Atrial fibrillation

Atrial fibrillation (AF or afib) is a cardiac arrhythmia (abnormal heart rhythm) that involves the two upper chambers (atria) of the heart. It is defined as being irregularly irregular, and can often be identified as such when taking a pulse. Atrial fibrillation is the most common arrhythmia; risk increases with age, with 8% of people over 80 having AF. In atrial fibrillation, the electrical impulses that are normally generated by the sinoatrial node are replaced by disorganized activity in the atria, leading to irregular conduction of impulses to the ventricles that generate the heartbeat. The result is an irregular heartbeat. This may be continuous (persistent or permanent AF) or alternating between periods of a normal heart rhythm (paroxysmal AF). The natural tendency of atrial fibrillation is to become a chronic condition. Chronic AF leads to an increased risk of death.^[1]

Atrial fibrillation is often asymptomatic, and is not in itself generally life-threatening, but may result in palpitations, fainting, chest pain, or congestive heart failure. Patients with atrial fibrillation are at significantly increased chance of stroke (about 2 to 7 times the regular population), and AF is a leading cause of stroke.^[2]

Atrial fibrillation may be treated with medications which either slow the heart rate or revert the heart rhythm back to normal. Synchronized electrical cardioversion may also be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent recurrence of atrial fibrillation in certain individuals. People with AF are often given anticoagulants such as warfarin to protect them from stroke.

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Classification

The American Heart Association, American College of Cardiology, and the European Society of Cardiology have proposed the following classification system based on simplicity and clinical relevance.^[3]

• First detected atrial fibrillation: any patient newly diagnosed with atrial fibrillation fits in this category, as the exact onset and chronicity of the disease is often uncertain.
• Recurrent atrial fibrillation: any patient with 2 or more identified episodes of atrial fibrillation is said to have recurrent atrial fibrillation. This is further classified into paroxysmal and persistent based on when the episode terminates without therapy. Atrial fibrillation is said to be paroxysmal when it terminates spontaneously within 7 days, most commonly within 24 hours. Persistent or chronic atrial fibrillation is AF established for more than seven days. Differentiation of paroxysmal from chronic or established AF is based on the history of recurrent episodes and the duration of the current episode of AF.^[3][4][5]
• Lone atrial fibrillation (LAF) is defined as atrial fibrillation in the absence of clinical or echocardiographic findings of cardiopulmonary disease.^[3] Patients with LAF who are under 65 have the best prognosis.

Signs and symptoms

Atrial fibrillation is usually accompanied by symptoms related to the rapid heart rate. Rapid and irregular heart rates may be perceived as palpitations, exercise intolerance, and occasionally 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, stroke symptoms resolving within 24 hours). It is not uncommon to identify atrial fibrillation on a routine physical examination or electrocardiogram (ECG/EKG), as it may be asymptomatic in many cases.^[3]

As most cases of atrial fibrillation 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 previous history of stroke or TIA, as well as hypertension (high blood pressure), diabetes, heart failure and rheumatic fever, may indicate whether someone with atrial fibrillation is at a higher risk of complications.^[3]

Diagnosis

The evaluation of atrial fibrillation involves diagnosis, determination of the etiology of the arrhythmia, and classification of the arrhythmia. A minimal evaluation performed should be performed in all individuals with atrial fibrillation. This includes a history and physical examination, surface electrocardiogram, transthoracic echocardiogram, and routine bloodwork. Certain individuals may benefit from an extended evaluation which may include an evaluation of the heart rate response to exercise, exercise stress testing, a chest x-ray, trans-esophageal echocardiography, and other studies.

Screening

Screening for atrial fibrillation is not generally performed, although a study of routine pulse checks or electrocardiograms during routine office visits, found that the annual rate of detection of atrial fibrillation in elderly patients improved from 1.04% to 1.63%; selection of patients for prophylactic anticoagulation would improve stroke risk in that age category.^[6]

Routine primary care visit

This estimated sensitivity of the routine primary care visit is 64%. This low result probably reflects the pulse not being checked routinely or carefully.^[6]

Minimal evaluation

The minimal evaluation of atrial fibrillation should generally be performed in all individuals with atrial fibrillation. 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 be then performed.

History and physical examination

The history of the individual's atrial fibrillation episodes is likely the most important part of the evaluation. Distinctions should be made to those who are entirely asymptomatic when they are in atrial fibrillation (in which case the atrial fibrillation is found as an incidental finding on an electrocardiogram or physical examination) and those who have gross and obvious symptoms due to atrial fibrillation and can pinpoint whenever they go into atrial fibrillation and 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.^[3]

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.^[3]

Electrocardiogram

Main article: Electrocardiogram

Atrial fibrillation is diagnosed on an electrocardiogram, an investigation performed routinely whenever irregular heart beat is suspected. Characteristic findings are the absence of P waves, with unorganized electrical activity in their place, and irregularity of R-R interval due to irregular conduction of impulses to the ventricles.^[3]

When electrocardiograms 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:^[7]:

• 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%

If paroxysmal AF is suspected but the electrocardiogram shows a regular rhythm, episodes may be documented with the use of Holter monitoring (continuous ECG recording for 24 hours). If the symptoms are very infrequent, longer periods of continuous monitoring may be required.^[3]

Echocardiography

Main article: Echocardiogram

A transthoracic (non-invasive) echocardiogram 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 increase the risk of stroke manifold), 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 ventricular hypertrophy and pericardial disease.^[3]

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 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

Main article: Chest X-ray

A chest X-ray is generally only performed if a pulmonary cause of atrial fibrillation is suggested. This may reveal an underlying problem in the lungs or the blood vessels in the chest. ^[3] 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) is preferred.^[3]

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 most commonly is formed in the setting of atrial fibrillation or flutter. TEE has a very high sensitivity for locating thrombus in this area^{[citation needed]} and can also detect sluggish bloodflow in this area that is suggestive of thrombus formation.^{[citation needed]}

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

Ambulatory holter monitoring

Main article: Holter monitor

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

Main article: Cardiac stress test

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 due to 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.

Etiology

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")
• Hyperthyroidism
• Carbon monoxide poisoning
• Dual-chamber pacemakers in the presence of normal atrioventricular conduction.^[8]
• A family history of AF increases risk by 30%.^[9] Various genetic mutations may be responsible.^[10]

Pathophysiology

Morphology

The primary pathologic change seen in atrial fibrillation is the progressive fibrosis of the atria. This fibrosis is primarily due to atrial dilatation, however genetic causes and inflammation may have a cause in some individuals.

Dilatation of the atria can be due to most 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 dilatation 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,^{[citation needed]} suggesting that dysfunction of the SA node is progressive with prolonged episodes of atrial fibrillation.

Electrophysiology

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

In atrial fibrillation, the regular impulses produced by the sinus node to provide rhythmic contraction of the heart are overwhelmed by the rapid randomly generated electrical discharges produced by larger areas of atrial tissue, often localized to the pulmonary veins. It can be distinguished from atrial flutter, which is a more organized electrical circuit usually in the right atrium that produces characteristic saw-toothed p-waves on the electrocardiogram; in atrial flutter, the discharges circulate rapidly (at a rate of 300 beats per minute) around the atrium; in AF, there is no regularity of this kind at all.

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

Treatment

The main goals of treatment of atrial fibrillation are to prevent temporary circulatory instability and to prevent stroke. Rate and rhythm control are principally used to achieve the former, while anticoagulation may be required to decrease the risk of the latter.^[11] In emergencies, when circulatory collapse is imminent due to uncontrolled tachycardia, immediate cardioversion may be indicated.^[3]

The primary factors determining atrial fibrillation treatment are duration and evidence of hemodynamic instability. Cardioversion is indicated with new onset AF (for less than 48 hours) and with hemodynamic instability. If rate and rhythm control can not be maintained by medication or cardioversion, electrophysiological studies with pathway ablation may be required.^[3]

Anticoagulation

Patients with atrial fibrillation, even lone atrial fibrillation without other evidence of heart disease, are at increased risk of stroke during long term follow up.^[12] A systematic review of risk factors for stroke in patients with nonvalvular atrial fibrillation concluded that a prior history of stroke or TIA is the most powerful risk factor for future stroke, followed by advancing age, hypertension, diabetes.^[13] The risk of stroke increases whether the lone atrial fibrillation was an isolated episode, recurrent, or chronic.^[14] The risk of systemic embolization (atrial clots migrating to other organs) depends strongly on whether there is an underlying structural problem with the heart (e.g. mitral stenosis) and on the presence of other risk factors, such as diabetes and high blood pressure. Finally, patients under 65 are much less likely to develop embolization compared with patients over 75. In young patients with few risk factors and no structural heart defect, the benefits of anticoagulation may be outweighed by the risks of hemorrhage (bleeding). Those at a low risk may benefit from mild (and low-risk) anticoagulation with aspirin (or clopidogrel in those who are allergic to aspirin). In contrast, those with a high risk of stroke derive most benefit from anticoagulant treatment with warfarin or similar drugs.

In the United Kingdom, the NICE guidelines recommend using a clinical prediction rule for this purpose.^[15] The CHADS/CHADS2 score is the best validated clinical prediction rule for determining risk of stroke (and therefore who should be anticoagulated); it assigns points (totaling 0-6) depending on the presence or absence of co-morbidities such hypertension and diabetes. In a comparison of seven prediction rules, the best rules were the CHADS2 which performed similarly to the SPAF^[16] and Framingham^[17] prediction rules. ^[18]

To compensate for the increased risk of stroke, anticoagulants may be required. However, in the case of warfarin, if a patient has a yearly risk of stroke that is less than 2%, then the risks associated with taking warfarin outweigh the risk of getting a stroke. ^[19][20]

Atrial fibrillation in the context of mitral stenosis is associated with a seventeen-fold increase in stroke risk.^[2]

Acute anticoagulation

If anticoagulation is required urgently (e.g. for cardioversion), heparin or similar drugs achieve the required level of protection much quicker than warfarin, which may take several days to reach adequate levels.

In the initial stages after an embolic stroke, anticoagulation may be risky, as the damaged area of the brain is relatively prone to bleeding (hemorrhagic transformation).^[21] As a result, a clinical practice guideline by National Institute for Health and Clinical Excellence recommends that anticoagulation should begin two weeks after stroke if no hemorrhage occurred.^[15]

Chronic anticoagulation

Among patients with "non-valvular" atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%. ^[22][23]. There is evidence that aspirin and clopidogrel are effective when used together, but the combination is still inferior to warfarin.^[24]

Warfarin treatment requires frequent monitoring with a blood test called the international normalized ratio (INR); this determines whether the correct dose is being used. In atrial fibrillation, the usual target INR is between 2.0 and 3.0 (higher targets are used in patients with mechanical artificial heart valves, many of whom may also have atrial fibrillation). A high INR may indicate increased bleeding risk, while a low INR would indicate that there is insufficient protection from stroke.

Elderly patients

The very elderly (patients aged 75 years or more) may benefit from anticoagulation provided that their anticoagulation does not increase hemorrhagic complications, which is a difficult goal. Patients aged 80 years or more may be especially susceptible to bleeding complications, with a rate of 13 bleeds per 100 person-years.^[25] A rate of 13 bleeds per 100 person years would seem to preclude use of warfarin; however, a randomized controlled trial found benefit in treating patients 75 years or over with a number needed to treat of 50.^[26] Of note, this study had very low rate of hemorrhagic complications in the warfarin group.

Rate control versus rhythm control

AF can cause disabling and annoying symptoms. Palpitations, angina, lassitude (weariness), and decreased exercise tolerance are related to rapid heart rate and inefficient cardiac output caused by AF. 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: rate control and rhythm control. Rate control treatments seek to reduce the heart rate to normal, usually 60 to 100 beats per minute. Rhythm control seeks to restore the normal heart rhythm, called normal sinus rhythm. Studies suggest that rhythm control is mainly a concern in newly diagnosed AF, while rate control is more important in the chronic phase. Rate control with anticoagulation is as effective a treatment as rhythm control in long term mortality studies, the AFFIRM Trial.^[27]

The AFFIRM study showed no difference in risk of stroke in patients who have converted to a normal rhythm with anti-arrhythmic treatment, compared to those who have only rate control.^[27]

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 down into the ventricles. This can be done with:^[3]

• Beta blockers (preferably the "cardioselective" beta blockers such as metoprolol, atenolol, bisoprolol)
• Cardiac glycosides (i.e. digoxin)
• Calcium channel blockers (i.e. diltiazem or verapamil)

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).

Cardioversion

Main article: Cardioversion

Rhythm control methods include electrical and chemical cardioversion:^[3]

• 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^[28], procainamide, ibutilide, propafenone or flecainide.

The main risk of cardioversion is systemic embolization of a thrombus (blood clot) from the previously fibrillating left atrium. Cardioversion should not be performed without adequate anticoagulation in patients with more than 48 hours of atrial fibrillation. Cardioversion may be performed in instances of AF lasting more than 48 hours if a transesophogeal echocardiogram (TEE) demonstrates no evidence of clot within the heart.^[3]

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

Maintenance of sinus rhythm

The mainstay of maintaining sinus rhythm is the use of antiarrhythmic agents. Recently, other approaches have been developed that promise to decrease or eliminate the need for antiarrhythmic agents.

Antiarrhythmic agents

Main article: Antiarrhythmic agent

The anti-arrhythmic medications often used in either pharmacological cardioversion or in the prevention of relapse to AF alter the flux of ions in heart tissue, making them less excitable, setting the stage for spontaneous and durable cardioversion. These medications are often used in concert with electrical cardioversion.

Radiofrequency ablation

In patients with AF where rate control drugs are ineffective and it is not possible to restore sinus rhythm using cardioversion, non-pharmacological alternatives are available. For example, to control rate it is possible to destroy the bundle of cells connecting the upper and lower chambers of the heart - the atrioventricular node - which regulates heart rate, and to implant a pacemaker instead. A more complex technique, which avoids the need for a pacemaker, involves ablating groups of cells near the pulmonary veins where atrial fibrillation is thought to originate, or creating more extensive lesions in an attempt to prevent atrial fibrillation from establishing itself.^[3]

Ablation is a newer technique and has shown some promise for cases of recurrent AF that are unresponsive to conventional treatments. Radiofrequency ablation (RFA) uses radiofrequency energy to destroy abnormal electrical pathways in heart tissue. The energy emitting probe (electrode) is placed into the heart through a catheter inserted into veins in the groin or neck. Electrodes that can detect electrical activity from inside the heart are also inserted, and the electrophysiologist uses these to "map" an area of the heart in order to locate the abnormal electrical activity before eliminating the responsible tissue.

Most AF ablations consist of isolating the electrical pathways from the pulmonary veins (PV)^[29], which are located on the posterior wall of the left atrium. All veins from the body (including neck and groin) lead to the right atrium, so in order to get to the left atrium the catheters must get across the atrial septum. This is done by piercing a small hole in the septal wall. This is called a transeptal approach. Once in the left atrium, the physician may perform Wide Area Circumferential Ablation (WACA) to electrically isolate the PVs from the left atrium.^[30]

Some more recent approaches to ablating AF is to target sites that are particularly disorganized in both atria as well as in the coronary sinus (CS). These sites are termed complex fractionated atrial electrogram (CFAE) sites.^[31]. It is believed by some that the CFAE sites are the cause of AF, or a combination of the PVs and CFAE sites are to blame. New techniques include the use of cryoablation (tissue freezing using a coolant which flows through the catheter), and microwave ablation, where tissue is ablated by the microwave energy "cooking" the adjacent tissue.

This is an area of active research, especially with respect to the RF ablation technique and emphasis on isolating the pulmonary veins that enter into the left atrium. The main problem in 2006 is that the procedure is only 70-80% effective at best -- and causes stroke in about 1% of patients.

Surgical Maze procedure

Main article: Maze procedure

James Cox, MD, and associates developed the Cox maze procedure, an open-heart surgical procedure intended to eliminate atrial fibrillation, and performed the first one in 1987. "Maze" refers to the series of incisions made in the atria, which are arranged in a maze-like pattern. The intention was to eliminate AF by using incisional scars to block abnormal electrical circuits (atrial macroreentry) that AF requires. This procedure required an extensive series of endocardial (from the inside of the heart) incisions through both atria, a median sternotomy (vertical incision through the breastbone) and cardiopulmonary bypass (heart-lung machine). A series of improvements were made, culminating in 1992 in the Cox maze III procedure, which is now considered to be the "gold standard" for effective surgical cure of AF. The Cox maze III is sometimes referred to as the "traditional maze", the "cut and sew maze", or simply the "maze".^[32]

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

Epidemiology

Atrial fibrillation is the most common arrhythmia found in clinical practice.^{[citation needed]} It also accounts for 1/3 of hospital admissions for cardiac rhythm disturbances^{[citation needed]}, and the rate of admissions for atrial fibrillation has risen in recent years.^[33] Approximately 2.2 million individuals in the United States and 4.5 million individuals in the European Union have atrial fibrillation.^[3][34]

The incidence of atrial fibrillation increases with age. The prevalence in individuals over the age of 80 is about 8%.^[35] In developed countries, the number of patients with atrial fibrillation is likely to increase during the next 50 years, due to the growing proportion of elderly individuals.^[36]

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.^[37] In the mid-eighteenth century, Jean-Baptiste de Sénac made note of dilated, irritated atria in people with mitral stenosis.^[38] 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".^[39] 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.^[40] Willem Einthoven published the first electrocardiogram showing AF in 1906.^[41] 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.^[42][43][44]

See also

• Atrial flutter
• Ashman phenomenon

References

[pt:Fibrilação auricular]]