Atrial Fibrillation Archives - Cardionerds

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Atrial Fibrillation Archives - Cardionerds episodes

May 21449. Atrial Fibrillation: Challenging Scenarios in Atrial Fibrillation Management with Dr. Bradley Knight
In this episode, CardioNerds Dr. Colin Blumenthal, Dr. Kelly Arps, and Dr. Yong Hao Yeo are joined by electrophysiology expert Dr. Bradley Knight to discuss atrial fibrillation (AF) management in challenging clinical scenarios. We explore arrhythmias in patients with pre-excitation syndromes, particularly Wolff-Parkinson-White (WPW) syndrome, and strategies for rhythm control. We also discuss AF management in pregnancy, adult congenital heart disease, and patients with tachycardia-bradycardia (tach-brady) syndrome. This episode provides essential insights into nuanced decision-making for the care of patients with complex arrhythmia profiles. Audio editing by CardioNerds academy intern, Grace Qiu.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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PEARLS
AF in WPW is a true emergency—AV nodal blocking agents can be deadly. In patients with WPW syndrome, AF can rapidly conduct through the accessory pathway, risking ventricular fibrillation and sudden death. Avoid AV nodal blockers like beta-blockers and calcium channel blockers.
Catheter ablation is the first-line rhythm control strategy in WPW. Catheter ablation carries a Class I recommendation and offers >90% success. If antiarrhythmic drugs are needed, sodium channel blockers like flecainide or propafenone are preferred in patients without structural heart disease.
In pregnancy, protecting the mother is protecting the fetus. An unstable mother means an unstable fetus. Rate control is the first step in AF with rapid ventricular responses and electrical cardioversion is safe when needed. Multidisciplinary care is essential.
AF in congenital heart disease is often outside the pulmonary veins. Surgical scars and chamber remodeling in ACHD patients often lead to AF from non-pulmonary vein foci. Electrogram-based mapping and targeted ablation strategies are essential to increase success rate of durable rhythm control.
Tachy-brady syndrome may require pacing to unlock therapy. AF may cause atrial myopathy and sinus node dysfunction. These patients often require permanent pacing to allow safe use of rate-controlling medications like beta-blockers and to prevent syncope or chronotropic incompetence.
Notes: Notes drafted by Dr. Yong Hao Yeo
Why is atrial tachycardia in patients with WPW syndrome dangerous?
Patients with WPW commonly present with supraventricular tachycardia (SVT) due to atrioventricular reentrant circuits, either orthodromic or antidromic. This SVT can degenerate into AF.
In the absence of AV nodal as the governor between the atrium and ventricles, the accessory pathway may conduct impulses rapidly and frequently. This can lead to dangerously high ventricular rates, predisposing patients to ventricular fibrillation and sudden cardiac arrest.
What are some strategies for rhythm control in patients with WPW and atrial tachycardia?
Catheter ablation is the first-line therapy (Class I recommendation), with a success rate of over 90%.
Ablation reduces the risk of sudden cardiac arrest, though some patients may remain prone to AF.
If ablation is not feasible/ contraindicated, sodium channel blockers such as flecainide and propafenone are good options in patients without ischemia or structural heart disease (Class IIa recommendation).
Amiodarone should be avoided because it has a long half-life, can accumulate in the system, and may delay definitive treatment with catheter ablation.
AV nodal blocking agents like beta blockers and calcium channel blockers should be avoided, as they are less effective at controlling ventricular rate in WPW and can increase conduction over the accessory pathway. These agents can also exacerbate the risk of rapid ventricular rates during AF and worsen left ventricular function.
What are some special considerations in managing AF in pregnant patients?
The primary goal in managing cardiovascular disease during pregnancy is to protect the mother, as fetal outcomes depend on maternal well-being. Therefore, while caution is necessary, we should avoid undertreating pregnant patients with AF.
In cases of AF with rapid ventricular response (RVR), rate control is usually the first-line strategy, with beta blockers preferred over digoxin or non-dihydropyridine calcium channel blockers. It is then reasonable to initially observe for spontaneous conversion in stable patients.
Antiarrhythmic drugs (AADs) are generally avoided during the first trimester, but clinical judgment on a case-by-case basis is essential.
Evidence for the safety of AADs in pregnancy is limited, often derived from their use in other conditions such as fetal SVT. Flecainide and sotalol are reasonable options for rhythm control (Class IIa recommendation).
Electrical cardioversion is considered safe in pregnancy and should be utilized when indicated (Do not forget!).
There is no pregnancy-specific thromboembolic risk stratification tool. CHA₂DS₂-VASc scoring and the presence of risk factors like mitral stenosis can help guide anticoagulation decisions, though the magnitude of thromboembolic risk during pregnancy remains unclear.
Rate control agents are typically continued during delivery due to the increased physiologic stress of labor and delivery.
Multidisciplinary care is crucial and should involve obstetrics, maternal-fetal medicine, cardiology, and electrophysiology specialists.
What are some key considerations for AF management in patients with adult congenital heart disease (ACHD)?
Patients with repaired congenital heart disease are at increased risk for arrhythmias due to two main factors: surgical scars that create arrhythmogenic foci and mechanical remodeling of the atria or ventricles resulting from the underlying disease.
In these patients with structural heart disease, sodium channel blockers may not be ideal antiarrhythmic options.
When selecting an antiarrhythmic drug, clinicians must consider the nature of structural or surgical impairments, such as right bundle branch block or prolonged QT interval.
It is also essential to assess renal and hepatic function (often impaired in patients with ACHD) to ensure appropriate metabolism and clearance of antiarrhythmic medications.
Electrogram-based ablation strategies (those leveraging artificial intelligence are developing!) may help identify effective ablation targets, which are often outside the pulmonary veins in patients with ACHD. These individualized approaches can improve ablation success rates in this complex patient population.
What makes tachycardia-bradycardia (tach-brady) syndrome a unique challenge in arrhythmia management?
Patients who present with both AF and bradycardia, especially with syncope, require a thoughtful diagnostic approach to identify the underlying rhythm disturbance.
Extended cardiac monitoring, including event monitors or implantable loop recorders, can help capture intermittent arrhythmias and correlate them with symptoms.
AF may lead to atrial myopathy, and since the sinus node resides within the atrium, this can result in sinus node dysfunction—a hallmark of tachy-brady syndrome.
Following spontaneous conversion from AF to sinus rhythm, sinus node dysfunction may persist, leading to prolonged pauses or chronotropic incompetence.
Management becomes more complex when beta-blockers are needed for AF with RVR, as they can exacerbate bradycardia. Permanent pacemaker implantation is often the next step to consider.
Permanent pacemaker implantation is often considered to facilitate safe rate control in these cases.
In younger patients, aggressive AF burden reduction may prevent atrial remodeling and the development of true atrial myopathy, potentially avoiding pacemaker implantation.
References
Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2023;149(1). doi:https://doi.org/10.1161/CIR.0000000000001193 ‌
Van IC, Rienstra M, Bunting KV, et al. 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). European Heart Journal. 2024;45(36). doi:https://doi.org/10.1093/eurheartj/ehae176 ‌
Joglar JA, Kapa S, Saarel EV, et al. 2023 HRS expert consensus statement on the management of arrhythmias during pregnancy. Heart Rhythm. Published online May 1, 2023. doi:https://doi.org/10.1016/j.hrthm.2023.05.017 ‌
Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: Executive Summary. Journal of the American College of Cardiology. 2019;73(12):1494-1563. doi:https://doi.org/10.1016/j.jacc.2018.08.1028 ‌
38 min
February 13441. Atrial Fibrillation: Ablation of Atrial Fibrillation with Dr. Jon Piccini
CardioNerds (Dr. Ramy Doss, Dr. Kelly Arps, and Dr. Naima Maqsood) dive into the nuances of atrial fibrillation (AF) ablation with Dr. Jon Piccini. They provide a high-yield overview of AF ablation, guiding listeners from patient selection through post-procedural management. We review appropriate candidacy for catheter ablation across AF phenotypes, key elements of pre-procedural evaluation including imaging and anticoagulation strategy, and the fundamental procedural steps with pulmonary vein isolation as the cornerstone. The discussion compares lesion set strategies in de novo ablation and reviews currently used energy sources—including radiofrequency, cryoablation, and pulsed-field ablation—highlighting differences in safety and efficacy. They also examine surgical and hybrid approaches for selected patients and outline essential components of post-ablation care, including rhythm monitoring, anticoagulation decisions, and management of complications. This episode integrates contemporary evidence with practical insights to support clinicians delivering comprehensive AF ablation care. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah.
NOTE: This episode was recorded in March 2025. Since then, the OCEAN trial showed that among patients who had had successful catheter ablation for atrial fibrillation at least 1 year earlier and had risk factors for stroke, treatment with rivaroxaban did not result in a significantly lower incidence of a composite of stroke, systemic embolism, or new covert embolic stroke than treatment with aspirin.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
CardioNerds Atrial Fibrillation Page
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PEARLS
Pulmonary veins (PVs) are the dominant triggers in early AF due to their unique myocardial sleeve electrophysiology.
Pulmonary vein isolation (PVI) remains the cornerstone of AF ablation by blocking PV triggers from reaching the left atrium. Posterior wall isolation is sometimes performed in persistent AFib, but large RCTs found no significant benefit over PVI alone.
Paroxysmal AF has the highest ablation success rates. Left atrial health remains the major determinant of outcome.
Ablation modalities include pulsed field ablation, radiofrequency ablation, and cryo-balloon ablation. PFA offers advantage of relative myocardial selectivity with near zero risk of atrio-esophageal fistula.
Long-term anticoagulation decisions after ablation currently depend on CHA₂DS₂-VASc score. Recent evidence suggests the safety of stopping anticoagulation in low-risk patients after ablation.
Early atrial arrhythmia recurrence during a blanking period after ablation (≤3 months) often reflects inflammation — not procedural failure. Late recurrence suggests PV reconnection or residual substrate and often requires repeat ablation.
Hybrid surgical and catheter Afib ablation represent an aggressive strategy for rhythm control in patients with persistent or long-standing persistent AF with extensive substrate and/or patients who have had multiple failed catheter ablations.
Notes
1. What is the mechanism behind AF initiation?
Atrial fibrillation (AF) is a progressive condition.
Early AF is primarily trigger-driven, most commonly from the pulmonary veins.
Pulmonary vein myocardial sleeves have unique electrophysiologic properties that promote premature beats and afterdepolarizations.
As AF progresses, atrial remodeling (fibrosis and scar) leads to a more substrate-driven arrhythmia.
2. How does early catheter ablation for atrial fibrillation work?
Electrical Isolation of pulmonary veins, blocking PV triggers from reaching the left atrium.
By reducing burden of atrial fibrillation, this may slow adverse atrial remodeling.
3. Which patients are good candidates for Afib ablation?
Functional Status: ambulatory, active patients derive the greatest benefit. Advanced frailty or severe end-stage cardiovascular disease reduces expected benefit.
Comorbidity Burden: CHA₂DS₂-VASc score helps risk-stratify not only stroke risk but also rhythm-control outcomes.
Type and Duration of AF
Paroxysmal AF → highest likelihood of success (burden reduction often 95–99%).
Long-standing persistent AF → lower suppression rates (often 50–80%).
Left Atrial Health: a major determinant of outcomes.
LA diameter >5.5 cm associated with significantly worse outcomes.
LA volume index (normal ≤34 mL/m²) is preferred over diameter for assessment.
4. What are the predictors of complications from AFib ablation procedures?
Low and high body mass index (BMI)
Chronic corticosteroid use
Severe enlargement of other cardiac chambers
Female gender is associated with a numerically higher risk of complications.
5. Role of preprocedural imaging with cardiac CT or MRI
Cardiac CT
Faster and convenient
Help define LA geometry and Pulmonary vein anatomy
Anatomic Variants as Right middle pulmonary vein, accessory pulmonary veins common pulmonary vein ostium, Atrial diverticula or Accessory left atrial appendage
Consider Cardiac MRI when:
Strong family history of atrial fibrillation or cardiomyopathy
Suspicion of occult structural heart disease
6. Key Procedural Steps in AF Ablation
There is significant variation across centers in anesthesia, mapping, and ablation strategies.
The following outline reflects a common contemporary approach.
Anesthesia & Monitoring
Most commonly performed under general anesthesia.
Benefits include improved catheter stability, enhanced patient comfort, and controlled ventilation (e.g., low-volume, high-frequency).
Invasive arterial line (A-line) is preferred for rapid detection of hypotension.
Vascular Access
Ultrasound-guided femoral venous access with multiple sheaths.
Micropuncture technique is ideal to minimize complications.
Intracardiac Echocardiography (ICE)
ICE catheter insertion.
Reduces complications, guides transseptal puncture, assesses catheter contact, and monitors for pericardial effusion.
Anticoagulation
Systemic heparin initiated before or immediately after transseptal access.
Activated clotting time (ACT) maintained in therapeutic range (typically >300 seconds).
Transseptal Puncture
Access to the left atrium via transseptal sheath.
Often uses electrocautery-assisted wire, with ICE guidance to improve safety.
Left Atrial Mapping
Creation of electroanatomic map (common in many centers).
Ideally performed in sinus rhythm.
Assesses left atrial geometry, voltage (for scar/substrate), and activation timing.
Ablation Strategy
Core component is pulmonary vein isolation (PVI).
Technology options include pulse field ablation (PFA), radiofrequency ablation, and cryoballoon ablation.
Additional ablation (case-dependent):
Posterior wall isolation
Targeting non-pulmonary vein triggers
Linear lesions
Ablation of organized atrial tachycardias/flutters
Emerging approaches include AI-guided strategies.
Post-Ablation Assessment
Confirm pulmonary vein entrance and exit block.
Remap left atrium (in many practices) to evaluate lesion completeness.
Check for complications (e.g., ICE assessment for pericardial effusion).
7. What is Electroanatomic Mapping?
Combines 3D geometry (anatomic reconstruction of cardiac chamber) with electrophysiology (electrical signals from tissue).
How it works:
Mapping catheter is moved along the atrial wall
Records electrograms
System generates:
3D chamber model
Voltage map (tissue health/scar)
Activation map (depolarization timing)
Key information provided
Voltage map (substrate assessment):
High voltage = healthy tissue
Low voltage = scar/fibrosis
Identifies areas needing additional ablation (e.g., posterior wall scar)
Activation map:
Visualizes wavefront propagation
Essential for diagnosing and ablating macroreentrant atrial flutters and organized atrial tachycardias
8. What is the current role of Afib ablaton outside pulmonary vein isolation?
While Pulmonary Vein Isolation (PVI) remains the cornerstone of atrial fibrillation (AF) ablation, adjunctive strategies are increasingly used for persistent AF, with varying levels of supporting data.
Non-PVI Triggers:
Arrhythmogenic foci found outside the pulmonary veins in 10% to 20% of patients.
Common sites include SVC, LAA, CS, and Crista Terminalis.
Identifying and ablating these inducible triggers—often provoked by isoproterenol—can reduce recurrence in persistent AF.
Posterior Wall Isolation (PWI):
The posterior wall is a driver for persistent AF.
Randomized evidence for routine PWI is conflicting.
Large RCTs found no significant benefit over PVI alone for first-time ablations.
Remains a primary adjunctive target for redo procedures.
AI-Guided Ablation:
Uses AI to identify “spatio-temporal dispersion” areas.
Recent TAILORED-AF trial demonstrate increased freedom from AF at 12 months compared to conventional PVI.
9. Comparison of ablation techniques
Pulsed Field Ablation (PFA) – Non-Thermal
Mechanism: irreversible electroporation
Key advantages:
Shorter procedural time
Comparable efficacy to thermal ablation
Higher myocardial tissue selectivity
No known risk of esophageal fistula or pulmonary vein stenosis
Low risk of phrenic nerve (usually transient)
Disadvantages:
Less flexibility for complex substrate
Hemolysis with possible AKI
Early and delayed coronary spasms
Skeletal muscle stimulation during energy delivery
Loss of all electrograms even with reversible injury can be misleading
Limited long term data
Radiofrequency Ablation (RFA) – Thermal (Heat)
Mechanism: resistive heating
Key advantages:
Highly versatile
Can tailor lesions
Long term experience
Disadvantages:
More procedural time (less with ultrahigh power RFA)
Very small risk of esophageal fistula (1/2000 but 50% mortality!)
Pulmonary vein stenosis
Rare Phrenic nerve palsy
Stem pops
Cryoballoon Ablation (CBA) – Thermal (Cold)
Mechanism: Uses extreme cold
Key Advantages:
Short learning curve
Single shot balloon
Highly reproducible
Good catheter stability (adhesion during freeze)
Low risk of thrombus
Disadvantages:
Similar to RFA
More phrenic nerve palsy
Less esophageal fistula and pulmonary vein stenosis
10. Other Complications of AF Catheter Ablation common to all modalities
Pericardial effusion/tamponade: 0.4–2.2%
Stroke/TIA: ~0.2–1.8%
In-hospital mortality: Very low (0.05–0.46%)
Often overstated in studies based on National Inpatient Sample (NIS) due to selection bias
Vascular access complications: Hematoma
11. Expert approach to Antiarrhythmic Drug (AAD) Therapy After AF Ablation
Continue AAD for the 3-month blanking period after catheter ablation.
Supported by multiple trials to reduce early AF recurrences.
Decreases hospitalizations during the healing phase by suppressing inflammation-related arrhythmias.
AADs do not clearly improve long-term freedom from AF.
At the 3-month follow-up:
If the patient is asymptomatic with no documented recurrence → discontinue AAD.
If recurrent AF occurs or high substrate burden persists → consider continuing AAD.
12. Expert approach to Anticoagulation After AF Ablation
All patients require anticoagulation for at least 3 months post–ablation.
Current guidelines recommend long-term anticoagulation decisions guided solely by CHA₂DS₂-VASc score.
Decisions should not be based on ablation success or arrhythmia burden.
New data support discontinuation in low-risk patients after careful shared decision-making.
In high-risk patients:
Observational data indicate ~2.5-fold increased stroke risk when anticoagulation is stopped.
OCEAN trial:
Generally low risk patients (mean CHA2DS2-VASc score 2.2).
Rivaroxaban did not significantly reduce composite stroke outcomes compared with aspirin.
13. Approach to recurrent Atrial Arrhythmias After AF Ablation
Early (≤3 months – blanking period):
True blanking probably less (6 weeks to 2 months)
Likely less with PFA
Often due to inflammation or lesion maturation
Should not be considered procedural failure
Management:
Continue or restart AAD
Electrical cardioversion for persistent symptomatic episodes
Avoid early repeat ablation
Late (>3 months) recurrences:
More likely due to pulmonary vein reconnection or residual atrial substrate
Arrhythmias include:
Recurrent atrial fibrillation
Atypical (macroreentrant) atrial flutter
Typical atrial flutter (cavotricuspid isthmus–dependent)
Focal atrial tachycardia
Management is often challenging and may include AAD, cardioversion, or repeat ablation.
14. When to Consider Hybrid Surgical and Catheter Ablation for Atrial Fibrillation?
Aggressive rhythm control strategy when standard endocardial approaches are insufficient.
Typically for persistent or long-standing persistent AF (>12 months).
Often used in patients with extensive substrate or multiple failed catheter ablations.
Can be performed during concomitant cardiac surgery or as a stand-alone hybrid procedure.
Benefits of surgical approach:
Epicardial posterior wall/dome ablation
PVI
Ligation of the ligament of Marshall
Left atrial appendage closure (e.g., AtriClip)
Approach:
Subxiphoid/minimally invasive surgical access
Endocardial EP confirmation
Additional PVI ablation and gap closure
Evidence suggests increased freedom from atrial arrhythmias at the expense of higher major adverse event risk.
54 min
December 25, 2025439. Atrial Fibrillation: Anti-Arrhythmic Drugs in the Management of Atrial Arrhythmias with Dr. Andrew Epstein
CardioNerds (Dr. Colin Blumenthal, Dr. Kelly Arps, and Dr. Natalie Marrero) discuss anti-arrhythmic drugs in the management of atrial fibrillation and atrial flutter with electrophysiologist Dr. Andrew Epstein. We discuss two major classes of anti-arrhythmic drugs, class IC and class III, as well as digoxin. Dr. Epstein explains their mechanisms of action, indications and specific patient populations in which they would be particularly helpful, efficacy, adverse side effects, contraindications, and key drug-drug interactions. We also elaborate on defining clinical trials and their clinical implications. Given the large burden of atrial fibrillation and atrial flutter in our patient population and the high prevalence of anti-arrhythmic drug use, this episode is sure to be applicable to many practicing physicians and trainees. Audio editing by CardioNerds academy intern, Grace Qiu.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
CardioNerds Atrial Fibrillation Page
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CardioNerds Academy
Cardionerds Healy Honor Roll
CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!
Pearls
Anti-arrhythmic drugs should not be thought of as an alternative to ablation but, instead, should be considered an adjunct to catheter ablation.
Class IC anti-arrhythmic drugs, flecainide and propafenone, are highly efficacious for acute cardioversion and a great option for patients with infrequent episodes of AF who do not have a history of ischemic heart disease.
Class III anti-arrhythmic drugs like ibutilide, sotalol, and dofetilide, are highly effective for acute conversion; however, they require hospitalization for close monitoring during initiation and dose titration given the risk of prolonged QT.
Amiodarone should not be used as a first line agent given its toxicities, prolonged half-life, large volume of distribution, and drug-drug interactions.
Dr. Epstein notes that, “All drugs are poisons with a few beneficial side effects,” when highlighting the many adverse side effects of anti-arrhythmic drugs, particularly amiodarone, and the importance of balancing their benefit in rhythm control with their side effect profile.
Notes
Notes: Notes drafted by Dr. Natalie Marrero.
What are the Class IC anti-arrhythmic drugs and what indications exist for their use?
Class IC anti-arrhythmic drugs are anti-arrhythmic drugs that work by blocking sodium channels and, thereby, prolonging depolarizing.
Class IC anti-arrhythmic drugs include flecainide and propafenone.
Class IC anti-arrhythmic drugs are good agents to use in patients that have infrequent episodes of AF and do not want daily dosing as these agents can be used by patients when they feel palpitations and desire acute conversion back to sinus rhythm (“pill in the pocket” approach).
What are the adverse consequences and/or contraindications to using a class IC agent?
Class IC anti-arrhythmic agents are contraindicated in patients with a history of ischemic heart disease based on increased mortality associated with their use in these patients in the CAST trial.
Given the results of the CAST trial, providers should screen annually for ischemia via a functional stress test in patients on these drugs at risk for coronary disease.
These drugs can increase 1:1 conduction of atrial flutter and, therefore, require concomitant use of a beta blocker.
These agents are generally well-tolerated without any organ toxicities; however, they can precipitate heart failure in patients with cardiomyopathies, cause sinus node depression, and unmask genetic arrythmias such as a Brugada pattern.
What are the class III agents and what are indications for their use?
Class III agents are drugs that block the potassium channel, prolonging the QT, and include Ibutilide, Sotalol, and Dofetilide.
Class III agents can be considered in patients with or without a history of ischemic heart disease that desire effective acute chemical cardioversion and are willing to go to the hospital for close monitoring during dose initiation and titration.
Other specific circumstances in which one can use these agents, specifically Ibutilide, are in patients with recurrent atrial fibrillation and Wolf Parkinson White (due to slowed conduction via the accessory pathway).
What are the adverse consequences and/or contraindications to using a class III agent?
Ibutilide, Sotalol, and Dofetilide prolong the QT and increase the risk of torsade de pointes, which is why they require ECG monitoring in-patient during drug initiation and dose titration.
These agents are generally well-tolerated.
Sotalol should be avoided or used cautiously in patients with left ventricular dysfunction, while dofetilide can be used and has dose-response beneficial effects in patients with left ventricular dysfunction.
Both sotalol and dofetilide are renally cleared with specific creatinine clearance cutoffs (CrCl < 20 for dofetilide and CrCl <40 for sotalol) and their dose should be adjusted based on the patient’s creatinine clearance (not eGFR).
What is the mechanism of action and indications for using amiodarone?
Amiodarone is a class III anti-arrhythmic agent, so it blocks the potassium channel prolonging the QT. Amiodarone is a “dirty drug” as it also has Class I (sodium channel blockade), Class II (antisympathetic action), and Class IV (calcium channel blockade) actions.
Amiodarone should be used as a second line agent.
Amiodarone can be considered in young, stable outpatients who are already in sinus rhythm especially greater than 60 beats per minute for outpatient loading.
What are the drawbacks of amiodarone?
Amiodarone, given its large volume of distribution and need to reach ~10 g for efficacy in conversion, takes a longer time to load and, therefore, a longer time to cardiovert.
Amiodarone is associated with multiple organ toxicities including pulmonary fibrosis, thyroid toxicity (both hypothyroidism and hyperthyroidism), peripheral neuropathy, sinus bradycardia, QT prolongation, corneal deposits, retinitis and vision loss.
Given the organ toxicities, patients on amiodarone should have their LFTs and TSH, a chest X-ray, and electrocardiogram checked at least every 6 months.
Amiodarone sensitizes patients to warfarin and increases digoxin levels, so if patients are on amiodarone with warfarin or digoxin, lower levels of warfarin or digoxin should be used.
What is dronedarone? How does it differ from amiodarone?
Dronedarone is a class III antiarrhythmic, which means it works by blocking the potassium channel and prolonging the QT.
Dronedarone differs from amiodarone in that it lacks iodine moiety and, therefore, does not have the associated thyroid toxicities. It also has a shorter half-life and smaller volume of distribution.
What are the contraindications to using dronedarone?
In the PALACE trial, dronedarone was associated with increased mortality in patients with heart failure, so it should be avoided in patients with clinical heart failure within the last six months.
What is the mechanism of action and indication for using digoxin?
Digoxin has several mechanisms of action including increasing vagal tone, inhibiting the sodium potassium ATPase, and acting as a positive inotrope.
Digoxin is indicated as a second line drug when better rate control is needed.
Digoxin improves rate control by increasing vagal tone and so may have an impact on resting rates. However, exertional rates may remain unctonrolled since these are mediated by sympathetic tone.
Digoxin is a good option in patients that are not particularly active given that it decreases ventricular rate at rest, but not with exercise.
Digoxin may be particularly beneficial in patients with heart failure given its positive ionotropic effects.
What are the adverse side effects of digoxin and special monitoring required for patients on digoxin?
Typically, digoxin levels are monitored, however they are usually not helpful as the levels are often drawn randomly. To be informative, the levels need to be a trough levels drawn right before the drug is given.
The literature contains conflicting results on the mortality associated with digoxin levels.
In general, the consensus in the field is that lower levels are better.
Digoxin is renally cleared, so levels should be closely monitored in patients with renal failure.
References
1. Mar PL, Horbal P, Chung MK, et al. Drug interactions affecting antiarrhythmic drug use. Circulation: Arrhythmia and Electrophysiology. 2022;15(5):e007955. https://doi.org/10.1161/CIRCEP.121.007955. doi: 10.1161/CIRCEP.121.007955.
2. Gianfranchi L, Luzi M, Solano A, et al. Outpatient treatment of recent-onset atrial fibrillation with the “pill-in-the-pocket” approach. N Engl J Med. 2004;351(23):2384–2391. https://doi.org/10.1056/NEJMoa041233. doi: 10.1056/NEJMoa041233.
3. Barker AH, Echt DS, Arensberg D, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. N Engl J Med. 1991;324(12):781–788. https://doi.org/10.1056/NEJM199103213241201. doi: 10.1056/NEJM199103213241201.
4. Markman Timothy M., Jarrah Andrew A., Ye T, et al. Safety of pill-in-the-pocket class 1C antiarrhythmic drugs for atrial fibrillation. JACC: Clinical Electrophysiology. 2022;8(12):1515–1520. https://doi.org/10.1016/j.jacep.2022.07.010. doi: 10.1016/j.jacep.2022.07.010.
5. Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS guideline for the diagnosis and management of atrial fibrillation: A report of the american college of cardiology/american heart association joint committee on clinical practice guidelines. Circulation. 2024;149(1):e1–e156. https://doi.org/10.1161/CIR.0000000000001193. doi: 10.1161/CIR.0000000000001193.
6. Ferrari F, Santander IRMF, Stein R. Digoxin in Atrial Fibrillation: An Old Topic Revisited. Curr Cardiol Rev. 2020;16(2):141-146. doi:10.2174/1573403X15666190618110941
7. Van Gelder I,C., Rienstra M, Bunting KV, et al. 2024 ESC guidelines for the management of atrial fibrillation developed in collaboration with the european association for cardio-thoracic surgery (EACTS): Developed by the task force for the management of atrial fibrillation of the european society of cardiology (ESC), with the special contribution of the european heart rhythm association (EHRA) of the ESC. endorsed by the european stroke organisation (ESO). Eur Heart J. 2024;45(36):3314–3414. https://doi.org/10.1093/eurheartj/ehae176. doi: 10.1093/eurheartj/ehae176.
8. Copaescu AM, Vogrin S, James F, et al. Efficacy of a Clinical Decision Rule to Enable Direct Oral Challenge in Patients With Low-Risk Penicillin Allergy: The PALACE Randomized Clinical Trial. JAMA Intern Med. 2023;183(9):944-952. doi:10.1001/jamainternmed.2023.2986
9. Kirchhof P, Camm AJ, Goette A, et al. Early Rhythm-Control Therapy in Patients with Atrial Fibrillation. N Engl J Med. 2020;383(14):1305-1316. doi:10.1056/NEJMoa2019422
10. Anderson JL, Platia EV, Hallstrom A, et al. Interaction of baseline characteristics with the hazard of encainide, flecainide, and moricizine therapy in patients with myocardial infarction. A possible explanation for increased mortality in the Cardiac Arrhythmia Suppression Trial (CAST). Circulation. 1994;90(6):2843-2852. doi:10.1161/01.cir.90.6.2843
11.Akiyama T, Pawitan Y, Greenberg H, Kuo C, Reynolds-Haertle R, The CI. Increased risk of death and cardiac arrest from encainide and flecainide in patients after non-Q-wave acute myocardial infarction in the cardiac arrhythmia suppression trial. Am J Cardiol. 1991;68(17):1551–1555. https://doi.org/10.1016/0002-9149(91)90308-8. doi: 10.1016/0002-9149(91)90308-8.
12. Parkash R, Wells GA, Rouleau J, et al. Randomized Ablation-Based Rhythm-Control Versus Rate-Control Trial in Patients With Heart Failure and Atrial Fibrillation: Results from the RAFT-AF trial. Circulation. 2022;145(23):1693-1704. doi:10.1161/CIRCULATIONAHA.121.057095
48 min
December 05, 2025437. Atrial Fibrillation: The Diagnosis and Management of Atrial Flutter with Dr. Joshua Cooper
In this episode, the CardioNerds (Dr. Naima Maqsood, Dr. Akiva Rosenzveig, and Dr. Colin Blumenthal) are joined by renowned educator in electrophysiology, Dr. Joshua Cooper, to discuss everything atrial flutter; from anatomy and pathophysiology to diagnosis and management. Dr. Cooper’s expert teaching comes through as Dr. Cooper vividly describes atrial anatomy to provide the foundational understanding to be able to understand why management of atrial flutter is unique from atrial fibrillation despite their every intertwined relationship. A foundational episode for learners to understand atrial flutter as well as numerous concepts in electrophysiology. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls
“The biggest mistake is failure to diagnose”. Atrial flutter, especially with 2:1 conduction, is commonly missed in both inpatient and outpatient settings so look carefully at that 12-lead EKG so you can mitigate the stroke and tachycardia induced cardiomyopathy risk
Decremental conduction of the AV node makes it more challenging to rate control atrial flutter than atrial fibrillation
Catheter Ablation is the first line treatment for atrial flutter and is highly successful, but cardioversion can be utilized as well prior to pursuing ablation in some cases.
Class I AADs like propafenone and flecainide may stability the atrial flutter circuit by slowing conduction and thus may worsen the arrhythmia. Therefore, the preferred anti-arrhythmic medication in atrial flutter are class III agents.
Atrial flutter can be triggered by firing from the left side of the heart, so in patients with both atrial fibrillation and flutter, ablating atrial fibrillation makes atrial flutter less likely to recur.
BONUS PEARL: Dr. Cooper’s youtube video on atrial flutter is a MUST SEE!
Notes
Notes: Notes drafted by Dr. Akiva Rosenzveig
What are the distinguishing features of atrial fibrillation and flutter?
Atrial flutter is an organized rhythm characterized by a wavefront that continuously travels around the same circuit leading to reproducible P-waves on surface EKG as well as a very mathematical and predictable relationship between atrial and ventricular activity
Atrial fibrillation is an ever changing, chaotic rhythm that consists of small local circuits that interplay off each other. Consequently, no two beats are the same and the relationship between the atrial activity and ventricular activity is unpredictable leading to an irregularly irregular rhythm
What are common atrial flutter circuits?
Cavo-tricuspid isthmus (CTI)-dependent atrial flutter is the most common type of flutter. It is characterized by a circuit that circumnavigates the tricuspid valve.
Typical atrial flutter is characterized by the circuit running in a counterclockwise pattern up the septum, from medial to lateral across the right atrial roof, down the lateral wall, and back towards the septum across the floor of the right atrium between the IVC and the inferior margin of the tricuspid valve i.e. the cavo-tricuspid isthmus. Surface EKG will show a gradual downslope in leads II, III, and AvF and a rapid rise at end of each flutter wave.
Atypical CTI-dependent flutter follows the same route but in the opposite direction (clockwise). Therefore, we will see positive flutter waves in the inferior leads
Mitral annular flutter is more commonly seen in atrial fibrillation patients who’ve been treated with ablation leading to scarring in the left atrium.
Roof-dependent flutter is characterized by a circuit that travels around left atrium circumnavigating a lesion (often from prior ablation), traveling through the left atrial roof, down the posterior wall, and around the pulmonary veins
Surgical/scar/incisional flutter is seen in people with a history of prior cardiac surgery and have iatrogenic scars in right atrium due to cannulation sites or incisions
How does atrial flutter pharmacologic management differ from other atrial arrhythmias?
The atrioventricular (AV) node is unique in that the faster it is stimulated, the longer the refractory period and the slower it conducts. This characteristic is called decremental conduction. In atrial fibrillation, the atrial rate is so fast that the AV node becomes overwhelmed and only lets some of those signals through to the ventricles creating an irregular tachycardia but at lower rates. In atrial flutter, the atrial rate is slower, therefore the AV node has more capability to conduct allowing for higher ventricular rates. Therefore, to achieve rate control one will need a higher dose of AV blocking medications. Atrial tachycardia may require even higher doses due to the increased ability of the AV node to conduct, as the atrial rates are slower than in atrial flutter.
Sodium channel blockers (Class I) such as flecainide and propafenone slow wavefront propagation, making it easier for the AV node to handle the atrial rates. This will end up leading to increased ventricular rates which can be dangerously fast. That is why AV nodal blockers should be used in conjunction with flecainide and propafenone.
What is the role of cardioversion in atrial flutter management?
Due to high success rate with atrial flutter ablation, ablation is the first line treatment. However, sometimes cardioversion may be utilized in patients depending on how symptomatic they are and how long it will take to get an ablation. Cardioversion may also be utilized preferentially when the atrial flutter was triggered by infection or cardiac surgery to see if it will come back.
If cardioversion is pursued, the patient will need to be anticoagulated due to the stroke risk after the procedure due to post-conversion stunning.
How effective is atrial flutter ablation?
The landmark Natale et al study in 2000 demonstrated 80% success rate after radiofrequency ablation as compared to 36% in patients on anti-arrhythmic therapy. The LADIP study in 2006 further corroborated these findings. Contemporary data shows above 90% success rate of atrial flutter ablation.
In patients who have had both atrial fibrillation and atrial flutter, most electrophysiologists would ablate both. However, in patients with atrial fibrillation, the atrial flutter usually is initiated by trigger spots firing in the left atrium. Once the atrial fibrillation is ablated, the flutter will become less likely. Therefore, there are those who say there’s no need to ablate the flutter circuit as well. Alternatively, if a patient has severe comorbidities and/or is high risk for ablation, one may consider performing the atrial flutter ablation only since atrial flutter is harder to manage medically compared with atrial fibrillation.
How do you manage atrial flutter in the acute inpatient setting?
In the inpatient setting, electrical cardioversion is often limited by blood pressure and the hypotensive effects of the sedatives required. If one is awake and too hypotensive, chemical cardioversion can be pursued. The most effective anti-arrhythmic for this is ibutilide. Amiodarone is not effective for acute cardioversion. Since ibutilide prolongs refractoriness in atrial and ventricular tissue, there’s a risk of long QT induced torsades de pointes. Pretreating with magneisum reduces the risk to 1-2%.
References
Jolly WA, Ritchie WT. Auricular flutter and fibrillation. 1911. Ann Noninvasive Electrocardiol. 2003;8(1):92-96. doi:10.1046/j.1542-474x.2003.08114.x
McMichael J. History of atrial fibrillation 1628-1819 Harvey – de Senac – Laënnec. Br Heart J. 1982;48(3):193-197. doi:10.1136/hrt.48.3.193
Lee KW, Yang Y, Scheinman MM; University of Califoirnia-San Francisco, San Francisco, CA, USA. Atrial flutter: a review of its history, mechanisms, clinical features, and current therapy. Curr Probl Cardiol. 2005;30(3):121-167. doi:10.1016/j.cpcardiol.200
2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(1):e167. doi:10.1161/
Cosío F. G. (2017). Atrial Flutter, Typical and Atypical: A Review. Arrhythmia & electrophysiology review, 6(2), 55–62. https://doi.org/10.15420/aer.2017.5.2
https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-11/Atrial-flutter-common-and-main-atypical-forms
Natale A, Newby KH, Pisanó E, et al. Prospective randomized comparison of antiarrhythmic therapy versus first-line radiofrequency ablation in patients with atrial flutter. J Am Coll Cardiol. 2000;35(7):1898-1904. doi:10.1016/s0735-1097(00)00635-5
Da Costa A, Thévenin J, Roche F, et al. Results from the Loire-Ardèche-Drôme-Isère-Puy-de-Dôme (LADIP) trial on atrial flutter, a multicentric prospective randomized study comparing amiodarone and radiofrequency ablation after the first episode of symptomatic atrial flutter. Circulation. 2006;114(16):1676-1681. doi:10.1161/CIRCULATIONAHA.106.638395
https://www.acc.org/Membership/Sections-and-Councils/Fellows-in-Training-Section/Section-Updates/2015/12/15/16/58/Atrial-Fibrillation#:~:text=The%20first%20’modern%20day’%20account,in%20open%20chest%20animal%20models.&text=In%201775%2C%20William%20Withering%20first,(purple%20foxglove)%20in%20AFib.
31 min
November 20, 2025435. Atrial Fibrillation: Chronic Management of Atrial Fibrillation with Dr. Edmond Cronin
CardioNerds (Dr. Kelly Arps, Dr. Naima Maqsood, and Dr. Elizabeth Davis) discuss chronic AF management with Dr. Edmond Cronin. This episode seeks to explore the chronic management of atrial fibrillation (AF) as described by the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. The discussion covers the different AF classifications, symptomatology, and management including medications and invasive therapies. Importantly, the episode explores current gaps in knowledge and where there is indecision regarding proper treatment course, as in those with heart failure and AF. Our expert, Dr. Cronin, helps elucidate these gaps and apply guideline knowledge to patient scenarios. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls
Review the guidelines- Catheter ablation is a Class I recommendation for select patient groups
Appropriately recognize AF stages- preAF conditions, symptomatology, classification system (paroxysmal, persistent, long-standing persistent, permanent)
Be familiar with the EAST-AFNET4 trial, as it changed the approach of rate vs rhythm control
Understand treatment approaches- lifestyle modifications, management of comorbidities, rate vs rhythm control medications, cardioversion, ablation, pulmonary vein isolation, surgical MAZE
Sympathize with patients- understand their treatment goals
Notes
Notes: Notes drafted by Dr. Davis.  
What are the stages of atrial fibrillation?
The stages of AF were redefined in the 2023 guidelines to better recognize AF as a progressive disease that requires different strategies at the different therapies
Stage 1 At Risk for AF: presence of modifiable (obesity, lack of fitness, HTN, sleep apnea, alcohol, diabetes) and nonmodifiable (genetics, male sex, age) risk factors associated with AF
Stage 2 Pre-AF: presence of structural (atrial enlargement) or electrical (frequent atrial ectopy, short bursts of atrial tachycardia, atrial flutter) findings further pre-disposing a patient to AF
Stage 3 AF: patient may transition between these stages
Paroxysmal AF (3A): intermittent and terminates within ≤ 7 days of onset
Persistent AF (3B): continuous and sustained for > 7 days and requires intervention
Long-standing persistent AF (3C): continuous for > 12 months
Successful AF ablation (3D): freedom from AF after percutaneous or surgical intervention
Stage 4 Permanent AF: no further attempts at rhythm control after discussion between patient and clinician
The term chronic AF is considered obsolete and such terminology should be abandoned
What are common symptoms of AF?
Symptoms vary with ventricular rate, functional status, duration, and patient perception
May present as an embolic complication or heart failure exacerbation
Most commonly patients report palpitations, chest pain, dyspnea, fatigue, or lightheadedness. Vague exertional intolerance is common
Some patients also have polyuria due to increased production of atrial natriuretic peptide
Less commonly can present as tachycardia-associated cardiomyopathy or syncope
Cardioversion into sinus rhythm may be diagnostic to help determine if a given set of symptoms are from atrial fibrillation to help guide the expected utility of more aggressive rhythm control strategies.
What are the current guidelines regarding rhythm control and available options?
COR-LOE 1B: In patients with reduced LV function and persistent (or high burden) AF, a trial of rhythm control should be recommended to evaluate whether AF is contributing to the reduced LV function
COR-LOE 2a-B: In patients with reduced LV function and persistent (or high burden) AF, a trial of rhythm control should be recommended to evaluate whether AF is contributing to the reduced LV function. In patients with a recent diagnosis of AF (<1 year), rhythm control can be useful to reduce hospitalizations, stroke, and mortality. In patients with AF and HF, rhythm control can be useful for improving symptoms and improving outcomes, such as mortality and hospitalizations for HF and ischemia. In patients with AF, rhythm-control strategies can be useful to reduce the likelihood of AF progression.
COR-LOE 2b-C: In patients with AF where symptoms associated with AF are uncertain, a trial of rhythm control (eg, cardioversion or pharmacological therapy) may be useful to determine what if any symptoms are attributable to AF.
COR-LOE 2b-B: In patients with AF, rhythm-control strategies may be useful to reduce the likelihood of development of dementia or worsening cardiac structural abnormalities.
While both rate and rhythm control can improve AF symptoms, several studies (such as AF-CHF) show improved quality of life with rhythm control
EAST-AFNET 4 was significant in that it showed rhythm control was associated with a 25% reduction in the combined endpoint of mortality rate, stroke, and hospitalizations due to HF or ACS
Acute rhythm control can be achieved with electrical or pharmacological cardioversion. Electrical is more effective and faster than pharmacological and is preferred for patients with hemodynamic instability attributable to AF. However, both approaches involved considerations for anticoagulation and thromboembolic risk. Pharmacologic options for cardioversion include ibutilide, amiodarone, flecainide, propafenone, procainamide, dofetilide, and sotalol.
COR-LOE 1-A: In patients with symptomatic AF in whom antiarrhythmic drugs have been ineffective, contraindicated, not tolerated or not preferred, and continued rhythm control is desired, catheter ablation is useful to improve symptoms.
AF ablation is also a suitable first-line option in some patients with paroxysmal AF to reduce recurrence and burden. Patient selection is important. Younger patients, those with minimal atrial enlargement, less myocardial fibrosis, and less persistent forms are more likely to have successful ablations, meaning less likely to have recurrence of AF after ablation.
HFrEF patients derive greater benefit than others from AF ablation in terms of improved functional status, LV function, and cardiovascular outcomes
Surgical ablation can be considered in those undergoing cardiac surgery for some other etiology such as valve surgery or CABG and is associated with increased survival, but some risk of pacemaker placement and renal dysfunction
How would you monitor for AF recurrence in post-ablation or cardioversion? Is there a role for monitoring in every patient?
Cardiac monitoring may be advised to AF patients for various reasons, such as for detecting recurrences, screening, or response to therapy
Long-term surveillance to detect recurrent AF can be beneficial and can be accomplished by various modalities, including wearable devices, smart watches, random monitoring (Holter, event, mobile telemetry), and implantable loop recorders. This is especially helpful in those who had AF-induced cardiomyopathy, especially if their LVEF recovered after rate/rhythm control. This is a population in whom recurrence of AF would want to be promptly noted and addressed.
Loop recorders can also be helpful in detecting subclinical AF or in patients with stroke or TIA of undetermined cause (COR-LOE 2a-B)
What AF burden warrants intervention?
It is important to recognize that AF is a chronic condition and tends to recur, so treatment often is focused on reducing risk of recurrence
Patient-clinician shared decision making is important when deciding when/how to intervene, as there is no cut-off for “significant” burden (COR-LOE 1-B)
What are some options for antiarrhythmic drugs and their characteristics?
Antiarrhythmic drugs are reasonable for long-term maintenance of sinus rhythm for patients with AF who are not candidates for, or decline, catheter ablation, or who prefer antiarrhythmic therapy
Amiodarone can be used in patients with or without HFrEF, as opposed to many other anti-arrhythmics that are (relatively) contraindicated in HFrEF or should be used with caution in such patients, such as flecainide, propafenone, dronedarone, and sotalol. However, due to its adverse effects and multiple drug interactions, is should be used only in patients in which other antiarrhythmic drugs are contraindications, ineffective, or not preferred. Dofetilide can also be used in patients with HFrEF.
In patients on amiodarone, labs should be checked regularly for thyroid, liver and kidney functions. There is also a role for pulmonary function testing and chest x-rays to monitor for pulmonary fibrosis, but frequency is not clearly established. It should be noted that amiodarone-induced lung toxicity occurs between 6 months and 2 years of use.
Flecainide is well tolerated, but is contraindicated in patients with significant coronary artery disease and possibly structural heart disease in general. It can also lead to the development of atrial flutter.
Dofetilide and sotalol require regular renal function monitoring and QTC monitoring
When should AV node ablation (AVNA) be considered?
In patients with AF and uncontrolled rapid ventricular response refractory to rate-control medications (who are not candidates for or in whom rhythm control has been unsuccessful), AVNA can be useful to improve symptoms and QOL (COR-LOE 2a-B)
AVNA is effective for rate control and does not require continuation of medications; however, patients become dependent on pacing and lifelong pacemaker implantation, and the potential for device complications
AVNA does not prevent progression or recurrence of AF
The type of device is dependent on patient comorbidities but the advent of conduction system pacing may improve outcomes in these patients compared with RV pacing.
What are some recommendations for managing atrial fibrillation in the perioperative period?
In patients with AF (excluding those with recent stroke or TIA, or a mechanical valve) and on oral anticoagulation with either warfarin or DOAC who are scheduled to undergo an invasive procedure or surgery, temporary cessation of oral anticoagulation without bridging anticoagulation is recommended (COR-LOE 1-B)
In patients with AF on DOAC that has been interrupted for an invasive procedure or surgery, in general, resumption of anticoagulation the day after low bleeding risk surgery and between the evening of the second day and the evening of the third day after high bleeding risk surgery is reasonable, as long as hemostasis has been achieved and further bleeding is not anticipated (COR-LOE 2a-B)
Preop prophylaxis to prevent AF after cardiac surgery with either beta blocker or amiodarone shows mixed benefit and carries a 2a-B recommendation; however, beta blocker is a class 1-A recommendation in patients who do develop AF in the postop period
It should be noted that patients who develop AF in the setting of an acute illness or surgery are at risk of recurrence
References
Joglar, J, Chung, M. et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. JACC. 2024 Jan, 83 (1) 109–279. https://doi.org/10.1016/j.jacc.2023.08.017
Fuster F, Rydén L, et al. ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology. Circulation. 2001 Oct, 104 (17). https://doi.org/10.1161/circ.104.17.2118
Kirchhof P, Camm A, et al. Early Rhythm-Control Therapy in Patients with Atrial Fibrillation. N Engl J Med. 2020 Aug, 383 (14) 1305-1416. DOI: 10.1056/NEJMoa2019422
Olshansky, B, Rosenfeld, L, Warner, A. et al. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study: Approaches to control rate in atrial fibrillation. JACC. 2004 Apr, 43 (7) 1201–1208.https://doi.org/10.1016/j.jacc.2003.11.032
Whitlock R, Belley-Cote E, et al. Left Atrial Appendage Occlusion during Cardiac Surgery to Prevent Stroke. N Engl J Med. 2021 May, 384 (22) 2081-2091. DOI: 10.1056/NEJMoa2101897
Kirchhof P, Toennis T, et al. Anticoagulation with Edoxaban in Patients with Atrial High-Rate Episodes. N Engl J Med. 2023 Aug, 389 (13) 1167-1179. DOI: 10.1056/NEJMoa2303062
Healey J, Lopes R, et al. Apixaban for Stroke Prevention in Subclinical Atrial Fibrillation. N Engl J Med. 2023 Nov, 390 (2) 107-117. DOI: 10.1056/NEJMoa2310234
Roy D, Talajic M, et al. Rhythm Control versus Rate Control for Atrial Fibrillation and Heart Failure. N Engl J Med. 2008 Jun, 358 (25) 2667-2677. DOI: 10.1056/NEJMoa0708789
Gillinov A, Bagiella E, et al. Rate Control versus Rhythm Control for Atrial Fibrillation after Cardiac Surgery. N Engl J Med. 2016 Mar, 374 (20) 1911-1921. DOI: 10.1056/NEJMoa1602002
48 min
October 24, 2025431. Atrial Fibrillation: Acute Management of Atrial Fibrillation with Dr. Jonathan Chrispin
Dr. Naima Maqsood, Dr. Kelly Arps, and Dr. Jake Roberts discuss the acute management of atrial fibrillation with guest expert Dr. Jonathan Chrispin. Episode audio was edited by CardioNerds Intern Dr. Bhavya Shah.
This episode reviews acute management strategies for atrial fibrillation. Atrial fibrillation is the most common chronic arrhythmia worldwide and is associated with increasingly prevalent comorbidities, including advanced age, obesity, and hypertension. Atrial fibrillation is a frequent indication for hospitalization and a complicating factor during hospital stays for other conditions. Here, we discuss considerations for the acute management of atrial fibrillation, including indications for rate versus rhythm control strategies, treatment targets for these approaches, considerations including pharmacologic versus electrical cardioversion, and management in the post-operative setting.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Become a CardioNerds Patron!
Pearls
A key component to the management of acute atrial fibrillation involves addressing the underlying cause of the acute presentation. For example, if a patient presents with rapid atrial fibrillation and signs of infection, treatment of the underlying infection will help improve the elevated heart rate.
Selecting a rate control versus rhythm control strategy in the acute setting involves considerations of comorbid conditions such as heart failure and competing risk factors such as critical illness that may favor one strategy over another. Recent data strongly supports the use of rhythm control in heart failure patients. Patients should be initiated on anticoagulation prior to pursuing a rhythm control strategy.
There are several strategies for rate control medications with therapies including beta-blockers, non-dihydropyridine calcium channel blockers, and digoxin. The selection of which agent to use depends on additional comorbidities and the overall clinical assessment. For example, a patient with severely decompensated low-output heart failure may not tolerate a beta-blocker or calcium channel blocker in the acute phase due to hypotension risks but may benefit from the use of digoxin to provide rate control and some inotropic support.
Thromboembolic prevention remains a cornerstone of atrial fibrillation management, and considerations must always be made in terms of the duration of atrial fibrillation, thromboembolic risk, and risks of anticoagulation.
While postoperative atrial fibrillation is more common after cardiac surgeries, there is no major difference in management between patients who undergo cardiac versus non-cardiac procedures. Considerations involve whether the patient has a prior history of atrial fibrillation, surgery-specific bleeding risks related to anticoagulation, and monitoring in the post-operative period to assess for recurrence.
Notes
1. Our first patient is a 65-year-old man with obesity, hypertension, obstructive sleep apnea, and pre-diabetes presenting for evaluation of worsening shortness of breath and palpitations. The patient has no known history of heart disease. Telemetry shows atrial fibrillation with ventricular rates elevated to 130-140 bpm. What would be the initial approach to addressing the acute management of atrial fibrillation in this patient? What are some of the primary considerations in the initial history and chart review?
An important first step involves taking a careful history to understand the timing of symptom onset and potential underlying causes contributing to a patient’s acute presentation with rapid atrial fibrillation.
Understanding the episode trigger determines management by targeting reversible causes of the acute presentation and elucidating whether the episode is triggered by a cardiac or non-cardiac condition. For example, if a patient presents with a few days of infectious symptoms, treating the infection is likely to lead to improvements in heart rate.
Determining the tempo of symptoms has further importance for assessing the risk of thromboembolism and anticoagulation consideration.
2. How would the initial evaluation be different for patients who have a new diagnosis of atrial fibrillation compared to those who have a known prior history of this arrhythmia?
The acuity of symptom onset plays an essential role in these considerations. For example, a patient may describe symptoms that have been ongoing for several months, which indicate a diagnosis beyond the acute phase of their presentation and would involve different considerations than for a patient who first noticed symptoms within the past few hours.
One way to view RVR rates in a patient with longstanding or permanent atrial fibrillation is to consider this vital sign as that patient’s version of sinus tachycardia in response to another physiologic process. In that setting, you would not try an approach to directly lower their heart rate but would instead attempt to determine and address the underlying cause of their presentation.
An additional consideration for patients without known prior atrial fibrillation is that they have likely never been on any rate-controlling agents and may have variable initial responses to these interventions.
3. In cases for which acute rate control of atrial fibrillation is indicated, what is the recommended heart rate target and how quickly should we aim to reach that target?
The initial first step in management should focus on addressing the underlying cause of the patient’s elevated heart rate while in atrial fibrillation. Once those factors are addressed and elevated heart rates persist, a rate-controlling agent can be considered.
Often, a primary reason for rate control is for symptom relief since patients can be very symptomatic from an elevated heart rate alone.
A reasonable goal for the intermediate setting is to achieve a heart rate of less than 100-110 bpm. One study compared lenient (resting heart rate <110 bpm) versus strict (resting heart rate <80 bpm and heart rate during moderate exercise <110 bpm) rate control in patients with atrial fibrillation and found no difference in outcomes related to mortality, hospitalization for heart failure, stroke, embolism, bleeding, or life-threatening arrhythmic events but that lenient control was easier to achieve.1 For this reason, aggressive rate control in the acute setting may not have a significant impact apart from symptom relief. There are not often clear indications to rapidly lower a patient’s heart rate, for example, from 140 to 90 bpm. Conversely, lowering a patient’s heart rate too rapidly can be detrimental by causing bradycardia or hypotension with excessive use of nodal blocking agents.
4. What are some of the considerations for the selection of rate-controlling agents?
Beta-blockers and non-dihydropyridine calcium channel blockers remain the mainstay of therapies used for rate control. The choice between these agents often depends on the comorbidities present. For example, if a patient has a known reduced LVEF, you may often avoid calcium channel blockers and opt for careful titration of beta-blockers. Often, the use of beta-blockers also allows for the management of additional comorbidities, including heart failure and coronary disease.
Digoxin is another agent to consider when a patient presents with acutely decompensated heart failure with a low LVEF and may not tolerate a beta-blocker or calcium channel blocker due to the risk of hypotension or worsening cardiogenic shock. Digoxin provides rate control while adding some positive inotropy. In terms of chronic management, digoxin use can be more challenging with close follow-up required to monitor levels. In some cases, amiodarone can be used as an acute rate-control agent, but there is a risk of conversion to sinus rhythm and thromboembolism if not on anticoagulation.
5. In what clinical scenarios might it be more optimal to consider an upfront rhythm control strategy?
Recent data support the benefit of an upfront rhythm control approach in heart failure patients, with complications including cardiovascular death, stroke, or hospitalization for worsening of heart failure or for acute coronary syndrome, reduced in heart failure patients managed with any early rhythm control strategy.2,3
In certain patients with known atrial fibrillation and heart failure, cardioversion can be considered as a strategy to help improve their heart failure symptoms. In these patients, initiating an anti-arrhythmic drug (AAD) prior to cardioversion can improve the likelihood of remaining in sinus rhythm after cardioversion.
6. Our second patient is a 58-year-old woman with a history of heart failure with reduced EF presenting to the ED with progressive lower extremity swelling and shortness of breath. She has a prior diagnosis of paroxysmal atrial fibrillation, and her most recent echo demonstrated an LVEF of 35%. She is found to have bilateral lower extremity pitting edema to her knees and elevated jugular venous pressure while requiring 2L of oxygen by nasal cannula. She is in rapid atrial fibrillation on presentation. Interrogation of her primary prevention ICD shows that she has been in atrial fibrillation for the past 3 weeks. In this scenario involving a patient with an acute heart failure exacerbation, are there considerations for a more upfront rhythm control strategy and perhaps electrical cardioversion?
In this scenario, there is an indication for utilizing an early rhythm control strategy. Even if an initial trial of diuresis and beta-blockers is used initially, the fact that this patient has been in atrial fibrillation for several weeks with only prior paroxysmal episodes indicates that her arrhythmia is likely contributing to her decompensation and therefore should be addressed during hospitalization. This patient should be considered for AAD initiation and careful considerations should be made to ensure that this patient is appropriately anticoagulated. Once anticoagulation has been established, interventions including electrical cardioversion can be considered.
For this patient with a reduced LVEF, AAD initiation should be considered prior to cardioversion with options limited to amiodarone or dofetilide. For patients with renal disease and concerns for QT prolongation, amiodarone can be used as a reasonable short-term solution to bridge the patient to more definitive long-term strategies for rhythm control. This patient can be initiated on AAD and, if she does not convert on medication, can be considered for electrical cardioversion. The timing of cardioversion would depend on when the patient is optimized from a heart failure standpoint, including when the patient has become more euvolemic. With dofetilide, electrical cardioversion is typically attempted after the fourth dose is given to ensure that the patient can stay in sinus rhythm after cardioversion.
7. A common scenario in which we often find ourselves managing atrial fibrillation is in the postoperative setting. What are some of the management strategies for postoperative atrial fibrillation and how does this vary between patients who underwent cardiac versus non-cardiac procedures?
Compared to non-cardiac surgery, in cardiac surgery there is an increased risk for developing postoperative atrial fibrillation, with rates of occurrence ranging from 30-60%.4,5 While there are higher rates of post-operative atrial fibrillation in patients undergoing cardiac surgeries, there is no significant difference in the strategies used to treat patients who underwent cardiac versus non-cardiac surgeries.
For patients who have no prior history of atrial fibrillation prior to developing post-operatively, historical teaching endorsed the idea that this arrhythmia developed in response to inflammation occurring during acute recovery and should not have long-term consequences; however, more recent data suggests that if a patient develops atrial fibrillation post-operatively, they are more likely to have recurrence of this arrhythmia in the future.6
Current guidelines support anticoagulation based on the CHADSVASc score for at least 60 days post-operatively while monitoring for persistence of the arrhythmia.7 Further, data suggest that rhythm approaches post-operatively lead to better long-term outcomes in terms of re-hospitalizations and mortality.
In patients who underwent surgeries with high bleeding risk during recovery and have contraindications to anticoagulation, rate-control strategies are most appropriate initially.
If a patient has new atrial fibrillation without a prior diagnosis, they will need monitoring for recurrence for 30-60 days post-operatively.
8. What are some of the considerations for a pill-in-the-pocket strategy for those patients who experience infrequent episodes of symptomatic atrial fibrillation?
In this strategy, the patient takes medication when they are having symptoms with the intention of terminating the atrial fibrillation episode acutely.
When initiating this approach, it is essential to do so in a monitoring setting because of the effects that can result from giving high doses of these medications to treat acute episodes. For example, with flecainide, a dose of 300 mg may be given at one time compared to a dose of 50-150 mg twice daily to reach the maintenance dose. When medications such as flecainide are given in these loading doses, it is important to monitor for any acute toxicity.
Given the potential toxicities and challenges inherent to a pill-in-the-pocket approach, the desire to prevent rather than reactively treat episodes of atrial fibrillation, and improvements in catheter ablation techniques, this strategy is now rarely used in practice, with patients managed either with a maintenance medication or ablation.
References
1.         Van Gelder IC, Groenveld HF, Crijns HJGM, et al. Lenient versus Strict Rate Control in Patients with Atrial Fibrillation. New England Journal of Medicine. 2010;362(15). doi:10.1056/nejmoa1001337
2.         Kirchhof P, Camm AJ, Goette A, et al. Early Rhythm-Control Therapy in Patients with Atrial Fibrillation. New England Journal of Medicine. 2020;383(14). doi:10.1056/nejmoa2019422
3.          Rillig A, Magnussen C, Ozga AK, et al. Early Rhythm Control Therapy in Patients With Atrial Fibrillation and Heart Failure. Circulation. 2021;144(11). doi:10.1161/CIRCULATIONAHA.121.056323
4.         Gaudino M, Di Franco A, Rong LQ, Piccini J, Mack M. Postoperative atrial fibrillation: From mechanisms to treatment. Eur Heart J. 2023;44(12). doi:10.1093/eurheartj/ehad019
5.         Perezgrovas-Olaria R, Alzghari T, Rahouma M, et al. Differences in Postoperative Atrial Fibrillation Incidence and Outcomes After Cardiac Surgery According to Assessment Method and Definition: A Systematic Review and Meta-Analysis. J Am Heart Assoc. 2023;12(19). doi:10.1161/JAHA.123.030907
6.         Gilbers MD, Kawczynski MJ, Bidar E, et al. Determinants and impact of postoperative atrial fibrillation burden during 2.5 years of continuous rhythm monitoring after cardiac surgery: Results from the RACE V prospective cohort study. Heart Rhythm. 2024;22(3):647-660. doi:10.1016/j.hrthm.2024.08.014
7.          Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(1). doi:10.1161/CIR.0000000000001193
38 min
September 15, 2025428. Atrial Fibrillation: The Impact of Modifiable Risk Factors and Lifestyle Management on Atrial Fibrillation with Dr. Prash Sanders
Dr. Kelly Arps, Dr. Naima Maqsood, and Dr. Sahi Allam discuss modifiable risk factors and lifestyle management of atrial fibrillation with Dr. Prash Sanders. Atrial fibrillation is becoming more prevalent across the world as people are living longer with cardiovascular disease. While much of our current focus lies on the pharmacological and procedural management of atrial fibrillation, several studies have shown that targeted reduction of risk factors, such as obesity, sleep apnea, hypertension, and alcohol use, can also significantly reduce atrial fibrillation burden and symptoms. Today, we discuss the data behind lifestyle management and why it is considered the “4th pillar” of atrial fibrillation treatment. We also explore ways to incorporate prevention strategies into our general cardiology and electrophysiology clinics to better serve the growing atrial fibrillation population. Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes.
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Pearls
More people have atrial fibrillation because it is being detected earlier using wearable technology, and patients are living longer with subclinical or clinical cardiovascular disease
There are 3 components of atrial fibrillation: an electrical “trigger” + a susceptible substrate (due to age, sex, genetics) + “perpetuators” that cause the trigger to continue stimulating the substrate (lifestyle risk factors such as obesity, smoking, diabetes, etc.)
Obesity is the highest attributable risk factor for atrial fibrillation. Treating obesity often helps to treat other risk factors, such as hypertension and sleep apnea.
Counseling is patient-dependent. Most patients are unable to make major behavioral changes cold-turkey and will need to make small, incremental changes.
Dr. Sanders’ tip: He tells his own patients that “atrial fibrillation is the body’s response to stress.” The key to treating atrial fibrillation is to control your underlying stressors – procedures and medications are simply band-aids that do not fix the root of the problem.
Notes
Notes drafted by Dr. Allam.
1. How common is atrial fibrillation?
Atrial fibrillation is the most common sustained arrhythmia. Currently, an estimated 50-60 million individuals worldwide are estimated to have atrial fibrillation, or roughly 1 in 4 individuals over the age of 45.1
The rising global prevalence of atrial fibrillation can be attributed to the aging of the population, increased rates of obesity, and greater accumulation of cardiovascular risk factors and survival with clinical cardiovascular disease.2 Atrial fibrillation is also being detected earlier through digital and wearable devices.2
Annually, we spend approximately $5,312 per adult on the management of atrial fibrillation in the United States.3
2. What is the underlying pathophysiology of atrial fibrillation? How do risk factors like sleep apnea or obesity “trigger” atrial fibrillation?
For atrial fibrillation to occur, there is an electrical “trigger”, a susceptible substrate (due to age, sex, genetics), and “perpetuators” that allow the trigger to continue stimulating the substrate.2
90% of electrical “triggers” come from the pulmonary veins
“Perpetuators” influence how the autonomic nervous system interacts with the triggers and substrate to perpetuate atrial fibrillation. Sleep apnea, obesity, and other risk factors are the “perpetuators”
Over time, as atrial fibrillation recurs, the substrate remodels to result in persistent atrial fibrillation.
3. What are some of the risk factors for atrial fibrillation and what are the possible benefits of controlling them?
Reference 4 provides an excellent review of the individual risk factors
Tobacco use
Nicotine patches/gums and counseling are associated with successful nicotine cessation in RCTs.
In the long term, nicotine itself can cause atrial fibrosis. However, it is safe to use patches and gums in the short term to abet cessation.
Obesity
The highest attributable risk factor for atrial fibrillation. Treating obesity often helps to treat other risk factors, such as hypertension and sleep apnea
In addition to regular exercise, reducing caloric intake can help combat obesity. Eating more fiber-laden food such as vegetables instead of carbohydrates, limiting portions, sugary drinks, and alcohol, and increasing fasting periods can all help decrease weight.
GLP-1 agonists can significantly reduce obesity and improve both symptoms and mortality for patients with comorbid conditions, such as HFpEF.
Obstructive sleep apnea
This is an evolving area of research with upcoming randomized trial data
Sleep apnea is probably not a static condition. Our likelihood of having sleep apnea changes with how rested we are, how much we’ve exercised, or whether we’ve consumed alcohol, etc. The testing and treatment of the future will reflect the changeable nature of sleep apnea.
Current data:
In the atrial fibrillation ablation population, treatment of sleep apnea was associated with an improvement in time to arrhythmia recurrence.
Another observational study from Norway, which included various patients who used dental sleep appliances, found no significant difference in atrial fibrillation between those who were treated for sleep apnea and those who were not. It was severely underpowered to detect a difference.
Caffeine
There is no evidence to support cessation of caffeine in patients with atrial fibrillation
For patients with bothersome palpitations, caffeine cessation can be tried if it improves their symptoms
Alcohol use
Per data from the UK Biobank, a single drink of alcohol daily does not increase your risk for developing atrial fibrillation. However, multiple drinks per day will increase your risk.
A proof-of-concept study showed that patients who abstained from alcohol for at least 6 months had complete resolution of atrial fibrillation. However, the dropout rate was very high as most patients could not completely abstain from alcohol
Dr. Sanders recommends alcohol consumption of ≤ 3 drinks/week, which is the cutoff used in lifestyle management studies.
Heart Failure
For patients with heart failure, the 4 pillars of heart failure management are also crucial to treating atrial fibrillation. SGLT2 inhibitors in particular are likely to confer benefits. 40-50% of patients in the SGLT2 inhibitor clinical trials had co-morbid atrial fibrillation.
About half of patients undergoing atrial fibrillation ablation appear to have HFpEF based on their hemodynamics.
4. Can atrial fibrillation be treated with only lifestyle modifications?
Potentially. This is an evolving area of research without much published data. Empirically, Dr. Sanders has noticed that in patients referred for atrial fibrillation ablation, aggressive lifestyle modifications result in 40% of them no longer requiring ablation. After a 10-year follow-up, 20% still do not require ablation.
However, ablation is still an effective modality to achieve rhythm control. It is also becoming a safer procedure owing to novel techniques, such as pulse field ablation.
In the future, we foresee most patients utilizing a combination of lifestyle modification and rhythm control strategies (ablation and/or medications) to control their atrial fibrillation.
5. What are the benefits of exercise in patients with atrial fibrillation? How much exercise do you recommend to your patients? Also, on the other end of the spectrum, does participation in endurance sports paradoxically promote atrial fibrillation?
The ACTIVE-AF study tested whether an intensive aerobic exercise regimen, up to 210 minutes per day, is safe and effective in controlling atrial fibrillation. Intensive exercise was associated with a significant reduction in atrial fibrillation burden and symptoms as well as an increase in quality of life and maintenance of sinus rhythm.5
Endurance athletes do have an approximately 5-fold higher risk of atrial fibrillation compared to sedentary people.6 However, this occurs at very high levels of exercise, exceeding 4 hours per day. Low to moderate levels of exercise have been shown to reduce rates of atrial fibrillation.4,5
6. How should we counsel patients about lifestyle management? Are there any good resources to use?
Dr. Sanders’ tip: Counseling is patient-dependent. For the majority of patients, the key to behavioral change is to make incremental adjustments over time, accompanied by encouragement. Some patients respond well to continuous feedback from digital devices. We can also supplement pharmacological therapies, such as medications to assist with weight loss or tobacco/alcohol cessation, to behavioral counseling.
Risk factor modification should be the central pillar of atrial fibrillation management and reviewed early on with patients in their atrial fibrillation course. It may be beneficial to have clinic sessions specifically dedicated to lifestyle counseling, which can be run by a multidisciplinary team of electrophysiologists, general cardiologists, and nurse educators.
7. How should we explain what atrial fibrillation is to our patients?
Dr. Sanders’ tip: He tells his own patients that “atrial fibrillation is the body’s response to stress. It occurs because the heart is not coping well with increased stress. Procedures and medications for atrial fibrillation are simply band-aids that do not fix the root of the problem, but controlling the risk factors contributing to increased stress will.”
He also emphasizes the increased stroke risk of atrial fibrillation.
References
1. Linz D, Gawalko M, Betz K, Hendriks J, Lip G, Vinter N. Atrial fibrillation: epidemiology, screening and digital health. The Lancet Regional Health – Europe. 2024;37(100786).
2. Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. Jan 02 2024;149(1):e1-e156.
3. Serpa F, Tale A, Zimetbaum P, Kramer D. Trends in health care expenditures and incremental health care cost in adults with atrial fibrillation in the United States. Heart Rhythm O2. 2025;6(1).
4. Chung MK, Eckhardt LL, Chen LY, et al. Lifestyle and Risk Factor Modification for Reduction of Atrial Fibrillation: A Scientific Statement From the American Heart Association. Circulation. Apr 21 2020;141(16):e750-e772. doi:10.1161/CIR.0000000000000748
5. Elliott AD, Verdicchio CV, Mahajan R, et al. An exercise and physical activity program in patients with atrial fibrillation. JACC: Clinical Electrophysiology. 2023;9(4):455-465. doi:10.1016/j.jacep.2022.12.002
6. Atrial fibrillation in competitive athletes. American College of Cardiology. Accessed February 22, 2025. https://www.acc.org/Latest-in-Cardiology/Articles/2019/08/16/08/20/http%3a%2f%2fwww.acc.org%2fLatest-in-Cardiology%2fArticles%2f2019%2f08%2f16%2f08%2f20%2fAtrial-Fibrillation-in-Competitive-Athletes
18 min
January 23, 2024 356. 2023 ACC/AHA/ACCP/HRS Atrial Fibrillation Guidelines – Key Takeaways with Dr. José Joglar and Dr. Mina Chung
CardioNerds Atrial Fibrillation Series Co-Chairs Dr. Colin Blumenthal (University of Pennsylvania Cardiology fellow) and Dr. Kelly Arps (Duke University Electrophysiology Fellow) join the 2023 atrial fibrillation guideline writing committee Chair Dr. José Joglar (UT Southwestern) and Vice Chair Dr. Mina Chung (Cleveland Clinic). They review the key takeaways from the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation. Audio editing by CardioNerds academy intern, student doctor Pace Wetstein.
This podcast was developed in collaboration with the American Heart Association. For more on these guidelines, access the AHA Science News AF Guideline landing page.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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56 min
December 29, 2023353. Atrial Fibrillation: Anticoagulation Pharmacology & Clinical Decision-Making with Dr. Ashley Lochman and Dr. Chris Domenico
CardioNerds co-founder Dr. Amit Goyal, series co-chair Dr. Colin Blumenthal, and episode lead Dr. Anushka Tandon to discuss pharmacologic anticoagulation options in atrial fibrillation with Drs. Ashley Lochman and Chris Domenico. The case-based review helps clarify some key concepts, such as when warfarin is preferred for anticoagulation, who may be a good DOAC (direct-acting oral anticoagulant) candidate, how to choose an appropriate DOAC agent, and how to manage anticoagulation therapy in patients already on antiplatelet therapies. Notes were drafted by Dr. Anushka Tandon. The episode audio was edited by student Dr. Shivani Reddy.
This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal.
This episode was planned and recorded prior to the release of the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation. Please refer to this guideline document for the most updated recommendations.
We have collaborated with VCU Health to provide CME. Claim free CME here!
This episode is made possible with support from Glass.Health – The first digital notebook designed for doctors. Follow @GlassHealthHQ for the latest product updates!
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls and Quotes – Anticoagulation Pharmacology
Avoid potentially fatal errors with this terminology tip for correctly referencing non-warfarin oral anticoagulant agents: it’s DOAC (like, please DO use AntiCoagulation), not NOAC (imagine someone interpreting that as “NO AntiCoagulation for this patient” at discharge – yikes)!
Sometimes, an oldie really is a goodie – warfarin is recommended over DOACs for patients with mechanical heart valves, moderate-to-severe mitral stenosis, anti-phospholipid antibody syndrome (APLS), left ventricular (LV) thrombus, higher INR goals, or DOAC failure. Patient preference and medication costs should also be considered – at the end of the day, “the best drug is the drug that a patient is willing to take!”
Standard-dose rivaroxaban or apixaban may be considered for use in patients weighing >120kg or with BMI >40; use of other DOACs should be limited to pts weighing =/< 120kg or with BMI =/< 40.
The pharmacists involved in this podcast promise they don’t have stock in apixaban! It just often happens to be the preferred DOAC option in certain scenarios – think patients with severe renal impairment (including ESRD) or with an increased risk for bleeding events (including older adults, those with a history of GI bleed, etc).
In general, dual therapy (DOAC or warfarin + P2Y12 inhibitor) is non-inferior to triple therapy (oral anticoagulant + P2Y12 inhibitor + aspirin) at preventing thrombotic events but is associated with a lower risk of bleeding events. Most patients can be transitioned to dual therapy after 7-30 days on triple therapy post-percutaneous coronary intervention.
What’s that on the horizon? Factor XI inhibitors may become the breakout stars of anticoagulation – multiple investigational agents are being studied for their potential to reduce thrombotic risk without significantly increasing bleeding risk in patients with indications for anticoagulation therapy…at least that’s the theorize hope. Watch this space!
Notes – Anticoagulation Pharmacology
In which cases is warfarin preferred over DOACs in patients with atrial fibrillation?
Long-term anticoagulation with warfarin is indicated in patients with atrial fibrillation and either a mechanical valve or moderate-to-severe mitral stenosis (i.e., valvular atrial fibrillation as defined in the 2019 AHA/ACC/HRS guidelines on atrial fibrillation [1]). The REALIGN trial [2] showed increased rates of thromboembolic and bleeding complications with dabigatran vs. warfarin in patients with mechanical valves, and the PROACT Xa trial [3] found similarly higher rates of thromboembolic events with apixaban vs. warfarin in patients with On-X mechanical valves. However, DOACs are appropriate for use in patients with bioprosthetic valves.
Warfarin is preferred over DOACs in patients with APLS (antiphospholipid syndrome). In triple-positive patients, DOACs should absolutely be avoided (as supported by the TRAPS study [4], which was stopped early due to findings of increased thromboembolic events with rivaroxaban vs. warfarin). Warfarin should also be preferentially used in single- and double-positive patients as well (as suggested by findings from the ASTRO-APS study [5]).
There are some newer data to suggest apixaban may be non-inferior to warfarin in treating patients with LV thrombus; however, data overall is very mixed, and anticoagulating these patients with warfarin currently remains the preferred and more cautious approach.
Other situations in which warfarin may be preferred are when a higher INR goal or a customized anticoagulation approach is required, in instances of DOAC failure, or in cases where cost or patient preference are driving factors.
What patient-specific factors should be considered when deciding whether someone is a good candidate for DOAC therapy?
Weight/BMI: previous guidance suggested against the use of DOACs in pts weighing >120kg or with a BMI >40. However, ISTH updated their guidance in 2021 [6] to support using rivaroxaban and apixaban for VTE treatment or prevention “regardless of body weight and BMI”; these DOACs are often used in patients with obesity for non-VTE indications (e.g., thromboprophylaxis in atrial fibrillation). Data to support this include a post-hoc analysis of the ARISTOTLE trial (apixaban in atrial fibrillation), which showed that patients weighing >120kg (~5% of the study population) had similar results to the overall study population. It’s important to use adjusted body weight when calculating CrCl to estimate renal function and determine DOAC dosing in obese patients. Other DOACs should be avoided in pts >120kg/with BMI >40 due to limited or unconvincing data at this time.
Hepatic impairment: DOACs have varying hepatic metabolism (apixaban is the most hepatically cleared and dabigatran the least), but limited data exist for DOAC dose adjustments in patients with hepatic impairment. DOACs should NOT be used in Child-Pugh Class C/severe hepatic disease, while rivaroxaban (and betrixaban)[GU1] should also NOT be used in moderate/CP Class B patients. DOACs should be avoided in patients with decompensated/unstable cirrhosis. Aside from these caveats, DOACs may be considered for use in mild-moderate (Class A/B) hepatic impairment (with exceptions as above).
Renal impairment: DOACs may be used in stable CKD with appropriate renal dose adjustments; DOAC therapies should be held in the context of AKI. Dabigatran is the most renally cleared and generally avoided for this reason. Apixaban is the least renally cleared and is generally the preferred agent in patients with renal impairment, including ESRD (in the context of which apixaban use is supported by data, including that from a 2022 cohort study [7] vs. warfarin).
Drug Interactions: rivaroxaban, apixaban, edoxaban, and dabigatran are all P-gp substrates that will be affected by P-gp inducers or inhibitors (e.g., dronedarone, amiodarone, digoxin, diltiazem, verapamil, antiepileptics, antifungals, chemotherapy agents, and St. John’s Wort). Rivaroxaban and apixaban are substrates of CYP450 enzymes, prominently 3A4, 3A5, and 2J2. Apixaban is also metabolized by 1A2 and 2C 8/9/19 to a lesser degree. Some DOACs may interact with atorvastatin or ticagrelor, but these interactions are not typically a barrier to concurrent therapy if clinically indicated. Running a drug interaction report or consulting a pharmacist to help evaluate and safely navigate drug interactions is extremely helpful in these scenarios.
*In addition to DOAC package inserts, the AHA guide to DOAC use [8] is a great resource that summarizes renal/hepatic dosing considerations, drug interactions, and anticoagulant transition recommendations.
What safety profile and bleeding risk considerations exist for warfarin versus DOACs?
Warfarin has been studied versus individual DOACs; generally, DOACs are preferred from a safety standpoint due to lower risk of bleeding. The RE-LY trial [9] showed no difference in major bleeding but less intracranial hemorrhage (ICH) with dabigatran when compared to warfarin. The ROCKET-AF [10] trial showed a greater Hgb drop/need for transfusion with rivaroxaban but higher critical/fatal bleeding (including ICH) incidence with warfarin. In the ARISTOTLE [11] trial, apixaban was associated with significantly lower bleeding outcomes than warfarin, except for GI bleeding (for which there was no significant difference between groups). Edoxaban had a lower incidence of overall GI bleed (upper and lower GI bleeding combined), but not individual upper or lower GI bleeding, than warfarin in the ENGAGE [12] trial.
There are no direct head-to-head trials comparing DOACs, though some data suggest apixaban is associated with a lower bleeding risk than rivaroxaban (no difference in ICH), and that rivaroxaban may be associated with a higher risk of hemorrhagic stroke.
In older adults, DOACs can be used without safety concerns over warfarin, though avoiding dabigatran may be suggested due to a signal for increased bleeding outcomes in older adult patients. The ELDERCARE-AF [13] trial from Japan showed no difference in major bleeding, but higher rates of GI bleeding and all bleeding, with edoxaban vs. placebo in adults >/= 80 years. Overall, apixaban is generally considered safe to use/the preferred DOAC option in patients with a history of GI bleeding.
What is the recommended anti-thrombotic approach for patients with indications for both antiplatelet therapy and anticoagulation (for example, patients with atrial fibrillation undergoing PCI)?
Assessing the appropriateness of dual vs. triple therapy involves balancing the risk of stent thrombosis vs. stroke risk.
Among P2Y12 inhibitors, clopidogrel is typically recommended over ticagrelor or prasugrel due to its lower incidence of bleeding events and because clopidogrel was also the most commonly used P2Y12 inhibitor in dual versus triple therapy trials.
The WOEST trial [14] found no increased thrombosis risk but a reduced bleeding risk in patients given dual therapy post-PCI with clopidogrel and warfarin vs. those given triple therapy with warfarin, clopidogrel, and aspirin. The REDUAL-PCI trial [15] found a similarly reduced bleeding risk without statistically increased thrombotic risk in patients receiving dual therapy with dabigatran + P2Y12i vs. continuing triple therapy with P2Y12i + aspirin + warfarin. The PIONEER-AF [16] trial found lower bleeding risk with rivaroxaban + P2Y12 therapy than with warfarin-DAPT triple therapy without differences in thrombotic outcomes; the caveat here is that the 15mg daily rivaroxaban dose used is not approved for stroke prevention (that dose is 20mg daily). The AUGUSTUS trial [17] showed dual apixaban + P2Y12i therapy to have lower bleeding risk and unchanged efficacy than VKA dual therapy or triple therapy with apixaban or VKA. Importantly, these trials were not powered to differentiate ischemic outcomes.
As for when patients should be transitioned from triple (OAC + P2Y12 + ASA) to dual therapy (OAC + P2Y12), data from medication-specific trials can help guide the approach. For patients anticoagulated with warfarin or dabigatran, a triple therapy duration of 30 days may be appropriate based on WOEST (up to 1 year) and REDUAL-PCI trials (up to 3 months for patients with a DES). In PIONEER-AF, patients were randomized directly to rivaroxaban + P2Y12 therapy without first receiving triple therapy, but in clinical practice, triple therapy is often instituted for 7-30 days before transitioning to dual therapy with rivaroxaban and P2Y12 inhibitor. For apixaban, a shorter 7-day course of triple therapy appears appropriate.
*The 2022 ACC ECDP is a fantastic reference resource to help guide the management of anticoagulation and antiplatelet therapy in patients with atrial fibrillation or VTE undergoing PCI or with ASCVD [18].
What’s the scoop on factor XI, which appears to be clinically important for thrombosis but not hemostasis, as a potential drug target? Might this be the future of anticoagulation pharmacotherapy?
Factor XI is a part of the contact pathway of coagulation. It is activated by thrombin and factor XIIa and is thought to activate factor IX. Factor XI appears to contribute to thrombin generation and thereby amplify thrombus growth; it may also reduce fibrin degradation. Higher levels of factor XI appear correlated to increased clotting risk, while factor XI levels are poorly correlated with bleeding risk. The excitement around factor XI as a drug target stems from the thought that XI inhibition may decrease thrombotic risk without significantly changing bleeding risk.
Currently, there are several drugs in development and multiple ongoing clinical trials examining therapeutic viability. Oral, intravenous, and subcutaneous formulations of factor XI inhibitors are all being studied, in forms including monoclonal antibodies, small molecules, and antisense oligonucleotides. Most data reported thus far relates to VTE prophylaxis in orthopedic surgery. However, ongoing/planned trials, like the PACIFIC and OCEANIC series, will look at factor XI inhibitors in the context of atrial fibrillation, stroke, and myocardial infarction. Comparator drugs in these studies include DOACs and enoxaparin.
Long-term impact for this class of investigational therapeutics remains to be seen, and cost will likely be a limiting factor in using these agents (especially as DOACs are anticipated to go generic in 5-10 years). However, early data seems promising! [19, 20].
References – Anticoagulation Pharmacology
January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society in Collaboration With the Society of Thoracic Surgeons [published correction appears in Circulation. 2019 Aug 6;140(6):e285]. Circulation. 2019;140(2):e125-e151. doi:10.1161/CIR.0000000000000665
Eikelboom JW, Connolly SJ, Brueckmann M, et al. Dabigatran versus warfarin in patients with mechanical heart valves. N Engl J Med. 2013;369(13):1206-1214. doi:10.1056/NEJMoa1300615
Wang TY, Svensson LG, Wen J, et al. Apixaban or Warfarin in Patients with an On-X Mechanical Aortic Valve. NEJM Evid 2023;May 6:[Epub ahead of print]. doi:10.1056/EVIDoa2300067
Pengo V, Hoxha A, Andreoli L, et al. Trial of Rivaroxaban in AntiPhospholipid Syndrome (TRAPS): Two-year outcomes after the study closure. J Thromb Haemost. 2021;19(2):531-535. doi:10.1111/jth.15158
Woller SC, Stevens SM, Kaplan D, et al. Apixaban compared with warfarin to prevent thrombosis in thrombotic antiphospholipid syndrome: a randomized trial. Blood Adv. 2022;6(6):1661-1670. doi:10.1182/bloodadvances.2021005808
Martin KA, Beyer-Westendorf J, Davidson BL, Huisman MV, Sandset PM, Moll S. Use of direct oral anticoagulants in patients with obesity for treatment and prevention of venous thromboembolism: Updated communication from the ISTH SSC Subcommittee on Control of Anticoagulation. J Thromb Haemost. 2021;19(8):1874-1882. doi:10.1111/jth.15358
Ellenbogen MI, Ardeshirrouhanifard S, Segal JB, Streiff MB, Deitelzweig SB, Brotman DJ. Safety and effectiveness of apixaban versus warfarin for acute venous thromboembolism in patients with end-stage kidney disease: A national cohort study. J Hosp Med. 2022;17(10):809-818. doi:10.1002/jhm.12926
Chen A, Stecker E, A Warden B. Direct Oral Anticoagulant Use: A Practical Guide to Common Clinical Challenges. J Am Heart Assoc. 2020;9(13):e017559. doi:10.1161/JAHA.120.017559
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1 hr 4 min
June 18, 2023309. Atrial Fibrillation: Situational Assessment of Stroke and Bleeding Risk with Dr. Hafiza Khan
Dr. Daniel Ambinder (CardioNerds Co-Founder), Dr. Kelly Arps (Series Co-Chair and EP fellow at Duke University), Dr. Stephanie Fuentes Rojas (FIT Lead and EP fellow at Houston Methodist), and Dr. Ingrid Hsiung (Cardiology Fellow at Baylor Scott & White Health) discuss situational assessment of stroke and bleeding risk with expert faculty Dr. Hafiza Khan (Electrophysiologist at Baylor Scott & White Health). In this episode, we discuss stroke and bleeding risk in specific situations such as prior to cardioversion, triggered episodes, and perioperatively. These are scenarios that are commonly encountered and pose specific challenges. Episode notes were drafted by Dr. Stephanie Fuentes. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian.
This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal.
This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds.
We have collaborated with VCU Health to provide CME. Claim free CME here!
Disclosures: Dr. Ellis discloses grant or research support from Boston Scientific, Abbott-St Jude, advisor for Atricure and Medtronic.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls and Quotes – Atrial Fibrillation: Situational Assessment of Stroke and Bleeding Risk
In patients with persistent atrial fibrillation with tachycardia induced cardiomyopathy, timely restoration of normal rhythm is important. In patients not on established oral anticoagulation one option is to wait 3 weeks on oral anticoagulation prior to considering cardioversion. Another option is to pursue TEE prior to cardioversion as TEE is currently the gold standard imaging modality to exclude a LAA thrombus.
Following cardioversion (chemical or electrical), anticoagulation must not be interrupted for 4 weeks due to atrial stunning. This is especially true for patients who have been in atrial fibrillation for an extended period of time.
Individualizing assessment of stroke and bleeding risk is imperative when determining perioperative anticoagulation (AC) management. ACC has a helpful app (ManageAnticoag App) to make this easier.
When considering AC in triggered atrial fibrillation (e.g., pneumonia, sepsis), it is important to consider the substrate that made the patient susceptible to developing atrial fibrillation. AC is favored in patients with high CHA2DS2-VAsC score and many traditional risk factors for atrial fibrillation as they are at high risk for future development of atrial fibrillation.
Atrial fibrillation is a marker of poor outcomes in patients who have undergone coronary artery bypass graft (CABG) surgery. It is unclear if patients should be started on long-term AC for new onset atrial fibrillation after CABG regardless of risk factors. This is currently being investigated in the PACES trial.
Notes – Atrial Fibrillation: Situational Assessment of Stroke and Bleeding Risk
How do we choose an imaging modality for excluding LAA thrombus exclusion prior to cardioversion?
TEE is the gold standard. It also provides other information that is important for management of atrial fibrillation (e.g. LA size/volume, presence/degree of mitral regurgitation/stenosis, ejection fraction).
Gated cardiac CTA may have a growing role for evaluation of LAA thrombus.
What is the data behind the recommendation for uninterrupted AC following cardioversion and what is atrial stunning?
All patients should be anticoagulated for four weeks after cardioversion, regardless of the mechanism of cardioversion or CHA2DS2-VAsC score. As discussed in prior episodes, those who meet long term criteria for AC should be anticoagulated indefinitely.
The term “atrial stunning” refers to the electro-mechanical dissociation of the LAA following cardioversion. The longer one is in atrial fibrillation, the longer it takes for the LAA contraction/LAA flow velocities to recover after restoration of normal rhythm. During the period of atrial stunning, there is increased risk of LAA thrombus formation, hence AC should not be interrupted. The first 72 hours post cardioversion are the highest risk for LAA thrombus formation followed by the subsequent 4 weeks.
What is the approach of perioperative AC management in patients with atrial fibrillation?
ACC has a helpful app (ManageAnticoag App), to individualize the decision of when/how to stop and resume AC peri-procedurally.
One needs to ascertain three factors: 1) surgical bleeding risk, 2) stroke risk, and 3) the patient’s individual bleeding risk (e.g., medications, supplements, renal function, etc.).
The BRDIGE trial investigated the need to bridge patients on and off anticoagulation perioperatively. The trial was small and patient characteristics of the study (mostly male, low percentage of patients with high CHADS score) do not allow for generalizability of study findings to all patients.
Many patients do not require perioperative bridging, but individual patient factors should be used to make this decision. High risk features that warrant heparin bridging include recent stroke, mechanical valve, or mitral stenosis. Should consider bridging in patients with high CHA2DS2-VAsC score as these patients only made up a small portion of the BRIDGE trial.
What is the approach to AC in patients with triggered atrial fibrillation?
Similar to a fire, atrial fibrillation requires a substrate (i.e., combustible material) and a trigger (i.e., a match) to initiate. Though you can treat and therefore remove the trigger (e.g., pneumonia), patients with a substrate conducive to atrial fibrillation remain at high risk of atrial fibrillation in the future. If they were to convert to atrial fibrillation without clear symptoms in the future, they would be at risk for stroke and might not be started on AC. As such, long-term AC should be evaluated in a similar manner to those with paroxysmal or persistent atrial fibrillation without a clear trigger.
The patient population with true “triggered” atrial fibrillation may be limited to those with thyrotoxicosis as hyperthyroidism can trigger atrial fibrillation even in patients with structurally normal hearts and background risk for future atrial fibrillation.
Atrial fibrillation after cardiac surgery (e.g., CABG, mitral valve repair/replacement) should be managed with a coordinated heart team approach. Anticoagulation should likely be favored if bleeding risk is acceptable and patient has known risk factors, especially in valve surgeries where patients often have had longstanding LA pressure or volume overload. Atrial fibrillation following CABG has been associated with poor outcomes, though it is currently unclear if patients without traditional risk factors require long-term AC. This is currently being studied in the PACES trial.
References
January, C.T, Wann, L.S, Alpert, J.S., Calkins, H, Cigarroa, J.E., Cleveland, J.C., Conti, J.B., Ellinor P.T et al 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American college of Cardiology/American heart Asocciation Task Force on Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology, 6421, e1-76.
Dagres N, Kornej J, Hindricks G, et al. Prevention of Thromboembolism After Cardioversion of Recent-Onset Atrial Fibrillation. J Am Coll Cardiol. 2013 Sep, 62 (13) 1193–1194.https://doi.org/10.1016/j.jacc.2013.06.019
32 min

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