BySteven Lome, MD

Fact checked byErik Swain

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Atrial Fibrillation Topic Review

BySteven Lome, MD

Fact checked byErik Swain

Pathophysiology
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Etiology
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Diagnosis
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Symptoms
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Treatment
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Special situations

Atrial fibrillation is the most common chronic arrhythmia. It is characterized by erratic atrial electrical activity with atrial rates of 400 to 600 beats per minute.

The P wave is absent on the surface electrocardiogram and may at times be replaced with “fibrillatory waves.”

Atrial flutter is similar to atrial fibrillation (AF) in regard to symptoms and thromboembolic risk, including stroke. However, the pathophysiology and management differ.

Symptoms of AF reflect loss of atrial mechanical activity (atrial contraction) and rapid ventricular heart rates, both of which may reduce the ability to increase cardiac output and, particularly when AF occurs in the setting of other heart disease, may lead to congestive heart failure. In addition, AF is associated with an increased risk for systemic thromboembolism and stroke.

Clinically, AF is classified as paroxysmal, persistent, longstanding persistent or permanent. [Joglar JA, et al. J Am Coll Cardiol. 2023;17a]

Paroxysmal AF is self-limiting; restoration of sinus rhythm occurs spontaneously. By definition, paroxysmal AF lasts for less than 7 days (usually less than 24 hours) [Hurst’s The Heart, 14th edition; Chapter 83, 11a] and does not require interventions such as electrical or chemical cardioversion to restore normal rhythm.

Persistent AF lasts for more than 7 days. The term persistent implies a rhythm control patient management strategy intended to return and maintain sinus rhythm.

Longstanding persistent AF lasts for more than 12 months. [Joglar JA, et al. J Am Coll Cardiol. 2023;17a]; Hurst’s The Heart, 14th edition; Chapter 83, 11a.]

Permanent AF is present when AF is continuously present for more than 7 days, and the patient and clinician decide not to intervene to restore sinus rhythm.

The term “chronic atrial fibrillation” and the abbreviation “PAF” should be avoided. The term “lone atrial fibrillation” is used when AF occurs in the absence of structural heart disease. AF has traditionally been classified as valvular or nonvalvular, but the 2023 American College of Cardiology/American Heart Association/American College of Clinical Pharmacy/Heart Rhythm Society Guideline for the Management and Diagnosis of Atrial Fibrillation advises abandoning the distinction. “We should no longer consider the classification of AF as ‘valvular’ or ‘nonvalvular’ for the purpose of defining the etiology of AF, since the term was specific for eligibility of stroke risk reduction therapies. Valvular and nonvalvular terminology should be abandoned,” the authors wrote. [Joglar JA, et al. J Am Coll Cardiol. 2023;18a]

“Recurrent” AF indicates that the patient has experienced two or more AF episodes.

Pathophysiology

AF occurs when irritable foci cause rapid action potentials that result in an atrial heart rate between 400 and 600 beats per minute (bpm). These foci are commonly in the superior pulmonary veins; this is an important factor in the electrophysiologic approach to atrial fibrillation, known as pulmonary vein isolation. Less commonly, the foci of AF can be within the right atrium; rarely, they are in the superior vena cava or in the coronary sinus.

In patients with AF, atrial tissue remodels, showing pathologic changes of fibrosis and inflammation. The exact mechanisms of this remodeling remain unclear. Almost any cardiac condition associated with increased left atrial pressure and left atrial enlargement will increase the risk for AF, including left heart failure (HF), chronic hypertension and mitral or aortic valvular heart disease. The larger the left atrium, the higher the risk for AF. Likewise, the larger the left atrium, the less likely that sinus rhythm can be maintained after cardioversion, especially without antiarrhythmic drugs.

Physiological atrioventricular (AV) nodal refractoriness prevents more than half of the 400 to 600 atrial action potentials per minute generated during AF from conduction to the ventricles. The typical ventricular heart rate in otherwise healthy patients with AF — in the absence of AV-blocking drugs— is 150 ± 20 bpm. Lower ventricular response rates in unmedicated older patients suggest underlying conducting system disease. [Kawaji T, et al. Circ J. 2018;4a-b]

In patients with Wolff-Parkinson-White (WPW) syndrome, an “accessory pathway,” which commonly has a short refractory period and is capable of rapid conduction, provides a direct electrophysiologic pathway from the atrium to the ventricles independently from the AV node. When patients with WPW develop AF, many more action potentials reach the ventricles, resulting in ventricular rates greater than 200 bpm. AV nodal blocking drugs such as beta-blockers or calcium channel blockers may paradoxically increase the ventricular heart rate, as more atrial action potentials can conduct through the accessory pathway. This paradoxical increase in ventricular heart rates may lead to ventricular fibrillation (ventricular rates of 400 to 600 bpm) and death. Procainamide or urgent electrical cardioversion is recommended to manage AF with rapid ventricular rates in patients with WPW.

When AF occurs, left atrial flow velocities are significantly decreased in the atrium, often with stasis in the left atrial appendage. This predisposes to thrombus formation and the atrial thrombi, often originating in the left atrial appendage, may embolize. Validated algorithms can identify individuals at higher risk for thromboembolism; see the CHADS2 Score Topic Review and the CHA2DS2-VASc Score Topic Review.

Etiology

Management of AF should include a careful search for the underlying cause, since appropriate treatment of the cause may prevent further arrhythmia. The mnemonic “PIRATES” encompasses the vast majority of the causes of AF:

Pulmonary embolus, pulmonary disease, postoperative, pericarditis
Ischemic heart disease, idiopathic (“lone atrial fibrillation”), intravenous central line (in right atrium)
Rheumatic valvular disease (specifically mitral stenosis or mitral regurgitation)
Anemia, alcohol (“holiday heart”), advanced age, autonomic tone (vagally mediated atrial fibrillation)
Thyroid disease (hyperthyroidism)
Elevated blood pressure (hypertension), electrocution
Sleep apnea, sepsis, surgery

Hypertension (blood pressure > 140 mm Hg systolic/90 mm Hg diastolic) accounts for almost 15% of all cases of AF, and the association is well-documented. Even though the relative risk for AF is only modestly increased in patients with hypertension, hypertension is so prevalent in the general population that it is the most important population-attributable risk factor.

Obstructive sleep apnea, commonly associated with hypertension and obesity, is present in about 40% of patients with AF. However, the proportion of AF resulting directly from obstructive sleep apnea remains unclear. [Andrade J, et al. Circ Res. 2014;4a]

Diagnosis

The diagnosis of AF is confirmed with a standard 12-lead ECG. P waves are absent, coarse “fibrillatory waves” can frequently be seen and sometimes no atrial activity can be identified.

fibrallatory waves — *Image: Learn the Heart*

The QRS complexes are “irregularly irregular”, with varying R-R intervals.

Two other supraventricular tachycardias may produce an apparently irregular ventricular response. The first, multifocal atrial tachycardia, usually occurs in association with chronic pulmonary disease and has distinct P waves of varying morphology. The second, atrial flutter with varying AV block, is characterized by typical flutter waves with multiple different R-R intervals. Sophisticated analysis of this arrhythmia suggests multiple levels of block within the AV node.

irregularly irregular rhythms — *Image: Learn the Heart*

The ventricular rate is frequently elevated; at rates above 150 bpm, it may be difficult to distinguish AF from atrial flutter, atrial tachycardia or atrioventricular nodal reentrant tachycardia (AVNRT). In this situation, administering adenosine will transiently slow the ventricular rate in patients with AF, allowing a definitive diagnosis. However, in patients with WPW syndrome, adenosine paradoxically increases the ventricular rate (as described above) and should not be administered.

Below are multiple full 12-lead ECG examples of AF:

On physical examination, the heart rhythm is “irregularly irregular” and frequently rapid. Findings of HF may be present depending on the ventricular rate, duration of AF and other factors. There will never be an S4 heart sound present during AF, as this heart sound is produced by atrial contraction with a noncompliant left ventricle. Normal atrial contraction is lost during AF.

Transesophageal echocardiography (TEE) or cardiac CT can document the presence or absence of left atrial thrombus if this information is required for patient management. On TEE, findings include direct visualization of a mobile echodensity within the appendage. To distinguish artifact or trabeculation from thrombus, the echodensity should move independently of the atrial wall. Pulse wave Doppler can be used to determine the flow velocity in the left atrial appendage; a velocity of less than 0.4 m per second indicates a higher risk for thromboembolism in general.

Symptoms of atrial fibrillation

Symptoms of AF relate either to palpitations caused by the irregularly irregular heartbeat or to HF with limited overall cardiac output resulting from the loss of atrial contraction and rapid ventricular rates. If AF occurs in association with structural heart disease, reduced cardiac output may cause hypotension, dizziness and even syncope (loss of consciousness).

symptoms chart — *Image: Learn the Heart*

Treatment of atrial fibrillation

Management of patients with AF requires the consideration of two distinct issues — electrophysiologic management and prevention of systemic thromboembolism. A summary image is below.

treatment management chart — *Image: Learn the Heart*

Alleviating symptoms

Electrophysiologic management includes two approaches: a “rate control” strategy and a “rhythm control” strategy.

In 2002, the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) randomized trial evaluated the outcomes of rate control vs. rhythm control in more than 4,000 patients, most of whom also received warfarin. At 5 years, mortality was higher in the rhythm-control group than in the rate-control group, but the difference did not achieve statistical significance. For the past 2 decades, an individualized management approach has been recommended, based on the severity of symptoms and the patient’s personal preference; this was reaffirmed in the 2023 AF guideline.

Rate control

Commonly, ventricular rate control with AV nodal blocking drugs in patients with AF results in symptomatic improvements, and no additional intervention is needed.

Selecting the appropriate AV blocking agent requires knowledge of other indications and contraindications for these drugs; assessment of left ventricular systolic function and renal function is particularly important in drug selection. AV blocking agents used in AF include beta-blockers, non-dihydropyridine calcium channel blockers and digoxin. [Joglar JA, et al. J Am Coll Cardiol. 2023;67a].

Beta-blockers (atenolol, metoprolol, carvedilol) antagonize beta-receptors, resulting in decreased conduction through the AV node, which reduces the heart rate in patients with AF. Caution is advised in patients with reactive airway disease (asthma), as antagonizing beta-2 receptors can cause bronchospasm. [Salpeter S, et al. Cochrane Database Syst Rev. 2002;5a, 9a]

Non-dihydropyridine calcium channel blockers (diltiazem, verapamil) slow AV conduction by antagonizing voltage gated calcium channels, decreasing intracellular calcium. Because these drugs reduce left ventricular inotropy (contractility) via the same mechanism, they are generally not recommended for use in patients with left ventricular systolic dysfunction (reduced ejection fraction).

Digoxin blocks the sodium/potassium ATPase pump and increases vagal tone. Digoxin effectively reduces ventricular rates at rest but not during physical activity. If used, digoxin should be prescribed in combination with a beta-blocker or a non-dihydropyridine calcium channel blocker.

Rarely, tolerable pharmacologic approaches do not adequately reduce the ventricular rate, and AV nodal ablation with permanent pacemaker implantation is needed. With the development of improved ablation techniques for AF, this approach is seldom employed.

Rhythm control

A rhythm control strategy can be employed when rate control is not successful in controlling symptoms of AF or if the ventricular rate is poorly controlled despite AV blocking drugs. Rhythm control may include cardioversion, antiarrhythmic drug therapy or AF ablation. Whether to pursue a rhythm control or rate control strategy should be based on shared decision-making, but based on recent evidence, the 2023 AF guideline endorses “early and continued management of patients with AF that should focus on maintaining sinus rhythm and minimizing AF burden.” [Joglar JA, et al. J Am Coll Cardiol. 2023;5a].

The term “cardioversion” is used to describe procedures performed to restore sinus rhythm, either electrically by direct current cardioversion (DCCV) or pharmacologically with class IA, class IC or class III antiarrhythmic drugs.

If sinus rhythm is successfully restored, antiarrhythmic drug therapy is often required to maintain it, especially if the risk for recurrence is high. Risk factors for recurrence include severe left atrial enlargement, hemodynamically significant valvular disease and uncontrolled sleep apnea.

Antiarrhythmic drugs

Numerous antiarrhythmic medications are used in the management of AF. They are listed below, by Vaughn-Williams class.

Class IA (quinidine, procainamide, disopyramide): These agents block cardiac sodium channels and depress phase 0 of the action potential. Although class IA drugs are effective for AF, they are not widely used due to adverse effects and significant risk for proarrhythmia, except in special situations, such as AF with WPW syndrome or vagally mediated AF. Disopyramide and quinidine prolong the QT interval and are associated with proarrhythmia and torsades de pointes. Therefore, the QT interval should be monitored during therapy. [Hurst’s The Heart, 14th edition; Chapter 83, 20b, 21a.] In addition to their cardiac effects, procainamide can cause drug-induced lupus erythematosus, detected by measuring anti-histone antibodies and quinidine can cause cinchonism. Disopyramide can cause urinary retention. Quinidine and disopyramide are not mentioned in the 2023 AF guideline, while procainamide may be considered for pharmacological cardioversion if other agents are contraindicated or not preferred, and is considered safe for use in pregnant patients with stable AF and structurally normal hearts. [Joglar JA, et al. J Am Coll Cardiol. 2023;82a;120a].

Class IB (lidocaine, mexiletine): These agents are not effective for AF. Both have been used for ventricular arrhythmias.

Class IC (flecainide, propafenone, moricizine): Flecainide and propafenone may be used to maintain sinus rhythm in patients with AF. Significant coronary artery disease is a contraindication due to increased risk for proarrhythmia and sudden cardiac death. Because class IC antiarrhythmics increase AV nodal conduction, they must be used in combination with an AV blocking agent in order to prevent rapid AF or atrial flutter conduction (1:1 conduction) through the AV node in the event of recurrent atrial tachyarrhythmia. Class IC drugs may be proarrhythmic in the setting of left ventricular hypertrophy (LVH; wall thickness > 1.4 cm). Flecainide and propafenone can be used as a “pill-in-the-pocket” approach in patients without heart disease who are in sinus rhythm, if documented to be safe and efficacious in the hospital setting. [Hurst’s The Heart, 14th edition; Chapter 83, 20c.] Note that propafenone is hepatically cleared (and thus not recommended with liver disease), whereas flecainide is renally cleared. Flecainide and propafenone are reasonable to use for long-term maintenance of sinus rhythm if the patient has no previous MI or structural heart disease, including HF with reduced ejection fraction (HFrEF). [Joglar JA, et al. J Am Coll Cardiol. 2023;85a].

Class III (amiodarone, sotalol, bretylium, dofetilide, dronedarone, ibutilide): These potassium channel blockers are also commonly used in AF management. Amiodarone has not received FDA approval for the treatment of AF. It is very effective, but has a very long half-life (approximately 42 days), and significant potential toxicity. Pulmonary fibrosis is a major concern. [Hurst’s The Heart, 14th edition; Chapter 83, 20d.] Sotalol is proarrhythmic in the setting of LVH. Amiodarone and dofetilide are preferred in patients with left ventricular systolic dysfunction (reduced EF). Dronedarone is not safe with HFrEF or in the setting of permanent AF. Bretylium is rarely used. Like the class IA antiarrhythmic disopyramide, sotalol and dofetilide prolong the QT interval and may cause proarrhythmia and torsades de pointes. Monitoring of the QT interval is therefore recommended when starting sotalol or dofetilide. [Hurst’s The Heart, 14th edition; Chapter 83, 20b.] Because of the risk for proarrhythmia, dofetilide therapy should not be initiated out of hospital. [Joglar JA, et al. J Am Coll Cardiol. 2023;85a] By contrast, dronedarone is typically started in the outpatient setting. Sotalol may be initiated out of hospital in patients with no structural heart disease who are in sinus rhythm and have normal QT and electrolyte status. [Hurst’s The Heart, 14th edition; Chapter 83, 20c]

Atrial fibrillation ablation

The majority of AF cases originate within the pulmonary veins. Ablation of AF — by pulmonary vein isolation (PVI) — electrically isolates the erratic electrical activity in the pulmonary veins (action potentials at a rate of 400 bpm to 600 bpm) from the rest of the left atrium, effectively eliminating the AF. Catheter ablation for AF is a complex procedure, usually performed via femoral venous access, with a transseptal approach to the left atrium and the pulmonary veins.

before and after ablation — *Image: Learn the Heart*

Higher success rates for AF ablation are achieved in patients with paroxysmal AF, smaller left atrial volumes and shorter duration of AF.

According to the 2023 AF guideline [Joglar JA, et al. J Am Coll Cardiol. 2023;93a], AF catheter ablation is indicated (recommendation class I) for:

Patients with symptomatic paroxysmal AF refractory or intolerant to at least one class I or III antiarrhythmic medication
In selected patients with symptomatic paroxysmal AF, generally younger with fewer comorbidities, it is indicated as a first-line therapy to improve symptoms and prevent progression to persistent AF

AF catheter ablation is reasonable (recommendation class IIa):

As a first-line therapy in patients (other than those younger and with few comorbidities) with symptomatic paroxysmal or persistent AF who are being managed with a rhythm control strategy

AF catheter ablation may be considered (recommendation class IIb) for:

Patients with asymptomatic or minimally symptomatic AF

The incidence of major periprocedural complications of AF ablation is estimated at 4% to 5%, and the risk for all-cause death at 0.1% to 0.2%. Intraoperative and postoperative complications include access site-related bleeding or vascular complications, pericardial effusion, tamponade, transient ischemic attack or stroke, and pulmonary congestion due to volume overload. [Piccini JP, et al. Lancet. 2016;8b] The most serious complication of AF ablation is atrioesophageal fistula, which is rare (incidence range: 0.03% to 0.08%) but life-threatening if not recognized and immediately treated. [Han HC, et al. Circ Arrhythm Electrophysiol. 2017;2a; Piccini JP, et al. Lancet. 2016;8a] Atrioesophageal fistula symptoms typically develop within 60 days of the ablation, and include nonspecific gastrointestinal, cardiac, neurological, and/or infective symptoms such as fever, fatigue, malaise, chest discomfort, nausea, vomiting, dysphagia, odynophagia, hematemesis, melena and dyspnea. [Han HC, et al. Circ Arrhythm Electrophysiol. 2017[7a]; Kapur S, et al. Circulation. 2017[7a].] The rate of AF recurrence after ablation is 30% to 40% in major clinical trials; and in general practice, 11% of U.S. patients have a repeat ablation within 1 year after their first ablation. [Joglar JA, et al. J Am Coll Cardiol. 2023;97a].

left atrial appendage — *Image: Learn the Heart*

Preventing thromboembolism

Thromboembolism and thromboembolic stroke occur due to detachment of a left atrial thrombus into the systemic circulation. In AF, the left atrium fulfills the elements of Virchow’s triad, including stasis, endothelial damage and activation of the coagulation system. [Watson T, et al. Lancet. 2009;1a]

Chronic oral anticoagulation for stroke prophylaxis reduces stroke risk and increases bleeding risk. Several risk/benefit decision aids have been developed and validated.

The most commonly used method is the CHA2DS2-VASc score. CHA2DS2 stands for Congestive heart failure, Hypertension, Age ≥ 75 years, Diabetes, previous Stroke/Transient Ischemic Attack (TIA). VASc stands for Vascular disease (peripheral arterial disease, previous MI, aortic atheroma), Age ≥ 65 years, Sex category (female). Each risk factor receives 1 point, with the exceptions of age greater than 75 years and stroke/TIA, which receive 2 points each. The 2023 AF guideline recommends chronic oral anticoagulation for patients with AF and a CHA2DS2-VASc score of 2 and higher for men or 3 and higher for women. (Joglar JA, et al. J Am Coll Cardiol. 2023;38a] In general, the higher the CHA2DS2-VASc score is, the higher the annual stroke risk; this is excellent information for clinicians to discuss with their patients.

According to the ACC/AHA/ACCP/HRS guidelines, all AF patterns are associated with greatly increased risk for thromboembolic ischemic stroke, and for patients with AF and an estimated annual stroke/thromboembolism risk of 2% or more, the selection of anticoagulant therapy should be based on thromboembolism risk regardless of AF pattern. [Joglar JA, et al. J Am Coll Cardiol. 2023;37a]

The choice of anticoagulation should be individualized. Options include warfarin and non-vitamin K antagonist oral anticoagulants (NOACs). Warfarin, a vitamin K antagonist, is effective for stroke risk reduction. For optimal safety and efficacy, the warfarin dose must be regularly monitored and adjusted to maintain an international normalized ratio (INR) between 2 and 3. [Hurst’s The Heart, 14th edition;Chapter 83, 17a.] NOACs, including dabigatran (Pradaxa, Boehringer Ingelheim), rivaroxaban (Xarelto, Janssen), edoxaban (Savaysa, Daiichi Sankyo) and apixaban (Eliquis, Bristol Myers Squibb/Pfizer), are target-specific anticoagulants approved by the FDA for thromboembolism prophylaxis in patients with AF. Dabigatran is a direct inhibitor of thrombin, while apixaban, edoxaban and rivaroxaban are direct inhibitors of activated factor X (factor Xa). [Hurst’s The Heart, 14th edition;Chapter 83, 18a.] These drugs do not require coagulation laboratory monitoring. Their predictable pharmacology and minimal drug/dietary interactions make them much more convenient for patients. The 2023 guideline states that renal function should be evaluated before NOAC therapy is initiated, and at least annually thereafter (depending on the degree of renal dysfunction and the likelihood of fluctuation in each individual patient). In patients with worsening renal function, dose adjustment or discontinuation may be required. [Joglar JA, et al. J Am Coll Cardiol. 2023;55a;61b]

In patients taking factor Xa inhibitors, hepatic function should also be evaluated at least once annually. In general, NOACs are not recommended for patients with severe hepatic dysfunction. [Joglar JA, et al. J Am Coll Cardiol. 2023;41a]

See the prescribing information for guidance for individual drugs.

The ACC/AHA guidelines recommend the use of NOACs rather than dose-adjusted warfarin for anticoagulation in patients with AF, except in patients with concomitant moderate-to-severe mitral stenosis or a mechanical heart valve. Warfarin is the recommended option for patients with mechanical heart valves. [Otto CM, et al. Circulation. 2020;e84-e85]

Two agents are currently available for urgent reversal of NOAC-mediated anticoagulation. Idarucizumab (Boehringer Ingelheim), a monoclonal antibody, binds to and inactivates dabigatran; it is FDA-approved and recommended for urgent reversal of dabigatran by the 2023 AF guideline (recommendation class I). [Joglar JA, et al. J Am Coll Cardiol. 2023;50a] Andexanet alfa (or “coagulation factor Xa [recombinant], inactivated-zhzo”), a bioengineered protein, is available as an antidote to the oral activated factor X (factor Xa) inhibitors, including apixaban and rivaroxaban. The FDA based its approval of andexanet alfa (Portola Pharmaceuticals) on data from healthy volunteers; the 2023 AF guideline gives it a class I recommendation for treatment of patients taking factor Xa inhibitors who experience life-threatening bleeding. [Joglar JA, et al. J Am Coll Cardiol. 2023;50a]

Direct surgical occlusion of the left atrial appendage during cardiac surgery for patients with atrial fibrillation who continue chronic oral anticoagulation postoperatively results in lower stroke rates as compared to similar patients who do not have atrial appendage closure. [Whitlock RP, et al. N Engl J Med. 2021;1a] These findings confirm the importance of the LA appendage in the pathophysiology of thromboembolic stroke.

More recently, left atrial appendage occlusion devices (Watchman, Boston Scientific and Amplatzer Amulet, Abbott) deployed by percutaneous catheter techniques for prevention of thromboembolism were developed. The Watchman and Amplatzer Amulet devices are FDA-approved. These devices isolate and occlude the left atrial appendage, reducing the risk for thromboembolism. The Watchman device is indicated “to reduce stroke risk in patients with nonvalvular atrial fibrillation who require an alternative to long-term oral anticoagulation”. However, even with a device in place, the left atrial appendage may still contain a thrombus. [Fauchier L, et al. J Am Coll Cardiol. 2018[1a-b].]

The 2023 AF guideline states that surgical and percutaneous left atrial appendage occlusion devices “have the potential to obviate the need for or supplement long-term oral anticoagulation in select patients.” [Joglar JA, et al. J Am Coll Cardiol. 2023;47b]

The guideline gives percutaneous left atrial appendage occlusion a class 2a recommendation in patients with AF at moderate or high risk for stroke who are contraindicated for oral anticoagulation, and a class 2b recommendation in patients with AF at moderate or high risk for stroke and high risk for bleeding on oral anticoagulation. [Joglar JA, et al. J Am Coll Cardiol. 2023;47a]

The Lariat device (SentreHeart) is used in a complex minimally invasive procedure requiring transseptal access to the left atrium and percutaneous access to the pericardial space in order to ligate the left atrial appendage. To date, clinical experience with the Lariat device is limited.

Patients with AF are at an increased risk for developing an acute coronary syndrome (ACS) such as myocardial infarction and unstable angina. [Kea B, et al. Curr Emerg Hosp Med Rep. 2016;1a] Percutaneous coronary intervention (PCI) is a nonsurgical modality for the treatment of ACS which requires modification to the anticoagulant and antiplatelet therapy in the context of AF. In 2020, the ACC released the Expert Consensus Decision Pathway for Anticoagulant and Antiplatelet Therapy in Patients with AF or Venous Thromboembolism Undergoing PCI, which includes algorithms for periprocedural, postprocedural and postdischarge management.

Prior to PCI, the current anticoagulant treatment (typically warfarin or a NOAC) is held or stopped, and aspirin is administered (325 mg for an elective PCI, 162-324 mg for an urgent or emergent PCI). During the procedure, a loading dose of a P2Y12 inhibitor (clopidogrel 600 mg orally preferred) is administered and a “bridging” anticoagulant (unfractionated heparin [UFH], low-molecular weight heparin [LMWH] or bivalirudin) is given intravenously. [Khumbani DJ, et al. J Am Coll Cardiol. 2020;10a, 21a-b]

After the procedure, the oral anticoagulant therapy is restarted and continued indefinitely. NOACs are preferred (even in patients who were previously on vitamin K antagonists such as warfarin), unless contraindicated (for example, because of inadequate renal function). Low-dose aspirin (81 mg daily) is given for at least 1 day following PCI, and may be extended for up to 30 days if thrombotic risk is high and bleeding risk low. When aspirin is co-administered with oral anticoagulants, the daily dose should not exceed 100 mg. Treatment with a P2Y12 inhibitor (clopidogrel is preferred over prasugrel and ticagrelor [Brilinta, AstraZeneca] because of a lower risk for bleeding) is continued for up to 12 months. To lower the risk for gastrointestinal bleeding, starting or continuing a proton pump inhibitor (or a histamine

H2-receptor antagonist in select cases) is recommended. [Khumbani DJ, et al. J Am Coll Cardiol. 2020;9a, 10a-c, 21a-b]

Special situations

Atrioventricular nodal ablation and permanent pacing

When high doses of AV blocking drugs do not control the ventricular response rate in AF, AV nodal ablation offers another option. Atrial action potentials must traverse the AV node to reach the ventricle. AV node ablation destroys this connection. This results in complete heart block. The ventricular His-Purkinje system has an intrinsic rate of 30 to 40 bpm, resulting in severe bradycardia after the AV node ablation, and a permanent pacemaker is required.

Vagally mediated atrial fibrillation

AF triggered by episodes of vagal stimulation has been well described (nausea, vomiting, abdominal pain, severe coughing, young healthy athletes with high vagal tone, etc). Disopyramide, an agent with significant anticholinergic activity, may be useful, although data are very limited. [Rattanawong P, et al. J Atr Fibrillation. 2020;1a]

Holiday heart

Ingestion of large amounts of alcohol (binge drinking, as frequently occurs during holidays) may trigger AF, even with a structurally normal heart. Clinicians refer to the familiar association of excessive alcohol intake and acute AF as “holiday heart.”

Atrial fibrillation in hypertrophic obstructive cardiomyopathy

Patients with hypertrophic obstructive cardiomyopathy (HOCM) do not tolerate the loss of atrial contraction and rapid ventricular rates that occur with acute AF. Effective atrial contraction is required to fill the noncompliant hypertrophied ventricle, and tachycardia shortens the available time for diastolic filling. These factors may result in severe hemodynamic compromise in patients with HOCM and acute AF (similar hemodynamic compromise may occur when AF develops in patients with severe left ventricular hypertrophy from hypertensive heart disease or aortic valve stenosis).

Because disopyramide has significant negative inotropic effects, it may occasionally be useful for management of AF in patients with HOCM, although sotalol is more attractive. [Miller CAS, et al. Am J Cardiol. 2019;1a]

Atrial fibrillation in Wolff-Parkinson-White syndrome

AF may be fatal in patients with WPW syndrome due to rapid conduction of the atrial impulses through the accessory pathway. This results in rapid ventricular rates, which can degenerate into ventricular fibrillation. AV nodal blocking agents should be avoided in this setting; these drugs slow AV conduction but increase the conduction in the accessory pathway, with very rapid ventricular rates.

Recognizing AF with WPW syndrome on ECG is crucial. The ECG below was recorded on a patient with AF and WPW syndrome. Note the wide-complex, irregularly irregular rhythm with “delta waves.” This ECG might initially be misinterpreted as showing polymorphic ventricular tachycardia (torsades de pointes); however, the QRS axis remains stable (no “twisting of the points”) in AF with WPW.

Procainamide is the appropriate therapy. Synchronized DC cardioversion is recommended for hemodynamic instability.

Patients with WPW syndrome and AF should be evaluated for accessory pathway ablation.