of atrial fibrillation.[42] Regular alcohol consumption also increases the risk of atrial fibrillation in several ways.[42] Thelong-term use of alcohol alters the physical structure and electrical properties of the atria.[42] Alcohol consumption does this by repeatedly stimulating thesympathetic nervous system, increasinginflammation in the atria, raisingblood pressure, lowering the levels ofpotassium andmagnesium in the blood, worseningobstructive sleep apnea, and by promoting harmful structural changes (remodeling) in the atria andventricles of the heart.[42] This remodeling leads to abnormally increased pressure in the left atrium, inappropriately dilates it, and increasesscarring (fibrosis) in the left atrium.[42] The aforementioned structural changes increase the risk of developing atrial fibrillation when paired with the harmful changes in how the left atrium conducts electricity.[42]
Hypertension is reportedly present in 49% to 90% of patients with atrial fibrillation.[58] According to the CHARGE Consortium, both systolic and diastolicblood 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 increases left atrial pressure, left atrial volume, size, and left ventricular hypertrophy, characteristic of chronic hypertension. All atrial remodeling is related to heterogeneous conduction and the formation of re-entrant electric conduction from thepulmonary veins.[7][56]
There is a relationship between risk factors such asobesity and hypertension, with the appearance of diseases such asdiabetes 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.[7]
Several medications are associated with an increased risk of developing atrial fibrillation.[59] Few studies have examined this phenomenon, and the exact incidence of medication-induced atrial fibrillation is unknown.[59] Medications that are commonly associated with an increased risk of developing atrial fibrillation includedobutamine and thechemotherapy agentcisplatin.[59] Agents associated with a moderately increased risk includenonsteroidal anti-inflammatory drugs (e.g.,ibuprofen),bisphosphonates, and other chemotherapeutic agents such asmelphalan,interleukin 2, andanthracyclines.[59] Other medications that rarely increase the risk of developing atrial fibrillation includeadenosine,aminophylline,corticosteroids,ivabradine,ondansetron, andantipsychotics.[59] This form of atrial fibrillation occurs in people of all ages but is most common in the elderly, in those with other atrial fibrillation risk factors, and afterheart surgery.[59]
The normalelectrical conduction system of the heart allows electrical impulses generated by the heart's own pacemaker (thesinoatrial node) to spread to and stimulate themuscular layer of the heart (myocardium) in both theatria and theventricles. When the myocardium is stimulated it contracts, and if this occurs in an orderly manner allows blood to be pumped to the body. In AF, the normal regular electrical impulses generated by the sinoatrial node are overwhelmed by disorganized electrical waves, usually originating from the roots of thepulmonary veins. These disorganized waves conduct intermittently through theatrioventricular node, leading to irregular activation of the ventricles that generate the heartbeat.[citation needed]
The primary pathologic change seen in atrial fibrillation is the progressivefibrosis 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 includesvalvular heart disease (such asmitral stenosis,mitral regurgitation, andtricuspid regurgitation), hypertension, and congestive heart failure. Any inflammatory state that affects the heart can cause fibrosis of the atria.
Once dilation of the atria has occurred, this begins a chain of events that leads to the activation of therenin–angiotensin–aldosterone system (RAAS) and subsequent increase in the matrixmetalloproteinases anddisintegrin, 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.[citation needed]
Fibrosis is not limited to the muscle mass of the atria and may occur in thesinus node (SA node) andatrioventricular node (AV node), correlating withsick sinus syndrome. Prolonged episodes of atrial fibrillation have been shown to correlate with prolongation of the sinus node recovery time; this suggests that dysfunction of the SA node is progressive with prolonged episodes of atrial fibrillation.
Along with fibrosis, alterations in the atria that predispose to atrial fibrillation affect theirelectrical properties, as well as their responsiveness to theautonomic nervous system. The atrialremodeling that includes the pathologic changes described above has been referred to asatrial myopathy.[60]
| Conduction | ||
Sinus rhythm | Atrial fibrillation | |
There are multiple theories about the cause of atrial fibrillation. An important theory is that 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 thepulmonary veins. Non-pulmonary vein sources of triggers for atrial fibrillation have been identified in 10% to 33% of patients.[61] These triggers include thecoronary sinus, the posterior wall of theleft atrium, theligament of Marshall, and theleft atrial appendage.[61][18]
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 in the left atrium near the pulmonary veins or in a variety of other locations through both the left or right atrium. Three fundamental components favor the establishment of a leading circle or a rotor: slow conduction velocity of thecardiac action potential, a shortrefractory period, and a smallwavelength. Meanwhile, the 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 the proper conditions, such wavelets can reform and spin around a center, forming an AF focus.[62]
In a heart with AF, the increased calcium release from thesarcoplasmic reticulum and increased calcium sensitivity can lead to an accumulation of intracellular calcium and causes downregulation ofL-type calcium channels. This reduces the duration of action potential and the refractory period, thus favoring the conduction of re-entrant waves. Increased expression ofinward-rectifier potassium ion channels can cause a reduced atrial refractory period and wavelength. The abnormal distribution ofgap junction proteins such asGJA1 (also known as connexin 43), andGJA5 (connexin 40) causes non-uniformity of electrical conduction, thus causing the arrhythmia.[63]
AF can be distinguished fromatrial 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 anECG, 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 such regularity, 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 heartbeat. A heartbeat results when an electrical impulse from the atria passes through theatrioventricular (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 severeventricular tachycardia, resulting in a severe reduction ofcardiac 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.[64]
Atrial fibrillation is diagnosed on anelectrocardiogram (ECG/EKG). The evaluation of atrial fibrillation involves a determination of the cause of the arrhythmia, and classification of the arrhythmia. Diagnostic investigation of AF typically includes a complete medical history and physical examination,ECG,transthoracic echocardiogram and blood tests.[30]
Numerous guidelines recommend opportunistic screening for atrial fibrillation in those 65 years and older. These organizations include the: European Society of Cardiology,[65]National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand,[66]European Heart Rhythm Society,[67][68]AF-SCREEN International Collaboration,[69]Royal College of Physicians of Edinburgh[70]European Primary Care Cardiovascular Society,[71] and Irish Health Information and Quality Authority.[72]
Single timepoint screening detects undiagnosed AF, which is often asymptomatic, in approximately 1.4% of people in people aged 65 years and older.[73][69] In 2022, theUnited States Preventive Services Task Force found insufficient evidence to determine the usefulness of routine screening.[74]
Some smartwatches may detect AF.[75]
Blood tests such ascomplete blood count,kidney function,electrolytes,glucose orHbA1c, andthyroid function is often determined in new-onset atrial fibrillation, to provide risk stratification and exclude certain etiology.[27]
Atrial fibrillation is diagnosed on an electrocardiogram (ECG), an investigation performed routinely whenever an irregular heartbeat 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.[29] At very fast heart rates, atrial fibrillation may look more regular, which may make it more difficult to separate from othersupraventricular tachycardias orventricular tachycardia.[76]
QRS complexes should be narrow, signifying that they are initiated by normal conduction of atrial electrical activity through theintraventricular 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 a 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 ambulatoryHolter 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 ambulatoryevent monitor.[27]
In general, a non-invasive transthoracicechocardiogram (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 identifyvalvular 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 predicts the 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.[29]
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.[citation needed]
A regular echocardiogram (transthoracic echocardiogram; TTE) has a low sensitivity for identifyingblood clots in the heart. If this is suspected (e.g. when planning urgent electrical cardioversion), atransesophageal echocardiogram (TEE, or TOE where British spelling is used) is preferred.[27]
The TEE has much better visualization of theleft atrial appendage than transthoracic echocardiography.[77] This structure, located in theleft atrium, is the place where a blood clot forms in more than 90% of cases in non-valvular (or non-rheumatic) atrial fibrillation.[78][79] TEE has a high sensitivity for locating thrombi in this area and can also detect sluggish blood flow in this area that is suggestive of blood clot formation.[77] If a blood clot is seen on TEE, then cardioversion is contraindicated due to the risk of stroke, and anticoagulation is recommended.
AHolter 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 regularly, 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.
| AF category | Defining characteristics |
|---|---|
| First detected | only one diagnosed episode |
| Paroxysmal | recurrent episodes that stop on their own in less than seven days |
| Persistent | recurrent episodes that last more than seven days |
| Long-standing Persistent | recurrent episodes that last more than twelve months |
| Permanent | AF that has been accepted, and for which a solely rate control strategy has been decided upon. |
TheAmerican College of Cardiology (ACC),American Heart Association (AHA), and theEuropean Society of Cardiology (ESC) recommend in their guidelines the following classification system based on simplicity and clinical relevance.[27][29]
All people with AF are initially in the category calledfirst 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 seven days and then another episode begins, later on, the category changes toparoxysmal AF. Although people in this category have episodes lasting up to seven days, in most cases of paroxysmal AF, the episodes will stop in less than 24 hours. If the episode lasts for more than seven days, it is unlikely to stop on its own and is then known aspersistent AF. In this case,cardioversion can be attempted to restore a normal rhythm. If an episode continues for a year or more, the rhythm is then known aslong-standing persistent AF. If a decision is made by the person and their medical team to accept persistent AF and not attempt restoration of a normal sinus rhythm but instead manage the AF by simply controlling the person's ventricular rate then the rhythm is referred to aspermanent AF. As a further subtype, AF that is detected only by an implanted or wearable cardiac monitor is known assubclinical AF.[27]
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 AF categories, which are mainly defined by episode timing and termination, the ACC/AHA and ESC guidelines describe additional outdated AF categories in terms of other characteristics of the person.[27]Valvular AF refers to AF attributable to moderate to severemitral valve stenosis or atrial fibrillation in the presence of amechanical artificial heart valve.[27] This distinction may be useful as it has implications on appropriate treatment, including differing recommendations for anticoagulation, but the term is discouraged as it may be confusing.[27][29] Other historically used definitions includelone AF – AF occurring in those aged under 60 in the absence of other cardiovascular or respiratory diseases. This description is also discouraged since it offers no clinical value.[29]Secondary AF refers to AF that occurs in the setting of another condition that have caused the AF, such asacute myocardial infarction,cardiac surgery,pericarditis,myocarditis,hyperthyroidism,pulmonary embolism,pneumonia, or another acute pulmonary disease.
Prevention of atrial fibrillation focuses primarily on preventing or controlling its risk factors. Many of its risk factors, such asobesity,smoking, lack of physical activity, andexcessive alcohol consumption, are modifiable and preventable with lifestyle modification or can be managed by a healthcare professional.[59]
Several healthy lifestyle behaviors are associated with a lower likelihood of developing atrial fibrillation. Accordingly, consensus guidelines recommend abstaining from alcohol and recreational drugs, stopping tobacco use, maintaining a healthy weight, and regularly participating in moderate-intensity physical activities.[59] Consistent moderate-intensityaerobic exercise, defined as achieving 3.0–5.9METs of intensity, for at least 150 minutes per week may reduce the risk of developing new-onset atrial fibrillation.[23] Few studies have examined the role of specific dietary changes and how it relates to the prevention of atrial fibrillation.[59]
The main goals of treatment are to preventcirculatory instability andstroke. Rate or rhythm control is used to achieve the former, whereasanticoagulation is used to decrease the risk of the latter.[80] If cardiovascularly unstable due to uncontrolledtachycardia, immediatecardioversion is indicated.[29] Manyantiarrhythmics, when used long term, increase the risk of death without any meaningful benefit.[81] An integrated management approach, which includes stroke prevention, symptoms control and management of associated comorbidities has been associated with better outcomes in patients with atrial fibrillation.[82][83][84][85]
This holistic or integrated care approach is summed up as the ABC (Atrial fibrillation Better Care) pathway,[86] as follows:
Regular aerobic exercise improves atrial fibrillation symptoms and AF-relatedquality of life.[23] The effect ofhigh-intensity interval training on reducing atrial fibrillation burden is unclear.[23] Weight loss of at least 10% is associated with reduced atrial fibrillation burden in people who are overweight or obese.[23]
For people who have both atrial fibrillation and obstructive sleep apnea, observational studies suggest thatcontinuous positive airway pressure (CPAP) treatment appears to lower the risk of atrial fibrillation recurrence after undergoing ablation.[23]Randomized controlled trials examining the role of obstructive sleep apnea treatment on atrial fibrillation incidence and burden are lacking.[23] Guideline-recommended lifestyle and medical interventions are recommended for people with atrial fibrillation and coexisting conditions such ashyperlipidemia, diabetes mellitus, or hypertension without specific blood sugar or blood pressure targets for people with atrial fibrillation.[23]
Bariatric surgery may reduce the risk of new-onset atrial fibrillation in people with obesity without AF and may reduce the risk of a recurrence of AF after an ablation procedure in people with coexisting obesity and atrial fibrillation.[23] It is important for all people with atrial fibrillation to optimize the control of all coexisting medical conditions that can worsen their atrial fibrillation, such ashyperthyroidism,diabetes,congestive heart failure,[87]high blood pressure,[88]chronic obstructive pulmonary disease,[89][90]stimulant use (e.g.,methamphetamine dependence), andexcessive alcohol consumption.[91]
Anticoagulation medication can be used to reduce the risk of stroke from AF. Anticoagulation medication is recommended in most people with increased risk of stroke,[13][92] which can be estimated using theCHA2DS2-VASc score.[29]
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.[93][94] The presence or absence of AF symptoms does not determine whether a person warrants anticoagulation and is not an indicator of stroke risk.[43]
Direct oral anticoagulant (DOAC) are recommended overwarfarin in atrial fibrillation.[29] In atrial fibrillation with presence of moderate to severe mitral stenosis or mechanical heart valve, warfarin is recommended over other therapies.[29] DOACs carry a lower risk of bleeding in the brain compared to warfarin,[94] although dabigatran is associated with a higher risk ofintestinal bleeding.[95]
Direct oral anticoagulant (DOAC), previously called "new", "novel", or "non-vitamin K antagonist" oral anticoagulant (NOAC), are medications taken orally that have another mechanism of action on thecoagulation cascade thanwarfarin.[96] DOACs recommended in atrial fibrillation includeapixaban,dabigatran,edoxaban andrivaroxaban.[29]
Antiplatelet drugs alone, such asaspirin ordual antiplatelet therapy withaspirin andclopidogrel, is not recommended as stroke prophylaxis in atrial fibrillation.[27][29][97][98][99][100][101][102] In those who are also on aspirin, DOACs appear to be better than warfarin.[103]
The optimal approach to anticoagulation in people with AF and who simultaneously have other diseases (e.g.,cirrhosis andend-stage kidney disease ondialysis) that predispose a person to both bleeding and clotting complications is unclear.[104][105]
Forvitamin K antagonists (VKA) such aswarfarin, time in therapeutic range (TTR) andINR variability are commonly used to assess the quality of VKA treatment. Patients who are unable to maintain a therapeutic INR on VKA, as indicated by low TTR and/or high INR variability, are at an increased risk of thromboembolic and bleeding events.[106] In these patients, treatment with a DOAC is recommended.[27] While there are no significant changes in adherence, persistence or clinical outcomes in patients switched from a VKA to a DOAC, an increase in therapy satisfaction has been reported.[107][108]
There are two ways to approach atrial fibrillation using medications: rate control and rhythm control. Both methods have similar outcomes.[109]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 long-term.
The risk of stroke appears to be lower with rate control versus attempted rhythm control, at least in those with heart failure.[110] 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.[111] 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.[112]
In those with a fast ventricular response, intravenousmagnesium significantly increases the chances of achieving successful rate and rhythm control in the urgent setting without major side-effects.[113] A person with poor vital signs, mental status changes, preexcitation, or chest pain often will go to immediate treatment with synchronized direct current cardioversion.[29] Otherwise, the decision of rate control versus rhythm control using medications is made. This is based on several criteria that include whether or not symptoms persist with rate control.
Rate control to atarget heart rate of fewer than 110 beats per minute is recommended in most people.[29] Lower heart rates may be recommended in those with left ventricular hypertrophy or reduced left ventricular function.[114] Rate control is achieved with medications that work by increasing the degree of the block at the level of theAV node, decreasing the number of impulses that conduct into the ventricles. This can be done with:[29][102]
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.[29]
After successful cardioversion, the heart may be stunned, which means that there is a normal rhythm, but the restoration of normal atrial contraction has not yet occurred.[117]
Catheter ablation (CA) is a procedure performed by anelectrophysiologist, acardiologist who specializes in heart rhythm problems, to restore the heart's normal rhythm by destroying, or electrically isolating, specific parts of the atria. A group of cardiologists led by DrHaïssaguerre fromBordeaux University Hospital [fr] noted in 1998 that thepulmonary veins are an important source of ectopic beats, initiating frequent paroxysms of atrial fibrillation, with these foci responding to treatment with radio-frequency ablation.[118] Most commonly, CA electrically isolates the left atrium from thepulmonary veins, where most of the abnormal electrical activity promoting atrial fibrillation originates.[119] CA is a form of rhythm control that restores normal sinus rhythm and reduces AF-associated symptoms more reliably than antiarrhythmic medications.[119]
Electrophysiologists generally use three forms ofcatheter ablation: radiofrequency (RF) ablation, cryoablation ("cryo"), orpulsed field (PF).[citation needed] In young people with little-to-no structural heart disease where rhythm control is desired and cannot be maintained by medication or cardioversion, ablation may be attempted and may be preferred over several years of medical therapy.[29][120] Although radiofrequency ablation has become an accepted intervention in selected younger people and may be more effective than medication at improving symptoms and quality of life, there is no evidence that ablation reduces all-cause mortality, stroke, or heart failure.[119] Some evidence indicates CA may be particularly helpful for people with AF who also have heart failure.[121] AF may recur in people who have undergone CA and nearly half of people who undergo it will require a repeat procedure to achieve long-term control of their AF.[119]
In general, CA is more successful at preventing AF recurrence if AF isparoxysmal as opposed topersistent.[122] As CA does not reduce the risk of stroke, many are advised to continue their anticoagulation.[119] Possible complications include common, minor complications such as the formation ofa collection of blood at the site where the catheter goes into the vein (access site hematoma), but also more dangerous complications including bleeding around the heart (cardiac tamponade),stroke, damage to theesophagus (atrio-esophagealfistula), or even death.[119][123] Use of pulsed field ablation as a non-thermal method of inducingelectroporation avoids damage to the phrenic nerve, esophagus, and blood vessels, while being at least as effective as thermal ablation methods.[124]
A hybrid convergent procedure has been developed which combines endocardial ablation with epicardial ablation, which can reduce AF recurrence to less than 5% for over one year.[125] The epicardial ablation is performed first, with a minimally invasive surgical approach.[126]
An alternative to catheter ablation is surgical ablation. Themaze 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. 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.[127] 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 is more likely to lead to the person being free from atrial fibrillation and off medications long-term after surgery and Cox-Maze IV procedure is the gold standard treatment. There is a slightly increased risk of needing a pacemaker following the procedure.[128][129][130] Less invasive modifications of the maze procedure have been developed, designated asminimaze procedures.
There is growing evidence thatleft atrial appendage occlusion therapy may reduce the risk of stroke in people with non-valvular AF as much as warfarin.[131][132] The addition of left atrial appendage isolation to catheter ablation has reduced AF recurrence by 80% in patients with persistent AF.[133]
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 the hospital varies from hours to days. This depends on the problem, the length of the operation, and whether or not general anesthetic 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.
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 three 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.[134] When AF occurs, management should primarily be rate and rhythm control. However, cardioversion may be used if the patient is hemodynamically unstable, highly symptomatic, or AF persists for six weeks after discharge. In persistent cases, anticoagulation should be used.
Atrial fibrillation can progress from infrequent occurrences to more frequent occurrences, ultimately becoming permanent.[135] Some cases do not progress, especially among patients with a healthy lifestyle.[136]
Many mechanisms contribute to cardiacremodeling leading to a worsening of atrial fibrillation, includingfibrosis,fatty infiltration,amyloidosis, andion channel modifications.[61] Fatty infiltration helps explain why obesity is a risk factor for atrial fibrillation in one fifth of patients.[61]
Atrial fibrillation increases the risk ofheart failure by 11 per 1000, kidney problems by 6 per 1000, death by 4 per 1000, stroke by 3 per 1000, andcoronary heart disease by 1 per 1000.[137] Women have a worse outcome overall than men.[138] Evidence increasingly suggests that atrial fibrillation is independently associated with a higher risk of developing dementia.[139]
Determining the risk of anembolism causing astroke is important for guiding the use ofanticoagulants. The most accurateclinical prediction rules is theCHA2DS2-VASc score.[13][140] The addition of blood based biomarkers such asNT-proBNP andneurofilament light chain improves risk prediction significantly.[141] A CHA2DS2-VASc score of zero is considered very low risk.[142]
In atrial fibrillation, the lack of an organized atrial contraction can result in some stagnant blood in the left atrium (LA) orleft atrial appendage (LAA). This lack of movement of blood can lead tothrombus formation (blood clotting). If the clot becomes mobile and is carried away by the blood circulation, it is called anembolus. An embolus proceeds through smaller and smallerarteries until it plugs one of them and prevents blood from flowing through the artery. This process results inend organ damage due to the loss of nutrients, oxygen, and the removal of cellular waste products. Emboli in the brain may result in anischemic stroke or atransient ischemic attack (TIA).
More than 90% of cases of thrombi associated with non-valvular atrial fibrillation evolve in the left atrial appendage.[78] 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.[143]
Atrial fibrillation has been independently associated with a higher risk of developingcognitive impairment,vascular dementia, andAlzheimer disease and with elevated levels ofneurofilament light chain in blood, a biomarker indicating neuroaxonal injury.[144][139][145] Several mechanisms for this association have been proposed, including silent small blood clots (subclinical microthrombi) traveling to the brain resulting in smallischemic strokes without symptoms, altered blood flow to the brain, inflammation, clinically silent small bleeds in the brain, and genetic factors.[146][139][145] Tentative evidence suggests that effective anticoagulation with direct oral anticoagulants or warfarin may be somewhat protective against AF-associated dementia and evidence of silent ischemic strokes onMRI but this remains an active area of investigation.[139][145]
Atrial fibrillation is the most common arrhythmia and affects more than 33 million people worldwide.[23] In Europe and North America, as of 2014[update], it affects about 2% to 3% of the population.[4] In the developing world, rates are about 0.6% for males and 0.4% for females.[4] The number of people diagnosed with AF has increased due to better detection of silent AF, increasing age and increase of conditions that predispose to it such asobesity and increasing survival from other forms ofcardiovascular disease.[27][29]
The rate of hospital admissions for AF has risen.[147] AF is the cause for 20% of allischemic strokes.[27] After atransient ischemic attack or stroke, about 11% are found to have a new diagnosis of atrial fibrillation.[148] 3% to 11% of patients with AF have structurally normal hearts.[149]
The number of new cases each year of AF increases with age. In younger people theprevalence is estimated to be 0.05% and is associated withcongenital heart disease or structural heart disease in this demographic.[150] As of 2001, it was anticipated that in developed countries, the number of people with atrial fibrillation was likely to increase during the following 50 years, due to the growing proportion of elderly people.[151]
Atrial fibrillation is more common in men than in women when reviewed in European and North American populations.[152] In developed anddeveloping countries, there is also a higher rate in men than in women. The risk factors associated with AF are also distributed differently according to gender. In men,coronary disease is more frequent, while in women, high systolic blood pressure andvalvular heart disease are more prevalent.[7]
Rates of AF are lower in populations of African descent than in populations of European descent. African descent is associated with a protective effect for AF, due to the lower presence ofSNPs withguaninealleles. European ancestry has more frequentmutations.[7] The variant rs4611994 for the genePITX2 is associated with risk of AF in African and European populations.[7][51] Hispanic and Asian populations have a lower risk of AF than European populations. The risk of AF in non-European populations is associated with characteristic risk factors of these populations, such ashypertension.[153]
Atrial fibrillation is an uncommon condition in children but sometimes occurs in association with certain inherited and acquired conditions.Congenital heart disease andrheumatic fever are the most common causes of atrial fibrillation in children. Other inherited heart conditions associated with the development of atrial fibrillation in children includeBrugada syndrome,short QT syndrome,Wolff Parkinson White syndrome, and other forms ofsupraventricular tachycardia (e.g.,AV nodal reentrant tachycardia).[150] Adults who survived congenital heart disease have an increased risk of developing AF. In particular, people who hadatrial septal defects,Tetralogy of Fallot, orEbstein's anomaly, and those who underwent theFontan procedure, are at higher risk with prevalence rates of up to 30% depending on the heart's anatomy and the person's age.[33]
Because the diagnosis of atrial fibrillation requires measurement of the electrical activity of the heart, atrial fibrillation was not truly described until 1874, whenEdmé Félix Alfred Vulpian observed the irregular atrial electrical behavior that he termed"fremissement fibrillaire" in dog hearts.[154] In the mid-18th century,Jean-Baptiste de Sénac made note of dilated, irritated atria in people withmitral stenosis.[155] The irregular pulse associated with AF was first recorded in 1876 byCarl 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".[156] Correlation of delirium cordis with the loss of atrial contraction, as reflected in the loss ofa waves in thejugular venous pulse, was made by Sir James MacKenzie in 1904.[157]Willem Einthoven published the first ECG showing AF in 1906.[158] 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.[159][160][161]
Atrial fibrillation occurs in other animals, includingcats,dogs, andhorses.[162][163] Unlike humans, dogs rarely develop the complications that stem from blood clots breaking off from inside the heart and traveling through the arteries to distant sites (thromboembolic complications).[162] Cats rarely develop atrial fibrillation but appear to have a higher risk of thromboembolic complications than dogs.[162]
Cats and dogs with atrial fibrillation often have underlying structural heart disease that predisposes them to the condition.[162] The medications used in animals for atrial fibrillation are largely similar to those used in humans.[162] Electricalcardioversion is occasionally performed in these animals, but the need forgeneral anesthesia limits its use.[162]Standardbred horses appear to be genetically susceptible to developing atrial fibrillation.[163] Horses that develop atrial fibrillation often have minimal or no underlying heart disease, and the presence of atrial fibrillation in horses can adversely affect physical performance.[163]
Report No.: 18-EHC018-EFReport No.: 2018-SR-04
Multiple studies have compared pharmacological rate and rhythm strategies but have failed to identify a superior therapy, a finding that extends to patients with HF. ... Antiarrhythmic drug therapy is indicated as first-line therapy for AF that remains symptomatic despite adequate rate control.
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