Summary

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, affecting approximately 10.55 million adults in the US. It is characterized by rapid, disorganized electrical signals in the atria causing an irregular heart rhythm. AF is associated with significantly increased risk of stroke (2.4-fold), heart failure (5-fold), myocardial infarction (1.6-fold), dementia, chronic kidney disease, and mortality. Clinical presentation ranges from asymptomatic (10-40% of cases) to symptoms including palpitations, dyspnea, chest pain, and fatigue. Management focuses on stroke prevention with anticoagulation, rate or rhythm control strategies, and addressing modifiable risk factors. Early rhythm control with antiarrhythmic medications or catheter ablation is beneficial in select patients, particularly those with symptomatic paroxysmal AF or heart failure with reduced ejection fraction (HFrEF).

Definitions

The 2023 ACC/AHA/ACCP/HRS guideline writing group proposed 4 stages of AF evolution:

• Stage 1 (At-Risk): Patients with AF-associated risk factors like obesity or hypertension.
• Stage 2 (Pre-AF): Signs of atrial pathology on electrocardiogram or imaging without AF.
• Stage 3 (AF): Presence of paroxysmal (≤7 days) or persistent (>7 days) AF subtypes.
• Stage 4 (Permanent AF): Established AF where rhythm control is no longer pursued.

Valvular AF lacks a universally accepted definition but is generally categorized as AF in the presence of:

• Moderate to severe mitral stenosis (usually rheumatic in origin)
• Mechanical prosthetic heart valves

By contrast, non-valvular AF (NVAF) refers to AF occurring without these conditions, even if other valvular abnormalities (e.g., mitral regurgitation, aortic stenosis) are present.

The distinction is important because mitral stenosis and mechanical valves are primary drivers of thromboembolic risk, carrying a 10%+ annual risk of stroke without AC. Warfarin is preferred for AC in such patients because DOACs were primarily studied in NVAF with limited data in patients with valvular AF.

Etiology

The development of atrial fibrillation is multifactorial and involves both modifiable and non-modifiable risk factors:

• Age: The strongest risk factor for AF, with incidence increasing significantly after age 65. The incidence per 1000 person-years increased from 3.7 to 13.4 in men and 2.5 to 8.6 in women over 50 years of Framingham Heart Study surveillance. The lifetime risk of developing AFib for individuals over 40 years old is approximately 1 in 4.
• Cardiovascular conditions: Hypertension, heart failure, coronary artery disease, valvular heart disease (particularly mitral valve disease), and cardiomyopathies significantly increase AF risk.
• Other comorbidities: Diabetes, obesity, obstructive sleep apnea, chronic kidney disease, and hyperthyroidism are strongly associated with AF development.
• Lifestyle factors: Excessive alcohol consumption (>1 standard drink daily or binge drinking), smoking, and physical inactivity contribute to AF risk. Paradoxically, male endurance athletes have higher AF risk despite exercise generally being protective. Holiday Heart Syndrome is an Irregular heartbeat (i.e AFib) triggered by excessive alcohol, but also moderate alcohol, stress, dehydration, or lack of sleep.
• Genetic factors: Family history increases risk, with genetic variants affecting approximately 30% of AF risk. Compared with individuals in the lower third of both clinical and polygenic risk, those in the upper third have more than double the lifetime risk of AF (48.2% vs 22.3%).
• Acute medical conditions: Sepsis, surgery, and other acute medical illnesses can trigger new-onset AF, with 42-68% of these patients experiencing recurrence within 5 years.

The mnemonic "H PIRATES" can be used to remember common causes of AF: Hypertension, Pneumonia/Pericarditis/Post-op, Ischemia, Rheumatic valve disease, Atrial myxoma/Accessory pathway, Thyrotoxicosis, Ethanol/Excess volume, Sick sinus/Sepsis.

The PARASITE mnemonic (Pulmonary disease, Anemia, Rheumatic heart disease, Atrial myxoma, Sepsis, Ischemia, Thyroid disease, Ethanol) offers another structured way to remember common triggers for acute AFib episodes.

Pathophysiology

The pathophysiology of AFib involves complex interactions between triggering mechanisms and an abnormal atrial substrate that sustains the arrhythmia:

• Triggers: Ectopic atrial premature beats that initiate AF typically arise from myocardial sleeves extending from the pulmonary vein-atrial junction into the pulmonary veins. These ectopic foci can spark AF episodes when encountering vulnerable atrial tissue. In those with structurally normal hearts, most PAF episodes are triggered by premature atrial complexes (PACs), particularly those originating near the pulmonary veins.
• Substrate development: Disease-specific atrial electrophysiologic, structural, and histopathologic changes create a substrate that promotes electrical reentry and AF persistence:
  • Atrial fibrosis and hypertrophy: Hypertension activates the renin-angiotensin-aldosterone system, inducing atrial fibrosis and hypertrophy, which slows atrial conduction and promotes reentry.
  • Oxidative stress and inflammation: Obesity increases oxidative stress, systemic inflammation, and abnormal calcium cycling, increasing atrial ectopy and promoting arrhythmia maintenance.
  • Autonomic dysfunction: Conditions like sleep apnea alter atrial repolarization through autonomic dysfunction, creating a favorable environment for AF.
• AF-induced remodeling: Once established, AF itself causes additional electrical and structural remodeling ("AF begets AF"), making the arrhythmia more persistent and difficult to treat. This is one of the underpinings to more recent evidence that early rhythm control confers benefits. Electrophysiological changes can occur within hours of AFib onset (electrical remodeling), while structural remodeling (fibrosis and dilatation) develops over months.
• Bidirectional relationship with heart failure: AF and heart failure frequently coexist and predispose to each other, creating a vicious cycle. In patients with AF and newly diagnosed HFrEF, tachycardia-mediated cardiomyopathy should be considered when common etiologies have been excluded.

Signs and Symptoms

Atrial fibrillation presents with varying symptoms, though approximately 10-40% of patients are asymptomatic:

• Common symptoms:
  • Palpitations (sensation of rapid, irregular heartbeat)
  • Dyspnea (shortness of breath), especially with exertion
  • Chest discomfort or pain
  • Fatigue
  • Presyncope (light-headedness)
  • Reduced exercise tolerance
• Asymptomatic presentation:
  • More common in men (10% vs 3% in women)
  • More common in older adults (mean age 74 vs 62 years for symptomatic patients)
  • More common in those with diabetes
  • Often discovered during evaluation of complications (stroke, heart failure) or incidentally during routine examinations
• Physical examination findings:
  • Irregularly irregular pulse
  • Pulse deficit (difference between heart rate and pulse rate)
  • Variable first heart sound intensity
  • Absence of "a" waves in jugular venous pulsations
  • Apex-pulse deficit - difference betweem apical and radial pulse counted over 1 minute; a deficit of 10 or more is idicative of Afib; due to inadequate LV filling and stroke volume (Sens 62.8%, Spec 85.7%) (IJAMR, 2019)
  • Signs of underlying causes (e.g., mitral valve disease, thyroid abnormalities)
  • Signs of complications (e.g., heart failure)
  ‍

In patients presenting with stroke or infarction, the brain, kidneys, and spleen are the most likely targets of emboli in AFib.

Diagnostic Workup

Diagnosis of atrial fibrillation is based on electrocardiographic documentation and appropriate clinical evaluation:

1. Electrocardiographic confirmation:
   • 12-lead ECG showing irregular atrial activity (fibrillatory waves) without discrete P wave; make sure it’s actually afib and not just sinus rhythm with lots of PACs - look for the p-waves!
   • Episode lasting >30 seconds on rhythm strip or continuous monitoring
   • Classification based on pattern: paroxysmal (≤7 days), persistent (>7 days or requiring cardioversion), long-standing persistent (>1 year), or permanent (decision made not to pursue rhythm control)
2. Basic evaluation:
   • Complete history and physical examination: Assessing symptoms, risk factors, complications
   • Transthoracic echocardiogram: To assess cardiac structure, left atrial size, valvular disease, and ventricular function
   • Laboratory testing:
     • Complete blood count
     • Comprehensive metabolic panel
     • Thyroid function tests
     • Additional tests based on clinical suspicion
3. Extended monitoring (for suspected but undiagnosed AF):
   • Holter monitors (24-48 hours)
   • Event recorders or mobile telemetry (up to 30 days)
   • Implantable loop recorders (up to 4 years) - particularly useful after cryptogenic stroke
   • Wearable consumer devices may detect possible AF but require confirmation with standard ECG
4. Additional testing (when indicated):
   • Transesophageal echocardiography (to exclude left atrial appendage thrombus before cardioversion)
   • Cardiac CT or MRI (for pulmonary vein anatomy before ablation or to assess for structural heart disease)
   • Exercise testing (only when specific indications such as suspected ischemia)

Treatment

Management of atrial fibrillation follows a comprehensive approach targeting stroke prevention, symptom control, and addressing underlying risk factors:

Stroke Prevention

• Anticoagulation for patients with estimated stroke/thromboembolic risk ≥2% per year (generally CHA₂DS₂-VASc score ≥2 for men, ≥3 for women):
  • Calculating CHA₂DS₂-VASc score
    • Congestive heart failure (1)
    • Hypertension (1)
    • Age ≥75 (2)
    • Diabetes (1)
    • Stroke/TIA history (2)
    • Vascular disease (1)
    • Age 65-74 (1)
    • Sex category (female) (1)
  • Bleeding risk scores (i.e HAS-BLED) should NOT be used in isolation to determine eligibility for oral anticoagulation, but instead to identify and modify bleeding risk factors and to inform medical decision-making in patients deemed at high risk for stroke.
  • Direct oral anticoagulants (DOACs) are first-line for non-valvular AF:
    • Apixaban: 5 mg twice daily (2.5 mg twice daily if ≥2 of: age ≥80, weight ≤60 kg, serum creatinine ≥1.5 mg/dL); usually the best choice for CKD/ESRD
    • Rivaroxaban: 20 mg daily with food (15 mg daily if CrCl 15-50 mL/min)
    • Edoxaban: 60 mg daily (30 mg daily if CrCl 15-50 mL/min or weight ≤60 kg)
    • Dabigatran: 150 mg twice daily (110 mg twice daily if age >80 or high bleeding risk)
  • Warfarin (target INR 2.0-3.0) is indicated for:
    • Moderate-to-severe mitral stenosis
    • Mechanical heart valves
    • Patients with CrCl <15 mL/min who cannot take apixaban
• Left atrial appendage occlusion/closure (WATCHMAN, Amulet devices) may be considered for patients with contraindications to long-term anticoagulation; patients will often still need to be on AC for a period of time after a device is placed
• Antiplatelet therapy alone (aspirin) is NOT recommended for stroke prevention in AF due to inferior efficacy
• Dual vs Triple Therapy in CAD/ACS - After PCI, discontinue aspirin early (1-4 weeks) after PCI and continueAC plus P2Y12 inhibitor over triple antithrombotic therapy.
• AFib burden (duration and frequency of episodes) is associated with the risk of thromboembolic events, independent of CHADS2-VASC or ATRIA risk scores.
  • AFib episodes lasting longer than 17 to 24 hours impart significant risk.
  • There may be over twofold increase stroke risk for AF duration ≥1 hour compared with shorter durations.
  • There are no clear thresholds, however, and AFib episodes and strokes are not always temporally associated, but stroke risks is highest during the five days immediately after an episode of AFib.
  • Atrial high rate episodes (AHREs) are associated with increased risk of stroke and may be precursors to the development of AFib warranting initiation of AC.

Rate Control Strategies

The RACE II trial established a goal heart rate of <110 bpm for rate control. However, in patients with LV dysfunction or persistent symptoms, a HR of <80 is generally preferred. In critically-ill patients with AFib there is usually a more permissive HR, as quickly pushing the HR to <100 without breaking the rhythm can be dangerous.

• First-line agents:
  • Beta-blockers: Metoprolol (25-100 mg twice daily), atenolol (25-100 mg daily), or bisoprolol (2.5-10 mg daily); favored in hyperthyroidism
  • Non-dihydropyridine calcium channel blockers: Diltiazem (120-360 mg daily) or verapamil (120-360 mg daily); recent guidelines give a strong recommendation against using IV nondihydropyridine calcium channel blockers in patients with AFRVR and known moderate or severe left ventricular systolic dysfunction, with or without decompensated heart failure
• Second-line agents:
  • Digoxin: 0.125-0.25 mg daily, particularly useful in heart failure patients or as adjunctive therapy; not for acute management, as it takes 2 hours for onset
  • Amiodarone: Can be used for rate control when other agents fail
  • Procainamide: Generally preferred for patients with pre-excitation (WPW) present; in such cases, AV nodal blocking agents are contraindicated, as they can precipitate ventricular tachycardia or Vfib
• AV node ablation with pacemaker implantation: For patients with inadequate rate control despite optimal medical therapy

Rhythm Control Strategies

The EAST-AFNET trial showed some benefit for early rhythm control, though with a high number needed to treat (NNT of 333) for combined outcomes. In general, everyone with new AF deserves an early attempt at sinus rhythm either through chemical or electrical cardioversion. However, certain populations likely benefit the most from this.

• Indications for rhythm control:
  • Symptomatic AF despite adequate rate control
  • First episode of AF
  • AF with heart failure, especially HFrEF
  • Young patients
  • Athletes
  • Patient oreference for rhythm control
• Cardioversion options:
  • Electrical cardioversion: Synchronized direct current shock
    • Requires sedation.
    • Use anteroposterior pad placement (left parasternal region and left scapular region).
    • Synchronize to QRS (NEVER defibrilate).
    • Can start with 100J biphasic.
  • Pharmacological cardioversion:
    • Class Ic agents: Flecainide or propafenone (for patients without structural heart disease)
    • Class III agents: Amiodarone, dofetilide, or ibutilide
  • Short AFib duration and normal left atrial size are predictors of successful cardioversion
  • The use of antiarrhythmic drugs prior to (and after) shock delivery may increase the likelihood of success
  • Do not initiate antiarrhythmic drug therapy in patients with advanced conduction disturbances unless anti-bradycardia pacing (PPM, etc) is provided
• Maintenance of sinus rhythm:
  • Antiarrhythmic drugs:
    • Class Ic: Flecainide (50-200 mg twice daily) or propafenone (150-300 mg three times daily) - avoid in coronary artery disease and structural heart disease; can be used in a “Pill-In-Pocket” approach for patient-led cardioversion which is best for recent onset, infrequent episodes, and no structural or ischemic heart disease.
    • Class III: Amiodarone (200 mg daily), sotalol (80-160 mg twice daily), dofetilide (125-500 μg twice daily), dronedarone (400 mg twice daily)
  • Catheter ablation:
    • Pulmonary vein isolation to eliminate triggers
    • Particularly effective for:
      • Paroxysmal AF (70-80% success rate)
      • Patients with heart failure (improves outcomes)
      • Young patients with symptomatic AF
      • Those with AF refractory to antiarrhythmic drugs
    • AC after ablation is based on CHA₂DS₂-VASc score, and not on the rhythm

Risk Factor Modification

• Weight management: Target ≥10% weight reduction in overweight/obese patients with BMI >27
• Exercise: Moderate exercise 210+ minutes weekly (30 minutes daily), except in cases of AF due to excessive training
• Blood pressure control: Target <130/80 mmHg
• Management of sleep apnea: CPAP therapy when indicated
• Alcohol reduction or elimination: Particularly important for rhythm control; reduce to < 3 standard drinks per week
• Smoking cessation: Comprehensive support for tobacco cessation
• Glycemic control: Optimal diabetes management
• Caffeine abstinence is NOT advised to prevent episodes of AFib unless the patient feels that is exacerbates symptoms

Pearls

Epidemiology and General Information

• AF affects up to 1 in 3 people in their lifetime, with approximately 10.55 million adults in the US affected as of 2019.
• Lifetime risk of AF is significantly influenced by both clinical risk factors and genetics, with those in the highest risk category having >40% lifetime risk.
• Prevalence is higher in men (~28 million worldwide) compared to women (~25 million worldwide).
• 10-40% of patients with AF are asymptomatic, with asymptomatic presentation more common in men and older adults.
• New onset AF that occurs when patients are hospitalized or post-operatively should not be given a "free pass". These patients are now known to be at risk for recurrent AF and embolic events
• There is increasing identification of AFib via patient-initiated monitoring, like with Apple Watches

Pathophysiology

• Ectopic atrial beats that initiate AF typically arise from myocardial sleeves extending from the pulmonary vein-atrial junction.
• Ventricular rate variability depends on the speed of AVN conduction; younger patients can be more symptomatic and tachycardic
• AF typically begins as paroxysmal episodes but can progress to persistent and permanent forms due to progressive atrial remodeling ("AF begets AF").
• Atrial high-rate episodes (AHREs) lasting >6 minutes detected on cardiac implantable electronic devices are associated with 2.4-fold increased stroke risk.
• The probability of detecting AF increases with the duration of monitoring, making prolonged monitoring crucial in cases like cryptogenic stroke.
• Afib is distinct from multifocal atrial tachycardia

Etiology and Risk Factors

• Approximately 15% of individuals who develop AFib have no identifiable risk factors.
• Taller height is independently associated with increased AF risk, possibly due to larger atrial size.
• Vagally-mediated AF commonly occurs at night or in the early morning when vagal tone is normally predominant.
• Male endurance athletes have higher AF risk despite physical activity typically being associated with lower risk in the general population.
• New-onset AF during hospitalization for non-cardiac illness has 5-year recurrence rates of 42-68% and is associated with increased stroke and mortality risk. PAF recurrence is common, ranging from 70% at one year (without antiarrhythmic therapy) to 60-90% at 4-6 years.
• The rates of progression from paroxysmal AFib to persistent AFib is 8%, 12%, 18%, and 25% at 1, 2, 4, and 5 years respectively.
• Younger age, lower rates of HTN and heart failure, smaller LA diameter, and preserved LV systolic function are associated with a lower risk of progression to persistent AFib.
• Sodium-glucose cotransporter-2 (SGLT2) inhibitors are associated with reduced AF risk (RR 0.82) in patients with diabetes, heart failure, or kidney disease.

Clinical Presentation and Diagnosis

• AF diagnosis requires ECG documentation of irregular atrial activity without discrete P waves lasting >30 seconds.
• The true prevalence of PAF may be underestimated due to asymptomatic episodes, even those lasting >48 hours.
• The duration of recurrent AF episodes vary over time in each individual, and progression to persistent or permanent AF is common.
• The LOOP Study found that despite increased AF detection with implantable loop recorders (31.8% vs 12.2%), there was no significant reduction in stroke when anticoagulation was instituted.
• Consumer wearable devices (smartwatches) have relatively low positive predictive value for AF; in the Apple Heart Study, only 34% of notifications were subsequently confirmed as AF.
• In AF with concurrent heart failure, consider tachycardia-mediated cardiomyopathy if common etiologies have been excluded.
• At very high rates, AF may appear regular ("pseudo-regularization"), emphasizing the need to carefully evaluate ECGs at high heart rates.
• AF with RVR is more often a consequence of hypotension rather than the cause of it unless HR >150; however Afib can reduce preload via reduced “atrial kick” since there is no coordinated p-wave
• AFib itself can independently elevate D-dimer, troponin, and BNP levels, necessitating careful interpretation in the context of suspected PE, ACS, or heart failure
• Rapid ventricular rate in PAF may cause angina and ischemic ECG changes, potentially with troponin elevation, mimicking an acute coronary syndrome.
• Distinguishing between fib and flutter is not always straightforward - in flutter, the rhythm may be regularly irregular if atrial flutter occurs with a variable AV block occurring in a fixed pattern (2:1 or 4:1). On the other hand, the rhythm may be irregularly irregular with a variable block occurring in a nonfixed pattern.

Treatment

• DOACs reduce risk of intracranial hemorrhage by approximately 50% compared to warfarin.
• CHADS-VASc and AC use in Afib is not really validated in critically ill patients and is a much more nuanced decision based on risks and benefits
• Early rhythm control (within 1 year of diagnosis) reduces cardiovascular outcomes by 21% compared to rate control alone.
• Get baseline LFTs and TFTs before starting amiodarone
• Amiodarone can cause pulmonary fibrosis
• Amiodarone can still lead to hypotension initially, especially when bolused
• In unstable Afib RVR, the first pressor should generally be phenylephrine (avoids adrenergic agonism and can lead to reflex bradycardia); it doesn't make sense to use levo, especially if you had previously been giving beta blockers
• If starting pressors in patient with AFib RVR, generally also good to avoid epinephrine and dobutamine which are beta-adrenergic
• Catheter ablation is superior to medical therapy for AF with heart failure, reducing death or HF hospitalization by 38% in the CASTLE-AF trial; ablation is more effective than antiarrhythmics for maintaining sinus rhythm
• Left atrial appendage occlusion requires at least 45 days of anticoagulation followed by dual antiplatelet therapy for 6 months and lifelong aspirin.
• Atrial flutter is treated similarly, but tougher to successfully rate control and it will stay in the 150 range which represents the 2:1 transmission through the AV node; usually need to ablate the cavo-tricuspid isthmus
• The most important intervention for critically ill patients with AF is usually treating the cause(s) of AF.

Complications

• AF is associated with 2.4-fold increased risk of stroke, 5-fold increased risk of heart failure, 1.6-fold increased risk of myocardial infarction, and 1.5-fold increased all-cause mortality.
• The left atrial appendage is the source of ~90% of thombi who have CVA with AFib
• There is between a 1-7% chance of stroke with cardioversion if the patient is not anticoagulated
• Cardioversion can “stun” myocardium and leave patients prone to clot formationa and stroke risk; AC is still needed for at least the first 10 days after successful conversion; there is no clear endpoint for AC due to recurrence likelihood being a shigh as 50% annually
• AF is associated with increased risk of both Alzheimer's disease (aOR 1.4) and vascular dementia (aOR 1.7), even in stroke-free patients.
• AF is independently associated with cognitive decline, with anticoagulation potentially reducing this risk.
• AF management and outcomes show significant disparities by sex, race, ethnicity, and social determinants of health, with worse outcomes in disadvantaged populations.

Trials and Helpful Literature

Review Articles

• Atrial Fibrillation A Review (JAMA, 2025)
• Direct Oral Anticoagulants in Patients with ESRD (Kidney Int Rep, 2025)
• Catheter ablation for atrial fibrillation: indications and future perspective (Eur Heart J, 2024)

Clinical Trials

Rate and Rhythm Control

• AFFIRM - In patients with atrial fibrillation and risk factors for stroke, a rhythm-control strategy (cardioversion and antiarrhythmic drugs) did not reduce mortality compared to a rate-control strategy, and was associated with more hospitalizations and adverse drug effects. (NEJM, 2002)
• RACE II Trial - In patients with permanent atrial fibrillation, lenient rate control (HR <110) was noninferior to strict rate control (HR <80) in preventing a composite endpoint of death from cardiovascular causes, hospitalization for heart failure, stroke, systemic embolism, bleeding, and life-threatening arrhythmic events, while being easier to achieve. Strict rate control may be better in younger patients and those with heart failure (NEJM, 2010)
• EAST-AFNET 4 Trial - In patients with early atrial fibrillation (diagnosed ≤1 year) and cardiovascular conditions, early rhythm-control therapy (antiarrythmic or ablation) led to a lower risk of death from cardiovascular causes, stroke, or hospitalization for heart failure or acute coronary syndrome, when compared to usual care. (NEJM, 2020)

Ablation

• CASTLE-AF - In patients with heart failure and atrial fibrillation, catheter ablation led to significantly lower rates of death and hospitalization for worsening heart failure, when compared to medical therapy (either rate or rhythm control). (NEJM, 2018)
• CABANA Trial - In patients with atrial fibrillation (”all-comers”), catheter ablation did not significantly reduce the composite primary endpoint of death, disabling stroke, serious bleeding, or cardiac arrest when compared to conventional medical therapy, though it was associated with lower rates of recurrent atrial fibrillation and the secondary endpoint of death or cardiovascular hospitalization. (JAMA, 2019)

Anticoagulation

• ARISTOTLE - In patients with atrial fibrillation and at least one additional risk factor for stroke, apixaban was superior to warfarin in preventing stroke or systemic embolism, caused less bleeding, and resulted in lower mortality. (NEJM, 2011)
• ROCKET-AF - In patients with nonvalvular atrial fibrillation at moderate-to-high risk for stroke, the once-daily oral direct factor Xa inhibitor rivaroxaban was noninferior to adjusted-dose warfarin for the prevention of stroke or systemic embolism, when compared to warfarin. (NEJM, 2011)

AC Therapy in AFib with CAD/ACS

• AUGUSTUS - In patients with atrial fibrillation who have had an acute coronary syndrome or undergone PCI, apixaban led to less bleeding and fewer hospitalizations compared to vitamin K antagonists, without significant differences in ischemic events. Additionally, omitting aspirin resulted in less bleeding without significant differences in ischemic events when compared to regimens that included aspirin. (NEJM, 2019)
• AFIRE - In patients with atrial fibrillation and stable coronary artery disease more than 1 year after revascularization or with angiographically confirmed disease not requiring revascularization, rivaroxaban monotherapy led to fewer cardiovascular events and deaths while causing less bleeding, when compared to combination therapy with rivaroxaban plus a single antiplatelet agent. (NEJM, 2019)

Other Resources

• MD Calc
  • CHADS-VASc (one year risk of thromboembolic event in non-anticoagulated patient)
  • HAS-BLED (risk of bleed on DOAC)
• The Curbsiders Podcast - #363 Afib: Rythm Control, Catheter Ablation, Afib in the Hospital, and LAA Closure
• UCSF Hospitalist Handbook - Chapter 8 Atrial Fibrillation
• Internet Book of Critical Care - Atrial Fibrilation and Flutter Complicating Critical Illness - managing AFib in an ICU setting has distinct considerations discussed in this article

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