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Atrial Fibrillation

Updated: Aug 07, 2025
  • Author: Brooks J Willar, MD; Chief Editor: Jeffrey N Rottman, MD
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Overview

Background

Atrial fibrillation (AF) is characterized by an irregular and often rapid heartbeat (see the first image below).has strong associations with other cardiovascular diseases, such as heart failure (HF), coronary artery disease (CAD), valvular heart disease, diabetes mellitus (DM), and hypertension. It is characterized by an irregular and often rapid heartbeat (see the first image below). The exact mechanisms by which cardiovascular risk factors predispose to AF are not understood fully but are under intense investigation. Catecholamine excess, hemodynamic stress, atrial stress (ischemia/inflammation/fibrosis), metabolic stress, and neurohumoral cascade activation are all purported to promote AF.

Ventricular rate varies from 130 to 168 beats per minute. Rhythm is irregularly irregular. P waves are not discernible.
Atrial fibrillation pulmonary vein isolation (PVI) using pulse field ablation (PFA) technology. 3D electroanatomic mapping with Boston Scientific's Faraview Opal mapping system. Image credit: Brooks J Millar, MD.

Classification of AF begins with distinguishing a first detectable episode, irrespective of whether it is symptomatic or self-limited. Previously published guidelines from an ACC/AHA/HRS committee of experts on the treatment of patients with AF recommended classification of AF into the following patterns (also see the image below) [] :

  • Paroxysmal AF: Episodes of AF that terminate spontaneously within 7 days (most episodes last < 24 hours)

  • Persistent AF: Episodes of AF that last more than 7 days and may require either pharmacologic or electrical intervention to terminate

  • Long-standing persistent AF: AF that has persisted for more than 12 months, either because cardioversion has failed or because cardioversion has not been attempted

  • Permanent AF: When both patient and clinician have decided to abort any further restoration strategies after shared clinical decision making

Classification scheme for patients with atrial fibrillation (AF).

This classification schema pertains to cases that are not related to a reversible cause of AF (eg, thyrotoxicosis, electrolyte abnormalities, acute ethanol intoxication). In current clinical practice, AF secondary to acute myocardial infarction, cardiac surgery, pericarditis, sepsis, pulmonary embolism, or acute pulmonary disease is considered separately. This is because, in these situations, AF is thought to be less likely to recur once the precipitating condition has been treated adequately and has resolved.

However, data from the Framingham Heart Study suggest that over 60% of the participants with secondary AF developed recurrent AF over 15-years of follow-up. [] Furthermore, the long-term risks of stroke and all-cause mortality were similar between participants without a secondary precipitant and those with secondary precipitants. Thus, long-term AF screening strategies can be considered in these patients similar to the current standard of practice for patients with cryptogenic stroke. []

The 2023 ACC/AHA/American College of Chest Physicians (ACCP)/HRS guideline revised the classification of AF, which had been based on the duration of arrhythmia duration and thereby emphasized therapeutic interventions, to use stages instead to acknowledge AF as a disease continuum that necessitates different strategies at different stages. [] These stages include individuals at risk for AF; pre-AF; AF (substages: paroxysmal, persistent, long-standing persistent AF; successful AF ablation); and permanent AF.

The 2024 ESC classification of AF, like that of the 2023 ACC/AHA/ACCP/HRS, is based on the temporal pattern of AF, as follows: first-diagnosed, paroxysmal, persistent, and permanent AF. []

Paroxysmal AF

AF is considered to be recurrent when a patient has two or more episodes. If recurrent AF terminates spontaneously, it is designated as paroxysmal.

Some patients with paroxysmal AF, typically younger patients, have been found to have distinct electrically active foci within their pulmonary veins. These patients generally have many atrial premature beats noted on Holter monitoring. Isolation or elimination of these foci can lead to elimination of the trigger for paroxysms of AF.

Paroxysmal AF may progress to persistent AF, and aggressive attempts to restore and maintain sinus rhythm may prevent comorbidities associated with AF.

Persistent AF

If recurrent AF is sustained, it is considered persistent, irrespective of whether the arrhythmia is terminated by either pharmacologic therapy or electrical cardioversion.

Persistent AF may be either the first presentation of AF or the result of recurrent episodes of paroxysmal AF. Patients with persistent AF also include those with longstanding AF in whom cardioversion has not been indicated or attempted, often leading to permanent AF.

Patients can also have AF as an arrhythmia secondary to cardiac disease that affects the atria (eg, CHF, hypertensive heart disease, rheumatic heart disease, CAD). These patients tend to be older, and AF is more likely to be persistent.

Persistent AF with an uncontrolled, rapid ventricular heart rate response can cause a dilated cardiomyopathy and can lead to electrical remodeling in the atria (atrial cardiomyopathy). Therapy (eg, drugs, catheter ablation, atrioventricular nodal modification, and permanent pacemaker implantation) to control the ventricular rate can improve left ventricular (LV) function and improve quality-of-life scores.

Permanent AF

Permanent AF is recognized as the accepted rhythm, and the main treatment goals are rate control and anticoagulation. Although it is possible to reverse the progression, this task can be challenging.

Lone AF

In addition to the above schema, the term "lone atrial fibrillation" has been used to identify AF in younger patients without structural heart disease, who are at a lower risk for thromboembolism. The definition of lone AF remains controversial, but it generally refers to paroxysmal, persistent, or permanent AF in younger patients (< 60 y) who have normal echocardiographic findings. [] The ACC/AHA/HRS guidelines recommend against using "lone AF" as a separate entity and utilizing the standard AF management tools for all patients. []

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Pathophysiology

Three forms of atrial remodeling during a progression of AF have been described: electrical, contractile, and structural. [] Electrical remodeling is a consequence of high atrial rates and includes shortening of the refractory period of atrial myocytes and slowing of atrial conduction velocity. [] Structural remodeling is characterized both by changes in atrial myocytes [, ] in the interstitium, [, ] and by changes in extracellular matrix composition and deposition of fibrotic tissue. [] Changes at the level of atrial myocytes include the loss of contractile structures and expression of fetal-like proteins, and accumulation of glycogen in the atrial interstitium. []

Changes in the interstitium are primarily manifested by the deposition of collagen fibers around cardiomyocytes. [] Contractile remodeling is caused mainly by impaired calcium handling and may result in atrial mechanical dysfunction that may be transient or progress to irreversible dysfunction. Impaired contractility results from local changes in cell physiology and also from structural remodeling of atrial myocytes (loss of gap junctions).

Another observed morphologic feature related to AF is the presence of inflammatory cells in the atrial myocardium. [] The role of inflammation and myocardial inflammatory infiltrate was suggested by morphologic studies on atrial tissue removed at the time of cardiac surgery and by clinical studies that monitored serum levels of inflammatory cytokines in patients with AF. [, ] Despite the observed association between elevated plasma levels of inflammatory markers and AF, it remains unknown whether inflammation is a systemic or local phenomenon reflecting an active inflammatory process in the atria. [] It is also not known whether the inflammatory cells are a marker of local reaction to tissue injury caused by factors leading to AF or whether they actively participate in the maintenance of AF due to direct cytotoxic or profibrotic effects or due to indirect effects from released cytokines that may promote arrhythmogenesis. []

AF shares strong associations with other cardiovascular diseases, such as HF, CAD, valvular heart disease, DM, and hypertension. [] These factors have been termed upstream risk factors, but the relationship between comorbid cardiovascular disease and AF is incompletely understood and more complex than this terminology implies. The exact mechanisms by which cardiovascular risk factors predispose to AF are not understood fully but are under intense investigation. Catecholamine excess, hemodynamic stress, atrial stress (ischemia/inflammation/fibrosis), metabolic stress, and neurohumoral cascade activation are all purported to promote AF.

Because diabetes mellitus and obesity are increasing in prevalence and are associated with an elevated risk of AF, Fontes et al examined whether insulin resistance is an intermediate step for the development of AF. In a community-based cohort that included 279 patients who developed AF within 10 years of follow-up, no significant association was observed between insulin resistance and incident AF. []

Although the precise mechanisms that cause AF are incompletely understood, AF appears to require both an initiating event and a permissive atrial substrate. The importance of focal pulmonary vein triggers has been highlighted in multiple studies, but alternative and nonmutually exclusive mechanisms have also been evaluated. [] These mechanisms include multiple wavelets, mother waves, fixed or moving rotors, and macro-reentrant circuits. [] In a given patient, multiple mechanisms may coexist at any given time. The automatic focus theory and the multiple wavelet hypothesis appear to have the best supporting data.

Automatic focus

A focal origin of AF is supported by several experimental models showing that AF persists only in isolated regions of atrial myocardium. This theory has garnered considerable attention, as studies have demonstrated that a focal source of AF can be identified in humans and that isolation of this source can eliminate AF.

The pulmonary veins appear to be the most frequent source of these automatic foci, but other foci have been demonstrated in several areas throughout the atria. Cardiac muscle in the pulmonary veins appears to have active electrical properties that are similar, but not identical, to those of atrial myocytes. Heterogeneity of electrical conduction around the pulmonary veins is theorized to promote reentry and sustained AF. Thus, pulmonary vein automatic triggers may provide the initiating event, and heterogeneity of conduction may provide the sustaining conditions in many patients with AF.

Multiple wavelet

The multiple wavelet hypothesis proposes that fractionation of wave fronts propagating through the atria results in self-perpetuating "daughter wavelets." In this model, the number of wavelets is determined by the refractory period, conduction velocity, and mass of atrial tissue. Increased atrial mass, shortened atrial refractory period, and delayed intra-atrial conduction increase the number of wavelets and promote sustained AF. This model is supported by data from patients with paroxysmal AF demonstrating that widespread distribution of abnormal atrial electrograms predicts progression to persistent AF. [] Intra-atrial conduction prolongation has also been shown to predict recurrence of AF. [] Together, these data highlight the importance of atrial structural and electrical remodeling in the maintenance of AF [] —hence the phrase "atrial fibrillation begets atrial fibrillation."

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Etiology

AF is strongly associated with the following risk factors:

  • Hemodynamic stress

  • Atrial ischemia

  • Inflammation

  • Noncardiovascular respiratory causes, including chronic obstructive pulmonary disease and obstructive sleep apnea

  • Alcohol and drug use

  • Endocrine disorders

  • Neurologic disorders

  • Genetic factors

  • Advancing age

Hemodynamic stress

Increased intra-atrial pressure results in atrial electrical and structural remodeling and predisposes to AF. The most common causes of increased atrial pressure are mitral or tricuspid valve disease and LV dysfunction. Systemic or pulmonary hypertension also commonly predisposes to atrial pressure overload, and intracardiac tumors or thrombi are rare causes.

Atrial ischemia

CAD infrequently leads directly to atrial ischemia and AF. More commonly, severe ventricular ischemia leads to increased intra-atrial pressure and AF.

Inflammation

Myocarditis and pericarditis may be idiopathic or may occur in association with collagen vascular diseases; viral or bacterial infections; or cardiac, esophageal, or thoracic surgery.

Noncardiovascular respiratory causes

Pulmonary embolism, pneumonia, lung cancer, and hypothermia have been associated with AF.

Drug and alcohol use

Stimulants, alcohol, and cocaine can trigger AF. Acute or chronic alcohol use (ie, holiday or Saturday night heart, also known as alcohol-related cardiomyopathy) and illicit drug use (ie, stimulants, methamphetamines, cocaine) have been specifically found to be related to AF. Whereas the association of more than moderate chronic alcohol use and AF has been reported in multiple studies previously, a more recent community-based study found an association with even moderate alcohol use with an increased risk of AF. []

Endocrine disorders

Hyperthyroidism, diabetes, and pheochromocytoma have been associated with AF.

Neurologic disorders

Intracranial processes such as subarachnoid hemorrhage or stroke can precipitate AF.

Familial AF

A history of parental AF appears to confer increased likelihood of AF (and occasional family pedigrees of AF are associated with defined ion channel abnormalities, especially sodium channels). [] One cohort study suggests that familial AF is associated with an increased risk of AF. This increase was not lessened by adjustment for genetic variants and other AF risk factors. []

Advancing age

AF is strongly age-dependent, affecting 4% of individuals older than 60 years and 8% of persons older than 80 years.

Other

In a 15-year prospective cohort study of 132,250 Japanese subjects, Xu et al found that anemia and chronic kidney disease, alone and in combination, were associated with an increased risk of new-onset AF. [, ] During a mean follow-up of 13.8 years in 1232 patients with new-onset AF, multivariate analysis showed that those with an estimated glomerular filtration rate (eGFR) lower than 60 mL/min/1.73 m2 were 2.56 times more likely to experience new-onset AF compared with patients with normal kidney function; those whose hemoglobin levels were lower than 13 g/dL had a 1.5 times increased risk of new-onset AF relative to patients with normal hemoglobin levels (P < 0.0001 for both analyses). [, ] Patients with CKD and anemia had a threefold higher incidence of AF. []

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Epidemiology

AF is the most frequently encountered cardiac arrhythmia. [] It affects more than 2.7 to 6.1 million persons in the United States [] which is expected to rise to 12.1 million in 2030. [] AF is strongly age-dependent, affecting 4% of individuals older than 60 years and 8% of persons older than 80 years. Approximately 25% of individuals aged 40 years and older will develop AF during their lifetime. []

The prevalence of AF is 0.1% in persons younger than 55 years, 3.8% in persons 60 years or older, and 10% in persons 80 years or older. With the projected increase in the elderly population in the United States, the prevalence of AF is expected to more than double by the year 2050. AF is uncommon in childhood except after cardiac surgery. []

The incidence of AF is significantly higher in men than in women in all age groups, although this effect may be mediated through the difference in average height between men and women. [] AF appears to be more common in White individuals (30%-40% overall lifetime risk) than in Black persons (20% overall lifetime risk) and Chinese persons (about 15% overall lifetime risk), [] with Black individuals having less than half the age-adjusted risk of developing AF.

In 10-15% of cases of AF, the disease occurs in the absence of comorbidities. However, AF is often associated with other cardiovascular diseases, including hypertension; HF; diabetes-related heart disease; ischemic heart disease; and valvular, dilated, hypertrophic, restrictive, and congenital cardiomyopathies. [] The Atherosclerosis Risk in Communities (ARIC) Study suggests reduced kidney function and presence of albuminuria are strongly associated with AF. []

The rate of ischemic stroke in patients with nonrheumatic AF averages 5% a year, which is somewhere between 2 and 7 times the rate of stroke in patients without AF. The risk of stroke is not due solely to AF; it increases substantially in the presence of other cardiovascular diseases. [] The prevalence of stroke in patients younger than 60 years is less than 0.5%; however, in those older than 70 years, the prevalence doubles with each decade. [] The attributable risk of stroke from AF is estimated to be 1.5% for those aged 50-59 years, and it approaches 30% for those aged 80-89 years. Women are at a higher risk of stroke due to AF than men and some have suggested this may be due to undertreatment with warfarin. However, one study of patients 65 years or older with recently diagnosed AF found warfarin use played no part in the increased risk of stroke among female patients. []

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Prognosis

AF is associated with a 1.5- to 2-fold higher risk of death, [] which is in part due to the strong association between AF and thromboembolic events, according to data from the Framingham heart study. [] Mortality appears to be higher in women than in men. []

It had been thought that medical therapies aimed at rhythm control offered no survival advantage over rate control and anticoagulation on the basis of the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial, which addressed whether rate control and anticoagulation are sufficient goals for asymptomatic, elderly patients. [] Newer data and improved therapies have changed this paradigm. The Early Treatment of Atrial Fibrillation for Stroke Prevention (EAST-AFNET) trial found that patients who received early rhythm control with antiarrhythmic drugs (AADs) or AF ablation had a lower composite outcome of death from cardiovascular causes, stroke, or hospitalization from worsening HF or acute coronary syndrome than those who received usual care. []

AF is associated with increased morbidity and mortality, in part due to the risk of thromboembolic disease, particularly stroke, in AF and in part due to its associated risk factors. There is a 2.4-fold elevated stroke risk, 1.5-fold elevated risk of cognitive impairment or dementia; a 1.5-fold increased MI risk, a 2-fold SCD risk, a 5-fold HF risk, a 1.6-fold CKD risk, and 1.3-fold PAD risk. []

Studies have shown that individuals in sinus rhythm live longer than individuals with AF. Disruption of normal atrial electromechanical function in AF leads to blood stasis. This, in turn, can lead to development of thrombus, most commonly in the left atrial appendage. Dislodgement or fragmentation of a clot can then lead to embolic phenomena, including stroke.

Development of AF predicts HF and is associated with a worse New York Heart Association HF classification. AF may also worsen HF in individuals who are dependent on the atrial component of the cardiac output. Those with hypertensive heart disease and those with valvular heart disease are particularly at high risk for developing HF when AF occurs. In addition, AF may cause tachycardia-mediated cardiomyopathy if adequate rate control is not established.

In critically ill patients, new-onset AF is independently associated with in-hospital and post-ICU risk of death. []

Findings from the observational multicenter PLECTRUM study that evaluated the thromboembolic risk regarding the type and site of mechanical prosthetic heart valves, as well as the quality of anticoagulation and risk factors associated with thromboembolism, found that there was a low rate of bleeding and thromboembolic events in patients with these valves, even when anticoagulation control was suboptimal. [] There was no association between the thromboembolic risk and low time in therapeutic range, but the presence of AF and a history of thromboembolism and of mitral prosthesis were independent risk factors for thromboembolism. []

In a systematic review (13 studies) and meta-analysis (10 eligible studies) of death and adverse outcomes in 54,587 patients with AF and concomitant HF, investigators reported a significantly higher all-cause mortality in AF patients with reduced ejection fraction (rEF) compared to those with preserved EF (pEF). [] However, the rates of stroke and hospitalizations were similar between the groups.

The risk of stroke from AF that lasts longer than 24 hours is a major concern and is usually addressed by prescribing a blood thinner (warfarin, dabigatran, rivaroxaban, apixaban, or edoxaban). The CHADS2 prognostic scoring system was originally derived to estimate the risk of ischemic stroke in patients with AF. A higher CHADS2 score implies a higher risk of ischemic stroke; in older guidelines, a CHADS2 score of 2 or greater was considered an indication for using blood thinners. [] However, the CHADS2 score appears to underestimate the risk of embolic stroke in patients older than 75 years. [] Furthermore the CHADS2 score does not include some of the other risk factors associated with ischemic stroke in AF patients, such as female sex and vascular disease.

An analysis of the AFNET (Central Registry of the German Competence NETwork on Atrial Fibrillation) registry of 8847 patients with nonvalvular AF indicated that the CHA2DS2-VASc score is more sensitive than the CHADS2 score for risk stratification of thromboembolic events (ischemic stroke, transient ischemic attack [TIA], systemic embolism), particularly in patients with a CHADS2 score of 0 or 1 who would have otherwise not received prescribed anticoagulation therapy on the basis of previous guidelines. [, ] However, CHA2DS2-VAScc scoring—which adds age 65-74 years, arterial disease, and female sex as stroke risk factors to the CHADS2 score [] —placed 30.3% of those classified as CHADS2 0 or 1 into CHA2DS2-VASc 1 or 2 and higher, groups in which oral anticoagulation is now recommended.

In another investigation of over 47,000 participants with a CHADS2 score of 0 to 1 who were not on anticoagulation therapy, Olesen et al reported a serial increase in the risk of stroke/thromboembolism with an increase in CHA2DS2-VASc score. [] Furthermore, a regression model with the CHA2DS2-VASc score showed higher discrimination for predicting stroke than the model with the CHADS2 score. []

A post-hoc analysis of the ONTARGET and TRANSCEND studies, which evaluated the efficacy of treatment with ramipril plus telmisartan or telmisartan alone in reducing cardiovascular disease, used the Mini–Mental State Examination (MMSE) to measure the cognitive function of participants at baseline and after two and five years. Results show that AF is associated with an increased risk of cognitive decline, new dementia, loss of independence in performing activities of daily living and admission to long-term care facilities. []

Acute pericarditis is a known potential complication following catheter ablation for AF. Independent risk factors for postablation acute pericarditis appear to be younger age and the use of radiofrequency ablation. []

AF in association with acute myocardial infarction

AF is a common finding in patients presenting with an acute myocardial infarction. A meta-analysis pooled data from 43 studies and more than 278,800 patients. [] The study found that AF in the setting of acute myocardial infarction was associated with 40% increase in mortality compared to patients in sinus rhythm with acute myocardial infarction. The causes of death were unclear, but may be related to triple anticoagulation therapy with aspirin, clopidogrel, and warfarin, or may be related to hemodynamic consequences associated with the loss of atrial contraction. Whether AF is a complication of myocardial infarction or a marker for myocardial infarction severity is unclear.

A study by van Diepen et al suggests that patients with HF or AF have a significantly higher risk of noncardiac postoperative mortality than patients with coronary artery disease; thus, patients and physicians should consider this risk, even if a minor procedure is planned. []

Catheter ablation in association with mortality and stroke

A systemic review and meta-analysis comprising 30 studies and 78,966 patients (about one third receiving AF ablation and two thirds on medical therapy) with 233,990 patient-years of follow-up found a survival benefit for AF ablation relative to medical treatment alone, but these findings were only supported in the setting of HF and LV systolic dysfunction. []

In a meta-analysis of data from 24 trials comprising 5730 adults that compared catheter ablation (n = 2992) to medical therapy (n = 2738), there was a reduction in all-cause mortality in the catheter ablation group compared to medical therapy–only group, as well as a reduction in hospitalizations, improvement in LVEF, and greater freedom from atrial arrhythmia. []

In a trial of 363 patients with HFrEF (LVEF ≤35% with NYHA class II-IV HF) and symptomatic paroxysmal and persistent AF without response to AADs, had unacceptable side effects, or were unwilling to take AADs randomized to catheter ablation or medical therapy (rate or rhythms control), those who received catheter ablation had a significantly lower rate of death from any cause or hospitalization for worsening HF than those who received medical therapy. []

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Tables
  • ]
Table 1. Stroke Rate in Patients with Nonvalvular Atrial Fibrillation not Treated with Anticoagulation []

CHA2DS2-VASc Score

Unadjusted Stroke Rate (%/y)

0

0.2

1

0.6

2

2.2

3

3.2

4

4.8

5

7.2

6

9.7

7

11.2

8

10.8

9

12.2

Table 2. Recommendations for Antithrombotic Therapy in Patients with Nonvalvular Atrial Fibrillation

CHA2DS2-VASc Score

Recommended Therapy
0 No therapy
1

No therapy, or aspirin 81-325 mg daily, or anticoagulation therapy

(eg, warfarin [international normalized ratio (INR) goal 2-3], dabigatran, rivaroxaban, apixaban, edoxaban)

≥2

Anticoagulation therapy (eg, warfarin [INR goal 2-3], dabigatran, rivaroxaban, apixaban, edoxaban)

Contributor Information and Disclosures
Author

Brooks J Willar, MD Clinical Fellow, Department of Cardiovascular Medicine, Division of Cardiac Electrophysiology, University of Massachusetts Chan School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Tenes Joseph Paul, DO Fellow Physician, Department of Cardiovascular Medicine, Division of Cardiac Electrophysiology, University of Massachusetts Medical School

Tenes Joseph Paul, DO is a member of the following medical societies: Heart Rhythm Society, American College of Cardiology, American College of Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Lawrence Rosenthal, MD, PhD, FACC, FHRS Professor of Medicine, Director, Section of Cardiac Pacing and Electrophysiology, Director of EP Fellowship Program, Division of Cardiovascular Disease, University of Massachusetts Memorial Medical Center

Lawrence Rosenthal, MD, PhD, FACC, FHRS is a member of the following medical societies: American College of Cardiology, American Heart Association, Heart Rhythm Society, Massachusetts Medical Society

Disclosure: Nothing to disclose.

David D McManus, MD, MSc, FACC, FHRS Director, Atrial Fibrillation Program, Assistant Professor of Medicine and Quantitative Health Sciences, University of Massachusetts Medical School

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Additional Contributors

Mariclaire Cloutier Freelance editor, Medscape Drugs & Diseases

Disclosure: Nothing to disclose.

Mayank Sardana, MBBS Fellow in Cardiovascular Medicine, University of Massachusetts Medical School

Disclosure: Nothing to disclose.

Acknowledgements

Pierre Borczuk, MD Assistant Professor of Medicine, Harvard Medical School; Associate in Emergency Medicine, Massachusetts General Hospital

Pierre Borczuk, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Abraham G Kocheril, MD, FACC, FACP, FHRS Professor of Medicine, University of Illinois College of Medicine

Abraham G Kocheril, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, and Illinois State Medical Society

Disclosure: Nothing to disclose.

William Lober, MD, MS Associate Professor, Health Informatics and Global Health, Schools of Medicine, Nursing, and Public Health, University of Washington

Disclosure: Nothing to disclose.

Brian Olshansky, MD Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, and Heart Rhythm Society

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Ali A Sovari, MD, FACP Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois College of Medicine; Staff Physician and Hospitalist, St John Regional Medical Center, Cogent Healthcare, Inc

Ali A Sovari, MD, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Physiological Society, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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