[8] Healthy lifestyle changes, such as weight loss in people with obesity, increased physical activity, and drinking less alcohol, can lower the risk for AF and reduce its burden if it occurs.

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.

[7] Using genome-wide association study (GWAS), which screen the entire genome for single nucleotide polymorphism (SNP), three susceptibility loci have been found for AF (4q25, 1q21 and 16q22).

This favors remodeling processes of the atrium due to inflammation or alterations in the depolarization of cardiomyocytes by elevation of sympathetic nervous system activity.

[56] It is due to a remodeling of cardiac tissue,[57] and an increase in vagal tone, which shortens the effective refractory period (ERP) favoring re-entries from the pulmonary veins.

[61] Other medications that rarely increase the risk of developing atrial fibrillation include adenosine, aminophylline, corticosteroids, ivabradine, ondansetron, and antipsychotics.

Three fundamental components favor the establishment of a leading circle or a rotor: slow conduction velocity of the cardiac action potential, a short refractory period, and a small wavelength.

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.

General practice was identified as a 'preferred' setting for AF screening by the AF-SCREEN international collaboration report due to the availability of nursing support and the natural pathway to treatment.

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.

[29] In general, a non-invasive transthoracic echocardiogram (TTE) is performed in newly diagnosed AF, as well as if there is a major change in the person's clinical state.

[citation needed] 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).

An exercise stress test will evaluate the individual's heart rate response to exertion and determine whether the AV node blocking agents are contributing to the symptoms.

Non-contact AF detection technologies have been developed that utilize pulsatile changes in skin color using video photoplethysmography (VPG).

Many of its risk factors, such as obesity, smoking, lack of physical activity, and excessive alcohol consumption, are modifiable and preventable with lifestyle modification or can be managed by a healthcare professional.

Accordingly, consensus guidelines recommend abstaining from alcohol and recreational drugs, stopping tobacco use, maintaining a healthy weight, and regularly participating in moderate-intensity physical activities.

[61] Consistent moderate-intensity aerobic exercise, defined as achieving 3.0–5.9 METs of intensity, for at least 150 minutes per week may reduce the risk of developing new-onset atrial fibrillation.

[23] Randomized controlled trials examining the role of obstructive sleep apnea treatment on atrial fibrillation incidence and burden are lacking.

[124][125] Dual antiplatelet therapy with aspirin and clopidogrel is inferior to warfarin for preventing strokes or systemic embolism and has comparable bleeding risk in people with atrial fibrillation.

[87] While there are no significant changes in adherence, persistence or clinical outcomes in patients switched from a VKA to a DOAC, an increase in therapy satisfaction has been reported.

[134] In those with a fast ventricular response, intravenous magnesium significantly increases the chances of achieving successful rate and rhythm control in the urgent setting without major side-effects.

[135] A person with poor vital signs, mental status changes, preexcitation, or chest pain often will go to immediate treatment with synchronized DC cardioversion.

[137] Rate control is achieved with medications that work by increasing the degree of the block at the level of the AV node, decreasing the number of impulses that conduct into the ventricles.

A group of cardiologists led by Dr Haïssaguerre from Bordeaux University Hospital noted in 1998 that the pulmonary veins are an important source of ectopic beats, initiating frequent paroxysms of atrial fibrillation, with these foci responding to treatment with radio-frequency ablation.

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.

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

[161] Many mechanisms contribute to cardiac remodeling leading to a worsening of atrial fibrillation, including fibrosis, fatty infiltration, amyloidosis, and ion channel modifications.

[169] Atrial fibrillation has been independently associated with a higher risk of developing cognitive impairment, vascular dementia, and Alzheimer disease and with elevated levels of neurofilament light chain in blood, a biomarker indicating neuroaxonal injury.

In particular, people who had atrial septal defects, Tetralogy of Fallot, or Ebstein's anomaly, and those who underwent the Fontan procedure, are at higher risk with prevalence rates of up to 30% depending on the heart's anatomy and the person's age.

[185] 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.