Atrial fibrillation

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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
Patient UK Atrial fibrillation
MeSH D001281

Atrial fibrillation (AF or A-fib) is the most common abnormal heart rhythm. It may cause no symptoms, but is often associated with palpitations, fainting, chest pain, or congestive heart failure. The cause of an individual's AF may not be identified.

AF may be identified clinically when taking a pulse, and its presence can be confirmed with an electrocardiogram (ECG) that demonstrates the absence of P waves and an irregular ventricular rate.[1]

In AF, the normal regular electrical impulses generated by the sinoatrial node in the right atrium of the heart are overwhelmed by disorganized electrical impulses usually originating in the roots of the pulmonary veins. This leads to irregular conduction of ventricular impulses that generate the heartbeat. AF may occur in episodes lasting from minutes to days (paroxysmal AF) or may be permanent in nature. Many medical conditions increase the risk of AF, in particular mitral stenosis (narrowing of the mitral valve of the heart).

The risk of stroke is increased fivefold in individuals with AF.[2] The degree of increased risk may be substantial, depending on the presence of additional risk factors (such as high blood pressure). AF is often treated with medications to slow the heart rate to a normal range (known as rate control) or to correct the heart rhythm to normal sinus rhythm (known as rhythm control). Synchronized electrical cardioversion can also be used to convert AF to a normal heart rhythm. Surgical and catheter-based ablation may be used to prevent recurrence of AF in some individuals.

Depending on the risk of stroke and blood clot formation, people with AF may use anti-clotting medications such as warfarin, which substantially reduces these risks but may increase the risk of major bleeding, mainly in older patients. The prevalence of AF in a population increases with age; 8% of people over the age of 80 have AF. Chronic AF leads to a small increase in the risk of death.

Signs and symptoms[edit]

AF is usually accompanied by symptoms related to a rapid heart rate. Rapid and irregular heart rates may be perceived as palpitations or exercise intolerance and occasionally may produce anginal chest pain (if the high heart rate causes ischemia). Other possible symptoms include congestive symptoms such as shortness of breath or swelling. The arrhythmia is sometimes only identified with the onset of a stroke or a transient ischemic attack (TIA). It is not uncommon for a patient to first become aware of AF from a routine physical examination or ECG, as it is often does not cause symptoms.[3]

Since most cases of AF are secondary to other medical problems, the presence of chest pain or angina, signs and symptoms of hyperthyroidism (an overactive thyroid gland) such as weight loss and diarrhea, and symptoms suggestive of lung disease can indicate an underlying cause. A history of stroke or TIA, as well as high blood pressure, diabetes, heart failure, or rheumatic fever may indicate whether someone with AF is at a higher risk of complications.[3] The risk of a blood clot forming in the left atrium, breaking off, and then traveling in the bloodstream can be assessed using the CHADS2 score or CHA2DS2-VASc score.

Rapid heart rate[edit]

Presentation is similar to other forms of rapid heart rate and may be asymptomatic.[4] Palpitations and chest discomfort are common complaints.[4] 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,[4] shortness of breath when lying flat, and sudden onset of shortness of breath during the night. This may progress to swelling of the lower extremities. Due to inadequate blood flow, individuals with AF may also complain of light-headedness,[4] may feel like they are about to faint, or may actually lose consciousness.

AF can cause significant respiratory distress. Inadequate oxygen delivery may cause a blue appearance. By definition, the heart rate will be greater than 100 beats per minute. Blood pressure will be variable, and often difficult to measure as the beat-by-beat variability causes problems for most digital (oscillometric) non-invasive blood pressure monitors. Low blood pressure is most concerning. Respiratory rate will be increased in the presence of respiratory distress. Pulse oximetry may confirm the presence of hypoxia related to any precipitating factors such as pneumonia. Examination of the jugular veins may reveal elevated pressure (jugular venous distention). Lung exam may reveal crackles, which are suggestive of pulmonary edema. Heart exam will reveal a rapid irregular rhythm.

Associated conditions[edit]


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


Four types of genetic disorder are associated with atrial fibrillation:[11]



The primary pathologic change seen in atrial fibrillation is the progressive fibrosis of the atria. This fibrosis is due primarily to atrial dilation, however genetic causes and inflammation may have a cause in some individuals. One study found that atrial dilation can occur as a consequence of AF,[12] although another study found that AF by itself does not cause it.[13]

Dilation of the atria can be due to almost any structural abnormality of the heart that can cause a rise in the pressure within the heart. This includes valvular heart disease (such as mitral stenosis, mitral regurgitation, and tricuspid regurgitation), hypertension, and congestive heart failure. Any inflammatory state that affects the heart can cause fibrosis of the atria. This is typically due to sarcoidosis but may also be due to autoimmune disorders that create autoantibodies against myosin heavy chains. Mutation of the lamin AC gene is also associated with fibrosis of the atria that can lead to atrial fibrillation.

Once dilation of the atria has occurred, this begins a chain of events that leads to the activation of the renin aldosterone angiotensin system (RAAS) and subsequent increase in matrix metalloproteinases and disintegrin, which leads to atrial remodeling and fibrosis, with loss of atrial muscle mass. This process is not immediate, and experimental studies have revealed patchy atrial fibrosis may precede the occurrence of atrial fibrillation and may progress with prolonged durations of atrial fibrillation.

Fibrosis is not limited to the muscle mass of the atria, and may occur in the sinus node (SA node) and atrioventricular node (AV node), correlating with sick sinus syndrome. Prolonged episodes of atrial fibrillation have been shown to correlate with prolongation of the sinus node recovery time,[3][14][15] suggesting that dysfunction of the SA node is progressive with prolonged episodes of atrial fibrillation.


Sinus rhythm
Heart conduct sinus.gif
Atrial fibrillation
Heart conduct atrialfib.gif

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

There are multiple theories about the etiology of atrial fibrillation. An important theory is that, in atrial fibrillation, the regular impulses produced by the sinus node for a normal heartbeat are overwhelmed by rapid electrical discharges produced in the atria and adjacent parts of the pulmonary veins. Sources of these disturbances are either automatic foci, often localized at one of the pulmonary veins, or a small number of localized sources in the form of either reentrant electrical spiral waves (rotors) or repetitive focal beats; these localized sources may be found in the left atrium near the pulmonary veins or in a variety of other locations through both the left or right atrium.

Because recovery of the atria from excitation is heterogeneous, the electrical waves generated by the AF sources undergo repetitive, spatially distributed breakup and fragmentation in a process known as "fibrillatory conduction". Another theory is the multiple wavelet theory first formulated by Moe,[16] 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.[17]


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

The evaluation of atrial fibrillation involves determination of the cause of the arrhythmia, and classification of the arrhythmia. Diagnostic investigation of AF typically includes a complete history and physical examination, ECG, transthoracic echocardiogram, complete blood count, and serum thyroid stimulating hormone level.[4] Depending upon given resources, afflicted individuals may benefit from an in-depth evaluation that may include correlation of the heart rate response to exercise, exercise stress testing, chest X-ray, transesophageal echocardiography, and other studies.[citation needed]

If a patient presents with a sudden onset of severe symptoms, other forms of abnormal heart rhythm with high heart rate must be ruled-out, as some may be immediately life-threatening, such as ventricular tachycardia. While most patients will be placed on continuous cardiorespiratory monitoring, an ECG is essential for diagnosis. Provoking causes should be sought out. A common cause of any tachycardia is dehydration, as well as other forms of hypovolemia.[citation needed] Acute coronary syndrome should be ruled out.[citation needed] Intercurrent illness such as pneumonia may be present.[citation needed]


In general, screening for atrial fibrillation is not performed.[citation needed] Screening in those 65 years and older has been studied and been found to increase the number of cases of atrial fibrillation detected.[18]

Minimal evaluation[edit]

In general, the minimal evaluation of atrial fibrillation should be performed in all individuals with AF. The goal of this evaluation is to determine the general treatment regimen for the individual. If results of the general evaluation warrant it, further studies may then be performed.

History and physical examination[edit]

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[edit]

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


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.[3] At very fast heart rates atrial fibrillation may look more regular, which may make it more difficult to separate from SVT or ventricular tachycardia.[19]

QRS complexes should be narrow, signifying that they are initiated by normal conduction of atrial electrical activity through the intraventricular conduction system. Wide QRS complexes are worrisome for ventricular tachycardia, although in cases where there is disease of the conduction system, wide complexes may be present in A-Fib with rapid ventricular response.

If paroxysmal AF is suspected but an ECG during an office visit shows only a regular rhythm, AF episodes may be detected and documented with the use of ambulatory Holter monitoring (e.g., for a day). If the episodes are too infrequent to be detected by Holter monitoring with reasonable probability, then the patient can be monitored for longer periods (e.g., a month) with an ambulatory event monitor.[3]


In general, a non-invasive transthoracic echocardiogram (TTE) is performed in newly diagnosed AF, as well as if there is a major change in the patient's clinical state. This ultrasound-based scan of the heart may help identify valvular heart disease (which may greatly increase the risk of stroke), left and right atrial size (which indicates likelihood that AF may become permanent), left ventricular size and function, peak right ventricular pressure (pulmonary hypertension), presence of left atrial thrombus (low sensivity), presence of left ventricular hypertrophy and pericardial disease.[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 to be of a longer duration than the individual's symptoms.

Extended evaluation[edit]

In general, an extended evaluation is not necessary in most individuals with atrial fibrillation, and is performed only if abnormalities are noted in the limited evaluation, if a reversible cause of the atrial fibrillation is suggested, or if further evaluation may change the treatment course.

Chest X-ray[edit]

In general, a chest X-ray is performed only if a pulmonary cause of atrial fibrillation is suggested, or if other cardiac conditions are suspected (in particular congestive heart failure.) This may reveal an underlying problem in the lungs or the blood vessels in the chest.[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[edit]

A normal echocardiography (transthoracic or TTE) has a low sensitivity for identifying blood clots in the heart. If this is suspected (e.g., when planning urgent electrical cardioversion) a transesophageal echocardiogram (TEE or TOE where British spelling is used) is preferred.[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 a blood clot forms in more than 90% of cases in non-valvular (or non-rheumatic) atrial fibrillation or flutter.[20] TEE has a high sensitivity for locating thrombi in this area[21] and can also detect sluggish bloodflow in this area that is suggestive of blood clot formation.[22]

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

Ambulatory Holter monitoring[edit]

A Holter monitor is a wearable ambulatory heart monitor that continuously monitors the heart rate and heart rhythm for a short duration, typically 24 hours. In individuals with symptoms of significant shortness of breath with exertion or palpitations on a regular basis, a holter monitor may be of benefit to determine whether rapid heart rates (or unusually slow heart rates) during atrial fibrillation are the cause of the symptoms.

Exercise stress testing[edit]

Some individuals with atrial fibrillation do well with normal activity but develop shortness of breath with exertion. It may be unclear whether the shortness of breath is due to a blunted heart rate response to exertion caused by excessive atrioventricular node-blocking agents, a very rapid heart rate during exertion, or other underlying conditions such as chronic lung disease or coronary ischemia. An exercise stress test will evaluate the individual's heart rate response to exertion and determine if the AV node blocking agents are contributing to the symptoms.


Classification system
AF Category Defining Characteristics
  First detected   only one diagnosed episode
  Paroxysmal   recurrent episodes that stop on their own in less than 7 days
  Persistent   recurrent episodes that last more than 7 days
  Permanent   an ongoing long-term episode

The American College of Cardiology (ACC), American Heart Association (AHA), and the European Society of Cardiology (ESC) recommend in their guidelines the following classification system based on simplicity and clinical relevance.[3]

All patients with AF are initially in the category called first detected AF. These patients may or may not have had previous undetected episodes. If a first detected episode stops on its own in less than 7 days and then another episode begins later on, the category changes to paroxysmal AF. Although patients in this category have episodes lasting up to 7 days, in most cases of paroxysmal AF the episodes will stop in less than 24 hours. If the episode lasts for more than 7 days, it is unlikely to stop on its own,[23] and is then known as persistent AF. In this case, cardioversion can be used to stop the episode. If cardioversion is unsuccessful or not attempted and the episode continues for a long time (e.g., a year or more), the patient's AF is then known as permanent.

Episodes that last less than 30 seconds are not considered in this classification system. Also, this system does not apply to cases where the AF is a secondary condition that occurs in the setting of a primary condition that may be the cause of the AF.

Using this classification system, it is not always clear what an AF case should be called. For example, a case may fit into the paroxysmal AF category some of the time, while other times it may have the characteristics of persistent AF. One may be able to decide which category is more appropriate by determining which one occurs most often in the case under consideration.

In addition to the above four AF categories, which are mainly defined by episode timing and termination, the ACC/AHA/ESC guidelines describe additional AF categories in terms of other characteristics of the patient.[3]


The main goals of treatment are to prevent circulatory instability and stroke. Rate or rhythm control are used to achieve the former, whereas anticoagulation is used to decrease the risk of the latter.[24] If cardiovascularly unstable due to uncontrolled tachycardia, immediate cardioversion is indicated.[3]


Anticoagulation can be achieved through a number of means including the use of heparin, warfarin,[2] dabigatran, rivaroxaban[25] and apixaban.[25] 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.[2] The method used depends on a number of issues, including: cost, risk of stroke, risk of falls, compliance, and speed of desired onset of anticoagulation.[26] 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.[27]

For those with non-valvular atrial fibrillation, the new oral anticoagulants (rivaroxaban, dabigatran, apixaban) are not superior to warfarin in preventing non-hemorrhagic stroke and systemic embolic events but they do have a lower risk of intracranial bleeding compared to warfarin.[28]

Rate versus rhythm control[edit]

There are two ways to approach atrial fibrillation using medications: rate control and rhythm control. Both methods have similar outcomes.[29] Rate control lowers the heart rate closer to normal, usually 60 to 100 bpm, without trying to convert to a regular rhythm. Rhythm control restores normal heart rhythm in a process called cardioversion and maintains the normal rhythm with drugs. Studies suggest that rhythm control is most important in the acute setting AF, whereas rate control is more important in the chronic phase.

There is no difference in risk of stroke in people having converted to a normal rhythm with anti-arrhythmic treatment compared to those with only rate control.[30] 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.[31]

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.[32] However, the diagnosis and progression of atrial fibrillation and other cardiovascular disease requires further investigation.

In those with a fast ventricular response, intravenous magnesium significantly increases the chances of successful rate and rhythm control in the urgent setting without major side-effects.[33] A patient with fluctuating vital signs, mental status changes, preexcitation, or chest pain often will go to immediate treatment with synchronized DC cardioversion.[3] 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[edit]

Rate control is achieved with medications that work by increasing the degree of block at the level of the AV node, in effect decreasing the number of impulses that conduct into the ventricles. This can be done with:[3][34]

In addition to these agents, amiodarone has some AV node blocking effects (in particular when administered intravenously), and can be used in individuals when other agents are contraindicated or ineffective (particularly due to hypotension).

Diltiazem has been shown to be more effective than either digoxin or amiodarone.[35]


Cardioversion is a noninvasive conversion of an irregular heartbeat to a normal heartbeat using electrical or chemical means.[3]

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.[38]


In young patients with little-to-no structural heart disease where rhythm control is desired and cannot be maintained by medication or cardioversion, then radiofrequency ablation or cryoablation may be attempted and is preferred over years of drug therapy.[3][39] Although radiofrequency ablation is becoming an accepted intervention in select younger patients, there is currently a lack of evidence that ablation reduces all-cause mortality, stroke, or heart failure.[40] There are two ongoing clinical trials (CABANA [Catheter Ablation Versus Antiarrhythmic Drug Therapy for Atrial Fibrillation] and EAST [Early Therapy of Atrial Fibrillation for Stroke Prevention Trial]) that should provide new information for assessing whether AF catheter ablation is superior to more standard therapy.[41]

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.[42]

Following surgery[edit]

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.[43] 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.



See also: CHADS score

Prediction of embolism[edit]

Determining the risk of an embolism causing a stroke is important for guiding the use of anticoagulants. The most accurate clinical prediction rules are:[44]

Mechanism of thrombus formation[edit]

In atrial fibrillation, the lack of an organized atrial contraction can result in some stagnant blood in the left atrium (LA) or left atrial appendage (LAA). This lack of movement of blood can lead to thrombus formation (blood clotting). If the clot becomes mobile and is carried away by the blood circulation, it is called an embolus. An embolus proceeds through smaller and smaller arteries until it plugs one of them and prevents blood from flowing through the artery. This process results in end-organ damage due to loss of nutrients, oxygen, and removal of cellular waste products. Emboli in the brain may result in an ischemic stroke or a transient ischemic attack (TIA).

More than 90% of cases of thrombi associated with non-valvular atrial fibrillation evolve in the left atrial appendage.[20] 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.[45]

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.[46] This risk reduction may be due to a beneficial stirring effect of the MR blood flow into the LA.[47]

Mitral valve[edit]

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.[48]

With a sinus rhythm, the mitral annulus undergoes dynamic changes during the cardiac cycle. For example, at the end of diastole the annular area is smaller than at the end of systole. A possible reason for this dynamic size difference is that the coordinated contraction of the left atrium acts like a sphincter about the mitral annulus and reduces its size. This may be important for mitral valve competence so that it does not leak when the left ventricle pumps blood. However, when the left atrium fibrillates, this sphincter action is not possible and may contribute to, or result in, mitral regurgitation in some cases.[48]


Atrial fibrillation is the most common arrhythmia[3] affecting 0.4 to 1% of the population.[3] It also accounts for 1/3 of hospital admissions for cardiac rhythm disturbances,[3] and the rate of admissions for AF has risen in recent years.[49] Strokes from AF account for 6-24% of all ischemic strokes.[50] After a transient ischemic attack or stroke about 11% are found to have a new diagnosis of atrial fibrillation.[51] Between 3–11% of those with AF have structurally normal hearts.[12] Approximately 2.2 million individuals in the United States and 4.5 million in the European Union have AF.[3]

The incidence of atrial fibrillation increases with age. In individuals over the age of 80 it affects about 8%.[3] 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.[52]


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.[53] In the mid-eighteenth century, Jean-Baptiste de Sénac made note of dilated, irritated atria in people with mitral stenosis.[54] 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".[55] 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.[56] Willem Einthoven published the first ECG showing AF in 1906.[57] 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.[58][59][60]


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