atrial fibrillation

心房細動

WordNet

1. of or relating to a cavity or chamber in the body (especially one of the upper chambers of the heart)
2. muscular twitching involving individual muscle fibers acting without coordination
3. act or process of forming fibrils

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/02/14 20:52:48」(JST)

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Atrial fibrillation
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.
ICD-10	I48
ICD-9	427.31
DiseasesDB	1065
MedlinePlus	000184
eMedicine	med/184 emerg/46
MeSH	D001281

Atrial fibrillation (AF or A-fib) is the most common cardiac arrhythmia (heart rhythm disorder). It may cause no symptoms, but it is often associated with palpitations, fainting, chest pain, or congestive heart failure. In some cases, however, AF is caused by otherwise idiopathic or benign conditions.

AF may be identified clinically when taking a pulse, and its presence can be confirmed with an electrocardiogram (ECG or EKG) that demonstrates the absence of P waves and an irregular ventricular rate.

In AF, the normal regular electrical impulses generated by the sinoatrial node are overwhelmed by disorganized electrical impulses usually originating in the roots of the pulmonary veins, leading to irregular conduction of ventricles impulses that generate the heartbeat. AF may occur in episodes lasting from minutes to days ("paroxysmal") or may be permanent in nature. A number of medical conditions increase the risk of AF, particularly 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 may be treated with medications to either slow the heart rate to a normal range ("rate control") or revert the heart rhythm to normal ("rhythm control"). Synchronized electrical cardioversion can 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 systemic embolism, people with AF may use anticoagulants such as warfarin, which substantially reduces these risks but may increase the risk of major bleeding, mainly in geriatric patients. The prevalence of AF in a population increases with age; 8% of people over 80 have AF. Chronic AF leads to a small increase in the risk of death.

Classification

Classification system

AF Category	Defining Characteristics
First detected	only one diagnosed episode
Paroxysmal	recurrent episodes that self-terminate 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 self-terminates in less than 7 days and then another episode begins later on, the case has moved into the category of paroxysmal AF. Although patients in this category have episodes lasting up to 7 days, in most cases of paroxysmal AF the episodes will self-terminate in less than 24 hours. If instead the episode lasts for more than 7 days, it is unlikely to self-terminate, and it is called persistent AF. In this case, the episode may be still terminated by cardioversion. If cardioversion is unsuccessful or not attempted and the episode is ongoing for a long time (e.g., a year or more), the patient's AF is called 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 which 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

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 angina (if the rate is faster and puts the heart under strain) and congestive symptoms of shortness of breath or edema. Sometimes the arrhythmia will be identified only 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 may be asymptomatic in many cases.

As most cases of AF are secondary to other medical problems, the presence of chest pain or angina, symptoms of hyperthyroidism (an overactive thyroid gland) such as weight loss and diarrhea, and symptoms suggestive of lung disease would indicate an underlying cause. A history of stroke or TIA, as well as hypertension (high blood pressure), diabetes, heart failure and rheumatic fever, may indicate whether someone with AF is at a higher risk of complications. A higher risk of embolus can be assessed using the CHADS2 score.

Rapid heart rate

Presentation is similar to other forms of rapid heart rate and in some cases may be asymptomatic. The patient may complain of palpitations or chest discomfort. 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 (paroxysmal nocturnal dyspnea), and may progress to swelling of the lower extremities (peripheral edema). Owing to inadequate blood flow, patients may also complain of light-headedness, may feel like they are about to faint (presyncope), or may actually lose consciousness (syncope).

The patient may be in significant respiratory distress. Because of inadequate oxygen delivery, the patient may appear blue (cyanosis). 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. It is most worrying if consistently lower than usual (hypotension). 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 an irregular but rapid rhythm.

Association with other conditions

• Central sleep apnea (CSA) – A study found that the prevalence of atrial fibrillation among patients with idiopathic central sleep apnea was significantly higher than the prevalence among patients with obstructive sleep apnea or no sleep apnea (27%, 1.7%, and 3.3%, respectively). There was a total of 180 subjects with 60 people in each of the 3 groups. 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

Diagnosis

A 12 lead ECG showing atrial fibrillation at approximately 150 beats per minute

The evaluation of atrial fibrillation involves diagnosis, determination of the etiology of the arrhythmia, and classification of the arrhythmia. The evaluation of atrial fibrillation typically entails a 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 which may include correlation of the heart rate response to exercise, exercise stress testing, chest X-ray, trans-esophageal echocardiography, and other studies.

If a patient presents with a sudden onset of severe symptoms other forms of tachyarrhythmia 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 electrocardiogram 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.

Screening

Screening for atrial fibrillation is not generally performed, although a study of routine pulse checks or ECGs during routine office visits found that the annual rate of detection of AF in elderly patients improved from 1.04% to 1.63%; selection of patients for prophylactic anticoagulation would improve stroke risk in that age category.

This estimated sensitivity of the routine primary care visit is 64%. This low result probably reflects the pulse not being checked routinely or carefully.

When ECGs are used for screening, the SAFE trial found that electronic software, primary care physicians and the combination of the two had the following sensitivities and specificities:

• Interpreted by software: sensitivity = 83%, specificity = 99%
• Interpreted by a primary care physician: sensitivity = 80%, specificity = 92%
• Interpreted by a primary care physician with software: sensitivity = 92%, specificity = 91%

Minimal evaluation

The minimal evaluation of atrial fibrillation should generally 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.

Routine bloodwork

While many cases of AF have no definite cause, it may be the result of various other problems (see below). Hence, renal function and electrolytes are routinely determined, as well as thyroid-stimulating hormone (commonly suppressed in hyperthyroidism and of relevance if amiodarone is administered for treatment) and a blood count.

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.

Electrocardiogram

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. 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 only shows 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.

Echocardiography

A non-invasive transthoracic echocardiogram (TTE) is generally 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.

Extended evaluation

An extended evaluation is generally not necessary in most individuals with atrial fibrillation, and is only performed 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.

Chest X-ray

A chest X-ray is generally only performed if a pulmonary cause of atrial fibrillation is suggested, or if other cardiac conditions are suspected (particularly 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.

Transesophageal echocardiogram

A normal echocardiography (transthoracic or TTE) has a low sensitivity for identifying thrombi (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 thrombus is formed 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 thrombus formation.

If no thrombus is seen on TEE, the incidence of stroke, (immediately after cardioversion is performed), is very low.^{[citation needed]}

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 if 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 if the shortness of breath is due to a blunted heart rate response to exertion caused by excessive AV node blocking agents, a very rapid heart rate during exertion, or due to 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.

Causes

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

• 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-aged women who consumed more than 2 drinks daily were 60% more likely to develop AF.
• Hyperthyroidism
• 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.

Genetics

Four type 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

Pathophysiology

Pathology

The primary pathologic change seen in atrial fibrillation is the progressive fibrosis of the atria. This fibrosis is primarily due 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 intra-cardiac pressures. 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 metaloproteinases 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.

Electrophysiology

Conduction
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 (muscle of the heart). When the myocardium is stimulated, it contracts. It is the ordered stimulation of the myocardium that allows efficient contraction of the heart, thereby allowing blood to be pumped to the body.

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.

Management

Main article: Management of atrial fibrillation

The main goals of treatment are to prevent circulatory instability and stroke. Rate or rhythm control are used to achieve the former, while anticoagulation is used to decrease the risk of the latter. If cardiovascularly unstable due to uncontrolled tachycardia, immediate cardioversion is indicated.

Anticoagulation

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 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.

Rate control versus rhythm control using drugs

AF can cause disabling and bothersome symptoms. Palpitations, chest discomfort, anxiety, and decreased exercise tolerance are related to rapid heart rate and inefficient cardiac output caused by AF. Furthermore, AF with a persistent rapid rate can cause a form of heart failure called tachycardia induced cardiomyopathy. This can significantly increase mortality and morbidity, which can be prevented by early and adequate treatment of the AF.

There are two ways to approach these symptoms using drugs: rate control and rhythm control. 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, while rate control is more important in the chronic phase. As far as mortality is concerned, the AFFIRM trial showed that there is lower mortality using rate control with anticoagulation treatment versus rhythm control treatment and the difference increases up to 5 years (end of study).

There is no difference in risk of stroke in patients who have converted to a normal rhythm with anti-arrhythmic treatment compared to those who have only rate control. 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 patients 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

Rate control is achieved with medications that work by increasing the degree of block at the level of the AV node, effectively 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 (particularly 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.

Cardioversion

Cardioversion is a noninvasive conversion of an irregular heartbeat to a normal heartbeat using electrical or chemical means.

• 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.

Vernakalant, an investigational drug which is unavailable in the U.S., has been found to safely and rapidly convert new onset atrial fibrillation in one published study.

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.

Ablation

In young patients 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.

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.

Following surgery

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.

Prognosis

Thromboembolism

See also: CHADS score

Prediction of embolism

Accurate prediction of whether a embolism will occur and cause a stroke is essential for guiding the decision to use anticoagulants. The most accurate clinical prediction rules are:

• CHADS2
• CHA2DS2-VASc

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. Thrombus can form anywhere in the body, while emboli follow the blood circulation to specific points in the body. 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.

Mitral valve

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 normal 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.

Epidemiology

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. 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.

History

Because the diagnosis of atrial fibrillation requires measurement of the electrical activity of the heart, atrial fibrillation was not truly described until 1874, when Edmé Félix Alfred Vulpian observed the irregular atrial electrical behavior that he termed "fremissement fibrillaire" in dog hearts. 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.

References

External links

• Atrial fibrillation on the Open Directory Project

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

• 1. 心房細動の概要 overview of atrial fibrillation
• 2. 新規発症した心房細動のマネージメント management of new onset atrial fibrillation
• 3. 発作性心房細動 paroxysmal atrial fibrillation
• 4. 心房細動：塞栓予防のための抗血栓治療 atrial fibrillation anticoagulant therapy to prevent embolization
• 5. 心房細動の疫学および危険因子 epidemiology of and risk factors for atrial fibrillation

English Journal

• Vascular mechanisms in the pathogenesis of stroke.

• Sierra C, Coca A, Schiffrin EL.SourceDepartment of Medicine, Sir Mortimer B. Davis-Jewish General Hospital and Lady Davis Institute for Medical Research, McGill University, 3755 Cote-Ste-Catherine Road, Montreal, QC, H3T 1E2, Canada, csierra@clinic.ub.es.
• Current hypertension reports.2011 Jun;13(3):200-7.
• Stroke is one of the most devastating manifestations of two common diseases, atherosclerosis and hypertension. It represents the second leading cause of death and a major cause of disability worldwide. Besides age (a nonmodifiable risk factor), hypertension is the most important cardiovascular risk
• PMID 21331606

• Atrial fibrillation and percutaneous coronary intervention: stroke, thrombosis, and bleeding.

• Gutierrez A, Rao SV.SourceDepartment of Medicine, Duke University School of Medicine, DUMC 3850, Durham, NC, 27710, USA, antonio.gutierrez@duke.edu.
• Current treatment options in cardiovascular medicine.2011 Jun;13(3):203-14.
• OPINION STATEMENT: Currently available data suggest that patients with atrial fibrillation (AF) undergoing percutaneous coronary intervention (PCI) with stenting who do not continue oral anticoagulation are at increased risk for mortality and morbidity. In this patient population, therapy directed a
• PMID 21340701

Japanese Journal

• 肥大型心筋症の周術期管理 (特集 心筋症患者の周術期管理)

• 尾前 毅
• 麻酔 63(1), 16-21, 2014-01
• NAID 40019935795

• Impact of Atrial Fibrillation Termination Site and Termination Mode in Catheter Ablation on Arrhythmia Recurrence

• Miyazaki Shinsuke,Taniguchi Hiroshi,Kusa Shigeki [他]
• Circulation journal : official journal of the Japanese Circulation Society 78(1), 78-84, 2014-01
• NAID 40019925869

• Prediction of Congestive Heart Failure in Patients with Non Valvular Atrial Fibrillation

• Imai Koichiro,Okura Hiroyuki,Tamada Tomoko,Fukuhara Kenzo,Koyama Terumasa,Kume Teruyoshi,Hayashida Akihiro,Kawamoto Takahiro,Neishi Yoji,Yoshida Kiyoshi
• Internal Medicine 53(1), 7-12, 2014
• … Objective Patients with atrial fibrillation (AF) have an increased risk of congestive heart failure (CHF) as well as ischemic stroke. …
• NAID 130003383772

Related Links

• Atrial Fibrillation Resource Biosense Webster - Atrial Fibrillation

Resource for the advancement of the diagnosis and treatment of atrial fibrillation and offers clinical and scientific information for the medical professional and patient education materials. Johnson and Johnson Medical NV/SA.

• Atrial fibrillationとは - goo Wikipedia (ウィキペディア)

The evaluation of atrial fibrillation involves diagnosis, determination of the etiology of the arrhythmia, and classification of the arrhythmia. The evaluation of atrial fibrillation typically entails a history and physical examination, ECG ...

• Atrial Fibrillation

Atrial Fibrillation (AF) and Risk of Stroke Stroke is one of the most serious consequences of atrial fibrillation (AF): People with AF are up to 5 times more likely to have a stroke than someone without AF 2 In 2011, it is estimated that ...

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★リンクテーブル★

リンク元	「心房細動」「AF」「Af」
拡張検索	「nonvalvular atrial fibrillation」
関連記事	「atrial」

「心房細動」

　　[★]

英

atrial fibrillation, AF, AFIB

関

心房粗動、心室細動

定義

• 心房細動は心房が高頻度に、しかも同期せずに興奮する状態である。その結果、心房は心室に血液を送るための律動的な収縮を行えなくなり、また心室の興奮も不規則となる。 (参考2)

分類

参考2

• 発作性心房細動

• 自然停止する心房細動

• 持続性心房細動

• 停止に薬物などを必要とするものを持続性心房細動

• 孤立性心房細動

• 基礎心疾患を認めず，高血圧もない症例に出現した心房細動

• 永続性心房細動

原因

• 原発性

• 加齢によるもの

• 他の疾患に続発

• 若年性の心房細動は要注意

心房細動を合併しやすい病態

医学大事典

• 虚血性心疾患、高血圧症、リウマチ性心疾患、心筋症、呼吸器疾患、甲状腺機能亢進症、高齢者心房中隔欠損症、WPW症候群など

心房負荷で僧帽弁狭窄症を来しやすい

危険因子 QB.C-410

• 高齢者(65歳以上)
• 脳卒中の既往
• 高血圧
• 心不全
• 心房・心室拡大

症状

• 頻拍に因る：動悸、胸部圧迫感
• 拍出量低下による：(器質的心疾患のある場合)心不全
• 心房収縮低下による：心房内血栓形成　→　血栓塞栓症

• 血栓塞栓症は心房細動の時と心房細動から洞調律に復帰させるときに起こりやすい。

心電図

• 着目する誘導：P波 = II誘導、f波 = V1誘導
• 1. f波の出現(400-700/分(EAB.160), 350-600/分(PHD.295))←多数興奮旋回 multiple reentry
• 2. P波の欠如
• 3. RR間隔が不整　←　f波が時々心室に伝わるため

絶対性不整脈

[show details]

治療

QB.C-410

• 血行動態が不安定：電気的除細動
• 血行動態が安定　：2-3週間抗凝固療法を行ってから薬物的な除細動Class Ia(APD↑), Class Ic(APD±)

• 48-72時間以内に新規発症した心房細動では抗凝固療法不要
• 経食道心エコーにより左房内血栓を認めなければ、除細動施行。
• 慢性経過(6ヶ月程度)した慢性心房細動では除細動を行っても再発する率が高いので、除細動の適応にはならない？？？？

概要

• 薬物療法と抗凝固療法を施行する
• electrical direct-current cardioversionによる洞調律の回復は、頻脈の時にすべき(心房の興奮が心室に伝導しているとき)
• カテーテルアブレーションは症状があって、かつ他の内科的治療法が奏効しない特に行う
• 外科治療はMaze手術がある

薬物治療

• 心室への興奮の伝達を抑制：Class II, class IV, or digitalis
• 除細動　　　　　　　　　：Class Ia(APD↑), Class Ic(APD±), Class III

薬物治療 (不整脈薬物治療に関するガイドライン Guidelines for Drug Treatment of Arrhythmias (JCS 2004))

心機能の低下	第一選択	第二選択
正常*	Naチャネル阻害薬	Na チャネル遮断薬
	slow drug	intermediate
	ジソピラミド	プロカインアミド
	シベンゾリン	キニジン
	ピルジカイニド	プロパフェノン
		アプリンジン
軽度*	Na チャネル遮断薬
	intermediate
	プロカインアミド
	キニジン
	プロパフェノン
	アプリンジン
中度以上	Na チャネル遮断薬
	intermediate
	プロカインアミド
	キニジン
	アプリンジン

抗凝固療法

• ワーファリンはINR 1.6-2.5に調節。欧米では2.0-3.0。　(QB.C347)日本人ではPT-INRを1.5-2.0に設定。　治療域が狭く個人差が大きいのでPT-INRをモニターする。

• CHADS2

• C cardiac failure
• H hypertension
• A age >75yr
• D disbites mellitus
• S2 prior stroke or TIA

• score

0 LOW: aspirin 81-325 mg PO dialy

1 MODERATE: aspirin or warfarin

2 MODERATE: previous CVA/TIA/embolism? YES: warfarin/NO: aspirin or warfarin

3-6 HIGH: warfarin

外科的療法 (NSU.440)

• 適応

• 再発性の発作性心房細動で患者の社会生活に障害が生じているもの
• 塞栓症の既往のある心房細動
• 冠状動脈疾患、僧帽弁膜症、心房中隔欠損症などのため手術を受ける症例で、発作性あるいは慢性心房細動を有する症例

• 右心房、心房中隔、左心房に切り込みを入れ一方向性の伝導しか起こらなくする。
• Coxが創案し、手術法はMazeIII法と呼ばれる。

心房細動の存在により面倒くさくなること

• 僧帽弁狭窄症：心拍出量↓
• WPW症候群：偽性心室頻拍

• 心原性脳塞栓症

参考

• 1. 不整脈薬物治療に関するガイドライン（2009年改訂版）

[display]http://www.j-circ.or.jp/guideline/pdf/JCS2009_kodama_h.pdf

• 2. 不整脈薬物治療に関するガイドライン Guidelines for Drug Treatment of Arrhythmias (JCS 2004)

国試

• 103I060、100D014

「AF」

　　[★]

• 心房細動 atrial fibrillation
• 自律神経不全症 autonomic failure

「Af」

　　[★]

同

atrial fibrillation, 心房細動

「nonvalvular atrial fibrillation」

　　[★]

非弁膜性心房細動、非弁膜症心房細動

「atrial」

　　[★]

• adj.

• 心房性の、心房の

関

atria、atrium、heart atria、heart atrium