Differential Diagnosis for Atrial Fibrillation: A Comprehensive Guide for Auto Repair Experts

Introduction

Atrial fibrillation (AFib) stands as the most frequently encountered cardiac arrhythmia, significantly elevating the risk of stroke and other cardiovascular complications. Characterized by rapid and irregular electrical activity in the atria, AFib disrupts the heart’s normal rhythm, leading to inefficient blood flow and potential thrombus formation. While the primary article provides a foundational understanding of AFib, a deeper exploration into the Differential Diagnosis For Atrial Fibrillation is crucial for healthcare professionals, and surprisingly relevant for experts in fields requiring meticulous diagnostic skills, such as auto repair. Just as automotive specialists must differentiate between various mechanical issues presenting similar symptoms, clinicians must accurately distinguish AFib from other cardiac conditions that mimic its presentation. This detailed guide expands upon the original article, offering a comprehensive overview of the differential diagnosis of atrial fibrillation, ensuring a robust understanding for accurate identification and management.

Etiology of Atrial Fibrillation

Understanding the diverse etiologies of atrial fibrillation is fundamental to considering its differential diagnosis. AFib is not a disease in isolation but often a manifestation of underlying health issues. The original article correctly highlights several key causes, which we will reiterate and slightly expand upon here:

  1. Advanced Age: The risk of AFib significantly increases with age, making it a prevalent concern in older populations.
  2. Congenital Heart Disease: Structural abnormalities present from birth can predispose individuals to atrial fibrillation.
  3. Underlying Heart Disease: This broad category includes valvular heart disease, coronary artery disease, structural heart disease, and atrial ischemia. These conditions alter the heart’s electrical and mechanical function, fostering AFib development.
  4. Hypertension: Both systemic and pulmonary hypertension create added stress on the heart, increasing AFib risk.
  5. Increased Alcohol Consumption: Excessive alcohol intake is a well-established risk factor, capable of triggering acute AFib episodes or contributing to chronic development.
  6. Endocrine Disorders: Conditions like diabetes mellitus, pheochromocytoma, and hyperthyroidism disrupt metabolic balance and can impact cardiac rhythm.
  7. Genetic Factors: Family history and specific genetic mutations play a role in susceptibility to AFib.
  8. Neurologic Disorders: Subarachnoid hemorrhage and stroke can secondarily induce cardiac arrhythmias, including AFib.
  9. Hemodynamic Stress: Conditions such as mitral or tricuspid valve disease, left ventricular dysfunction, and pulmonary embolism impose significant hemodynamic stress on the atria.
  10. Obstructive Sleep Apnea: Sleep apnea-related hypoxia and autonomic nervous system fluctuations are linked to increased AFib incidence.
  11. Inflammation: Myocarditis and pericarditis, inflammatory conditions of the heart muscle and sac, can disrupt electrical conduction and trigger AFib.

It’s crucial to note that in some instances, AFib can be iatrogenic, resulting from medical treatments or procedures. Furthermore, the recurrence patterns of AFib – paroxysmal, persistent, long-standing persistent, and permanent – influence management strategies but do not fundamentally alter the differential diagnosis process. Recognizing these diverse causes is the first step in effectively differentiating AFib from other conditions.

Epidemiology of Atrial Fibrillation

The epidemiological data underscores the significance of atrial fibrillation as a widespread health concern, further emphasizing the need for accurate differential diagnosis. As the original article states, AFib is the most common cardiac rhythm disorder, and its prevalence is globally increasing. The aging population is a major driver, with prevalence rates dramatically rising with age. While approximately 1% of the global population has AFib, this figure jumps to around 9% in individuals over 75. Lifetime risk for developing AFib at age 80 escalates to approximately 22%. Interestingly, AFib is more frequently observed in males and individuals of White ethnicity compared to Black individuals. These epidemiological trends highlight the importance of considering AFib in a broad range of patient demographics and underscores the necessity for healthcare providers to be adept at its differential diagnosis across diverse populations.

Pathophysiology of Atrial Fibrillation

The pathophysiology of atrial fibrillation is complex and multifactorial, primarily revolving around cardiac remodeling. Atrial remodeling, encompassing both structural and electrical changes, creates the substrate for the erratic rhythm characteristic of AFib. Structural remodeling involves alterations in myocytes and the extracellular matrix, with fibrosis playing a significant role in certain etiologies. Electrical remodeling involves changes in ion channels and action potential duration, often driven by tachycardia itself, leading to a shortened refractory period and increased vulnerability to AFib.

While the exact mechanisms are still being elucidated, conditions like hypertension, structural heart disease, valvular disease, and ischemic heart disease are strongly implicated in triggering both paroxysmal and persistent AFib. Genetic predispositions are also recognized, with research identifying gene mutations affecting cardiac ion channels, such as the alpha-subunit of the cardiac Ik5 channel. These genetic factors can alter membrane stability and refractory periods, facilitating AFib initiation and maintenance.

In most cases, AFib is non-genetic and stems from underlying cardiovascular disease. The process typically involves a trigger initiating ectopic electrical activity, often originating near the pulmonary veins, leading to unsynchronized atrial firing and fibrillation. This results in irregular ventricular rates and turbulent blood flow, reducing cardiac output and increasing the risk of thromboembolism, particularly from the left atrial appendage. Understanding this complex pathophysiology is crucial not only for managing AFib itself but also for differentiating it from other arrhythmias with potentially overlapping mechanisms and presentations.

History and Physical Examination in Atrial Fibrillation

A meticulous history and physical examination are paramount in the diagnostic process of atrial fibrillation, including its differential diagnosis. The clinical presentation of AFib is highly variable, ranging from asymptomatic individuals to patients experiencing severe complications like cardiogenic shock or stroke.

The history should comprehensively assess for symptoms such as palpitations (awareness of heart rhythm), chest pain, shortness of breath, peripheral edema, exertional dyspnea, and dizziness. Crucially, risk factor assessment is vital, including inquiries about hypertension, valvular, structural, or ischemic heart disease, obstructive sleep apnea, obesity, smoking, alcohol and illicit drug use, rheumatic fever/heart disease history, pericarditis, and hyperlipidemia. For patients with known AFib, the history should delve into symptom duration and frequency, identifiable triggers, prior successful termination methods, antiarrhythmic drug use, and pre-existing cardiac conditions.

The physical examination always begins with assessing airway, breathing, and circulation (ABCs), particularly in acute presentations. General examination findings in AFib may include tachycardia with an irregularly irregular pulse. Heart rates typically range from 110 to 140 beats per minute but can be much higher or lower. Assessment should include evaluating for edema, peripheral pulses, and signs of peripheral vascular disease.

A focused physical exam is crucial to identify potential underlying causes of AFib. Neck examination may reveal carotid artery disease or thyroid abnormalities. Pulmonary auscultation may disclose rales indicative of heart failure, or wheezing suggesting pulmonary diseases like asthma or COPD. Cardiovascular examination with careful auscultation of all cardiac areas and palpation of the apical impulse can identify valvular pathologies. Abdominal examination should assess for aortic abnormalities, bruits, hepatomegaly, and distension, which could indicate heart failure. Neurological examination is essential to detect signs of transient ischemic attack or stroke. This detailed approach to history and physical examination is not only vital for diagnosing AFib but also for guiding the differential diagnosis by identifying clues that point towards or away from AFib and towards other potential cardiac or non-cardiac conditions.

Evaluation of Atrial Fibrillation

Beyond history and physical examination, the electrocardiogram (ECG) is the cornerstone of atrial fibrillation diagnosis and essential for differential diagnosis. The characteristic ECG findings in AFib include a narrow complex, “irregularly irregular” rhythm devoid of discernible P-waves. Fibrillatory waves may be present but are not always prominent. Ventricular rates typically range from 80 to 180 bpm but can vary widely.

Laboratory investigations are crucial to evaluate for underlying causes and contributing factors. A complete blood count (CBC) can screen for infection, a basic metabolic panel (BMP) for electrolyte imbalances, and thyroid function tests for hyperthyroidism. A chest X-ray can identify thoracic abnormalities. Cardiac biomarkers and B-type natriuretic peptide (BNP) are often measured to assess for underlying cardiac disease. In some cases, cardiac catheterization may be necessary based on history and physical findings.

Pulmonary embolism (PE) should be considered in the differential diagnosis, and evaluation with D-dimer or spiral CT scan may be warranted as right heart strain from PE can induce atrial arrhythmias. Risk stratification for PE using PERC or Wells criteria can be helpful. A transesophageal echocardiogram (TEE) is often indicated, particularly prior to cardioversion, to rule out atrial thrombus and assess cardiac structure. This comprehensive evaluation, anchored by the ECG and supplemented by laboratory and imaging studies, is vital not only to confirm AFib but also to differentiate it from other arrhythmias and guide appropriate management.

Treatment and Management of Atrial Fibrillation

The management of atrial fibrillation, as described in the original article, is multifaceted and depends on the clinical context, including hemodynamic stability and risk stratification. In hemodynamically unstable patients with rapid ventricular response, immediate cardioversion is often necessary, sometimes even before TEE, alongside anticoagulation. For rate control in acute settings, beta-blockers or calcium channel blockers are typically first-line agents, often administered intravenously. Digoxin and amiodarone are generally reserved for second-line use in acute rate or rhythm control.

For patients with pre-existing AFib, stroke risk stratification using the CHA2DS2-VASc score is crucial to guide anticoagulation decisions. Higher scores necessitate anticoagulation, while lower scores may warrant antiplatelet therapy or no antithrombotic therapy. Bleeding risk assessment using the HAS-BLED score is also essential when considering anticoagulation. Rate or rhythm control strategies, employing medications like beta-blockers, calcium channel blockers, amiodarone, dronedarone, and digoxin, are tailored to individual patient needs and AFib characteristics. Non-pharmacological options, such as catheter ablation and, in rare cases, pacemaker implantation, are considered in specific scenarios. Current guidelines emphasize the use of non-vitamin K oral anticoagulants (NOACs) over warfarin for most patients, and advocate for comprehensive stroke and bleeding risk assessment in all AFib patients. While treatment strategies are important for overall AFib management, they are less directly relevant to the core concept of differential diagnosis, which focuses on distinguishing AFib from other conditions before initiating treatment.

Differential Diagnosis of Atrial Fibrillation: Key Distinctions

The differential diagnosis for atrial fibrillation is critical because several cardiac arrhythmias and other conditions can mimic its symptoms or ECG findings. Accurately distinguishing AFib from these conditions is essential for appropriate management and prognosis. The original article briefly mentions a few key differential diagnoses, which we will now expand upon:

  1. Atrial Flutter: Atrial flutter is another supraventricular tachyarrhythmia, often confused with AFib. The key differentiator lies in the rhythm regularity. While AFib is irregularly irregular, atrial flutter is typically regularly irregular or even regular, particularly in typical atrial flutter. ECG in atrial flutter often reveals characteristic “sawtooth” flutter waves, best seen in the inferior leads (II, III, aVF), which are absent in AFib. The atrial rate in flutter is usually more organized and slower than in AFib, typically around 250-350 bpm. Ventricular response in flutter can be regular (e.g., 2:1 conduction) or irregular, depending on AV node conduction. Clinically, atrial flutter may present with similar symptoms to AFib, but the ECG distinction is crucial for diagnosis and management, as ablation strategies and anticoagulation needs can differ.

    Image alt text: ECG tracing showing irregularly irregular rhythm characteristic of atrial fibrillation with absent P waves and variable R-R intervals.

  2. Atrial Tachycardia: Atrial tachycardia is a regular supraventricular tachycardia originating from a single ectopic focus within the atria. In contrast to the chaotic electrical activity of AFib, atrial tachycardia exhibits a more organized, rapid atrial rhythm. ECG typically shows regular, narrow QRS complexes with distinct P-waves preceding each QRS complex. However, P-waves in atrial tachycardia may be abnormal in morphology and axis compared to sinus P-waves, and the PR interval may be shortened or prolonged depending on the location of the ectopic focus. The atrial rate in atrial tachycardia is usually regular and faster than sinus rhythm, but slower and more organized than AFib. Differentiating atrial tachycardia from AFib is essential as their mechanisms, triggers, and optimal management strategies can differ.

  3. Multifocal Atrial Tachycardia (MAT): Multifocal atrial tachycardia is characterized by at least three different P-wave morphologies on ECG, along with an irregular atrial rhythm. This arrhythmia is often associated with pulmonary disease, hypoxemia, and electrolyte imbalances, particularly in elderly patients. While both MAT and AFib are irregular atrial rhythms, MAT has discernible P-waves of varying morphologies, whereas AFib lacks organized P-waves. The irregularity in MAT is often described as “wandering,” with varying P-P intervals, PR intervals, and P-wave morphologies. Distinguishing MAT from AFib is important because their underlying causes and treatment approaches differ significantly. MAT often resolves with treatment of the underlying pulmonary or metabolic issues, whereas AFib management focuses on rate control, rhythm control, and anticoagulation.

    Image alt text: Animated illustration depicting the chaotic and disorganized electrical activity within the atria during atrial fibrillation, contrasting with normal sinus rhythm.

  4. Wolf-Parkinson-White (WPW) Syndrome with Atrial Fibrillation: WPW syndrome is a pre-excitation syndrome characterized by an accessory pathway that bypasses the AV node, predisposing individuals to re-entrant tachycardias. When AFib occurs in the setting of WPW, it can be particularly dangerous. The accessory pathway can conduct atrial impulses directly to the ventricles at very rapid rates, potentially leading to ventricular fibrillation and sudden cardiac death. ECG in WPW with sinus rhythm shows a short PR interval and a delta wave (slurred upstroke of the QRS complex). During AFib in WPW, the ECG may show very rapid, irregular wide QRS complexes, as the accessory pathway conducts rapidly to the ventricles without the rate-limiting effect of the AV node. Differentiating AFib in WPW from typical AFib is critical because certain medications that slow AV nodal conduction (e.g., digoxin, verapamil, diltiazem) are contraindicated in WPW with AFib as they can paradoxically increase conduction down the accessory pathway and worsen the arrhythmia.

  5. Atrioventricular Nodal Reentry Tachycardia (AVNRT): AVNRT is the most common type of paroxysmal supraventricular tachycardia (PSVT). It is caused by a re-entry circuit within the AV node. AVNRT typically presents with sudden onset and termination of regular, rapid palpitations. ECG during AVNRT usually shows a regular, narrow complex tachycardia. P-waves are often not visible or are retrograde (inverted in inferior leads) and occur simultaneously with or shortly after the QRS complex, as atrial activation is retrograde from the AV node. While AVNRT is a regular rhythm unlike AFib’s irregularity, patients may initially perceive both as “palpitations.” The ECG is crucial to differentiate them. AVNRT is typically treated with vagal maneuvers or AV nodal blocking agents to terminate acute episodes, and catheter ablation is a highly effective long-term treatment.

    Image alt text: Diagram illustrating the irregular and rapid firing of electrical signals in the atria during atrial fibrillation, leading to an erratic heart rhythm.

In addition to these primary cardiac arrhythmia differentials, other non-cardiac conditions can mimic AFib symptoms and should be considered in the differential diagnosis:

  • Sinus Tachycardia: Physiological sinus tachycardia due to exercise, anxiety, fever, or hyperthyroidism can increase heart rate and cause palpitations, but the rhythm remains regular, and P-waves are normal.
  • Anxiety and Panic Attacks: These can cause palpitations, chest discomfort, shortness of breath, and dizziness, mimicking AFib symptoms, but ECG will show sinus rhythm.
  • Hyperthyroidism: Thyroid hormone excess can induce sinus tachycardia or even AFib, but other hyperthyroid symptoms (weight loss, heat intolerance, tremor) and thyroid function tests help differentiate it.
  • Anemia: Severe anemia can cause palpitations and shortness of breath due to increased cardiac output, but ECG will show sinus rhythm unless underlying cardiac issues are present.
  • Electrolyte Imbalances: Hypokalemia, hypomagnesemia, and other electrolyte disturbances can predispose to various arrhythmias, including AFib, but electrolyte levels should be assessed.
  • Pulmonary Embolism: As mentioned earlier, PE can present with shortness of breath, chest pain, and palpitations, and can even induce AFib, but PE-specific symptoms and risk factors should be evaluated.

A systematic approach to differential diagnosis for atrial fibrillation involves:

  1. Detailed History: Focusing on symptom characteristics, onset, duration, triggers, and associated symptoms.
  2. Thorough Physical Examination: Assessing heart rate, rhythm, presence of murmurs, signs of heart failure, and other systemic findings.
  3. ECG: The cornerstone of arrhythmia diagnosis, carefully analyzing rhythm regularity, P-waves, QRS morphology, and rate.
  4. Laboratory Tests: Including CBC, BMP, thyroid function tests, cardiac biomarkers, and potentially D-dimer or BNP.
  5. Echocardiography: To assess cardiac structure, function, and rule out valvular disease or other structural heart conditions.
  6. Consideration of Non-Cardiac Causes: Evaluating for underlying pulmonary, endocrine, metabolic, or psychological conditions that can mimic or exacerbate AFib.

By systematically considering these differential diagnoses and utilizing appropriate diagnostic tools, clinicians can accurately distinguish atrial fibrillation from other conditions and ensure optimal patient management.

Staging and Prognosis of Atrial Fibrillation

The staging or classification of atrial fibrillation, as outlined in the original article, is primarily based on the duration and pattern of episodes: paroxysmal, persistent, long-standing persistent, and permanent. This classification helps guide treatment strategies but is less directly relevant to the differential diagnosis process. Similarly, while the prognosis of AFib, including increased stroke risk, thromboembolism, and potential complications, is important for overall patient management, it does not directly aid in distinguishing AFib from other arrhythmias at the time of initial diagnosis.

Complications of Atrial Fibrillation

The complications of atrial fibrillation, most notably stroke and heart failure, underscore the clinical significance of this arrhythmia. However, like staging and prognosis, complications are not directly utilized in the initial differential diagnosis of AFib. Recognizing the potential for these complications reinforces the importance of accurate diagnosis and appropriate management once AFib is identified.

Pearls and Other Issues in Atrial Fibrillation

The “pearls” highlighted in the original article, such as the increasing prevalence of AFib with age and the risk of stroke due to thrombus formation in the fibrillating atria, are crucial reminders of the clinical impact of AFib. Emphasizing the need for patients to seek immediate medical attention for symptoms like chest pain, palpitations, and shortness of breath is vital for timely diagnosis and management. However, these “pearls” are more focused on the general understanding and management of AFib rather than the specific process of differential diagnosis.

Enhancing Healthcare Team Outcomes in Atrial Fibrillation

The importance of an interprofessional team approach to managing atrial fibrillation, as emphasized in the original article, is paramount for optimizing patient outcomes. Nurses, pharmacists, cardiologists, and other healthcare professionals play crucial roles in medication management, monitoring, patient education, and coordination of care. While effective team-based care is essential for managing AFib patients, it is not directly involved in the initial step of differential diagnosis. Accurate differential diagnosis precedes and informs the subsequent management strategies implemented by the healthcare team.

Outcomes in Atrial Fibrillation

The outcomes data presented in the original article, highlighting the rising prevalence of AFib and the increased stroke risk, further underscore the importance of effective AFib management. The fact that anticoagulation can significantly reduce stroke risk in AFib patients reinforces the need for accurate diagnosis and appropriate risk stratification. However, similar to other sections, outcome data is not directly utilized in the initial differential diagnosis process itself.

Conclusion

Accurate differential diagnosis for atrial fibrillation is a cornerstone of effective cardiac care. While AFib is the most common cardiac arrhythmia, a range of other conditions, both cardiac and non-cardiac, can mimic its presentation. Distinguishing AFib from atrial flutter, atrial tachycardia, multifocal atrial tachycardia, WPW syndrome, AVNRT, and other conditions requires a systematic approach encompassing detailed history, thorough physical examination, and, most importantly, careful ECG interpretation. Understanding the nuances of each differential diagnosis, recognizing key ECG features, and considering the clinical context are essential skills for healthcare professionals. Just as auto repair experts rely on meticulous diagnostics to pinpoint the precise cause of a vehicle malfunction, clinicians must master the art of differential diagnosis to ensure accurate identification and optimal management of atrial fibrillation, ultimately improving patient outcomes and reducing the burden of this prevalent arrhythmia.


Image alt text: Example ECG strip demonstrating atrial fibrillation with rapid ventricular response, showing irregular rhythm, absence of P waves, and fibrillatory baseline.

References

1.Markides V, Schilling RJ. Atrial fibrillation: classification, pathophysiology, mechanisms and drug treatment. Heart. 2003 Aug;89(8):939-43. [PMC free article: PMC1767799] [PubMed: 12860883]

2.Amin A, Houmsse A, Ishola A, Tyler J, Houmsse M. The current approach of atrial fibrillation management. Avicenna J Med. 2016 Jan-Mar;6(1):8-16. [PMC free article: PMC4759971] [PubMed: 26955600]

3.McManus DD, Rienstra M, Benjamin EJ. An update on the prognosis of patients with atrial fibrillation. Circulation. 2012 Sep 04;126(10):e143-6. [PMC free article: PMC3678907] [PubMed: 22949543]

4.Mohanty S, Trivedi C, Gianni C, Natale A. Gender specific considerations in atrial fibrillation treatment: a review. Expert Opin Pharmacother. 2018 Mar;19(4):365-374. [PubMed: 29424249]

5.Peters SAE, Woodward M. Established and novel risk factors for atrial fibrillation in women compared with men. Heart. 2019 Feb;105(3):226-234. [PubMed: 30158135]

6.Choi YJ, Choi EK, Han KD, Jung JH, Park J, Lee E, Choe W, Lee SR, Cha MJ, Lim WH, Oh S. Temporal trends of the prevalence and incidence of atrial fibrillation and stroke among Asian patients with hypertrophic cardiomyopathy: A nationwide population-based study. Int J Cardiol. 2018 Dec 15;273:130-135. [PubMed: 30150122]

7.Robert R, Porot G, Vernay C, Buffet P, Fichot M, Guenancia C, Pommier T, Mouhat B, Cottin Y, Lorgis L. Incidence, Predictive Factors, and Prognostic Impact of Silent Atrial Fibrillation After Transcatheter Aortic Valve Implantation. Am J Cardiol. 2018 Aug 01;122(3):446-454. [PubMed: 30201110]

8.Tarride JE, Quinn FR, Blackhouse G, Sandhu RK, Burke N, Gladstone DJ, Ivers NM, Dolovich L, Thornton A, Nakamya J, Ramasundarahettige C, Frydrych PA, Henein S, Ng K, Congdon V, Birtwhistle RV, Ward R, Healey JS. Is Screening for Atrial Fibrillation in Canadian Family Practices Cost-Effective in Patients 65 Years and Older? Can J Cardiol. 2018 Nov;34(11):1522-1525. [PubMed: 30144961]

9.Karnad A, Pannelay A, Boshnakova A, Lovell AD, Cook RG. Stroke prevention in Europe: how are 11 European countries progressing toward the European Society of Cardiology (ESC) recommendations? Risk Manag Healthc Policy. 2018;11:117-125. [PMC free article: PMC6112781] [PubMed: 30197544]

10.Laäs DJ, Naidoo M. Oral anticoagulants and atrial fibrillation: A South African perspective. S Afr Med J. 2018 Jul 25;108(8):640-646. [PubMed: 30182879]

11.Bai CJ, Madan N, Alshahrani S, Aggarwal NT, Volgman AS. Sex Differences in Atrial Fibrillation-Update on Risk Assessment, Treatment, and Long-Term Risk. Curr Treat Options Cardiovasc Med. 2018 Aug 27;20(10):79. [PubMed: 30146677]

12.Brieger D, Amerena J, Attia JR, Bajorek B, Chan KH, Connell C, Freedman B, Ferguson C, Hall T, Haqqani HM, Hendriks J, Hespe CM, Hung J, Kalman JM, Sanders P, Worthington J, Yan T, Zwar NA. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the diagnosis and management of atrial fibrillation 2018. Med J Aust. 2018 Oct 15;209(8):356-362. [PubMed: 30067936]

13.Pharithi RB, Ranganathan D, O’Brien J, Egom EE, Burke C, Ryan D, McAuliffe C, Vaughan M, Coughlan T, Morrissey E, McHugh J, Moore D, Collins R. Is the prescription right? A review of non-vitamin K antagonist anticoagulant (NOAC) prescriptions in patients with non-valvular atrial fibrillation. Safe prescribing in atrial fibrillation and evaluation of non-vitamin K oral anticoagulants in stroke prevention (SAFE-NOACS) group. Ir J Med Sci. 2019 Feb;188(1):101-108. [PubMed: 29860595]

14.Dan GA, Iliodromitis K, Scherr D, Marín F, Lenarczyk R, Estner HL, Kostkiewicz M, Dagres N, Lip GYH. Translating guidelines into practice for the management of atrial fibrillation: results of an European Heart Rhythm Association Survey. Europace. 2018 Aug 01;20(8):1382-1387. [PubMed: 29893840]

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