Atrial Fibrillation Topic Review

Introduction

Atrial fibrillation (AF) is the most common chronic arrhythmia, 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 in regard to symptoms and thromboembolic risk, including stroke. However, the pathophysiology and management differ.

Symptoms of atrial fibrillation 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, atrial fibrillation is classified as paroxysmal, persistent or permanent — the three Ps.

Paroxysmal atrial fibrillation is self-limiting; restoration of sinus rhythm occurs spontaneously. By definition, paroxysmal atrial fibrillation 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 atrial fibrillation 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.(January CT, et al. J Am Coll Cardiol. 2014[8a(e206)]; Hurst’s The Heart, 14th edition; Chapter 83, 11a.)

Permanent atrial fibrillation is present when atrial fibrillation is continuously present for more than 7 days, and there are no interventions planned 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. Atrial fibrillation may also be classified as valvular or nonvalvular. The term “nonvalvular AF”, as used in the current ACC/AHA Atrial Fibrillation Guidelines, describes AF in the absence of moderate-to-severe mitral stenosis or a mechanical heart valve. “Nonvalvular” does not imply a complete absence of valve disease, and can be used to describe AF in the context of mild mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation, and tricuspid regurgitation. (January CT, et al. J Am Coll Cardiol. 2019[6c-e(e130)].)

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

Pathophysiology – Atrial Fibrillation

Atrial fibrillation 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 atrial fibrillation can be within the right atrium; rarely, they are in the superior vena cava or in the coronary sinus.

In patients with atrial fibrillation, 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 atrial fibrillation, including left heart failure, chronic hypertension and mitral or aortic valvular heart disease. The larger the left atrium, the higher the risk for atrial fibrillation. Likewise, the larger the left atrium, the less likely that sinus rhythm can be maintained after cardioversion, especially without antiarrhythmic drugs.

Physiological AV nodal refractoriness prevents more than half of the 400 to 600 atrial action potentials/minute generated during atrial fibrillation from conduction to the ventricles. The typical ventricular heart rate in otherwise healthy patients with atrial fibrillation — 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 WPW patients develop atrial fibrillation, 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 400-600 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 – Atrial Fibrillation

Management of atrial fibrillation 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 atrial fibrillation:

Pulmonary embolus, pulmonary disease, post-operative, 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 > 140/90 mm Hg) accounts for almost 15% of all cases of atrial fibrillation and the association is well-documented. Even though the relative risk of AF is only modestly increased in hypertensives, hypertension is so prevalent in the general population that 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 atrial fibrillation. However, the proportion of atrial fibrillation resulting directly from obstructive sleep apnea remains unclear. (Andrade J, et al. Circ Res. 2014[4a].)

Diagnosis – Atrial Fibrillation

The diagnosis of atrial fibrillation 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.

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

Two other supraventricular tachycardias may produce an apparently irregular ventricular response. The first, multi-focal 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 arrythmia suggests multiple levels of block within the AV node.

The ventricular rate is frequently elevated; at rates above 150 bpm, it may be difficult to distinguish atrial fibrillation 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 atrial fibrillation, allowing a definitive diagnosis. However, in patients with Wolff-Parkinson-White syndrome, adenosine paradoxically increases the ventricular rate (as described above) and should not be administered.

Below are multiple full 12-lead ECG examples of atrial fibrillation:

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

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/s indicates a higher risk for thromboembolism in general.

Symptoms – Atrial Fibrillation

Symptoms of atrial fibrillation relate either to palpitations caused by the irregularly irregular heartbeat or to heart failure 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).

Treatment – Atrial Fibrillation

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

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.

Rate control

Commonly, ventricular rate control with AV nodal blocking drugs in patients with atrial fibrillation 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.

Beta-blockers (atenolol, metoprolol, carvedilol) antagonize beta-receptors, resulting in decreased conduction through the AV node, which reduces the heart rate in patients with atrial fibrillation. 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 atrial fibrillation, this approach is seldom employed.

Rhythm control

A rhythm control strategy is employed when rate control is not successful in controlling symptoms of atrial fibrillation or if the ventricular rate is poorly controlled despite AV blocking drugs. Rhythm control may include cardioversion, antiarrhythmic drug therapy or atrial fibrillation ablation.

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 of recurrence is high. Risk factors for recurrence include severe left atrial enlargement, hemodynamically significant valvular disease and uncontrolled sleep apnea.

Antiarrhythmic drug

Numerous antiarrhythmic medications are used in the management of atrial fibrillation. 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 atrial fibrillation, they are not widely used due to adverse effects and significant risk of proarrhythmia, except in special situations, such as atrial fibrillation with Wolff-Parkinson-White or vagally-mediated atrial fibrillation. Disopyramide and quinidine prolong the QT interval and are associated with proarrhythmia and torsade de pointes. Therefore, the QT interval should be monitored during therapy. (January CT, et al. J Am Coll Cardiol. 2014[32a(e230)]; 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.

Class IB (lidocaine, mexiletine): These agents are not effective for atrial fibrillation. 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 atrial fibrillation. Significant coronary artery disease is a contraindication due to increased risk of 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 atrial fibrillation 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 (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.

Class III (amiodarone, sotalol, bretylium, dofetilide, dronedarone, ibutilide): These potassium channel blockers are also commonly used in atrial fibrillation management. Amiodarone has not received FDA approval for the treatment of AF. It is very effective, but has a very long half-life (~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 ejection fraction). Dronedarone is not safe with systolic heart failure or in the setting of permanent atrial fibrillation. 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. (January CT, et al. J Am Coll Cardiol. 2014[32a(e230)]; Hurst’s The Heart, 14th edition; Chapter 83, 20b.) Because of the risk of proarrhythmia, dofetilide therapy should not be initiated out of hospital. (January CT, et al. J Am Coll Cardiol. 2014[30a(e228)].) 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 atrial fibrillation cases originate within the pulmonary veins. Ablation of atrial fibrillation — by pulmonary vein isolation (PVI) — electrically isolates the erratic electrical activity in the pulmonary veins (action potentials at a rate of 400-600 bpm) from the rest of the left atrium, effectively eliminating the atrial fibrillation. Catheter ablation for atrial fibrillation is a complex procedure, usually performed via femoral venous access, with a trans-septal approach to the left atrium and the pulmonary veins.

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

According to the ACC/AHA Guidelines (January CT, et al. J Am Coll Cardiol. 2014[36(e234)].), 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

AF catheter ablation is reasonable (recommendation class IIa) for:

  • Some patients with symptomatic persistent AF refractory or intolerant to at least one class I or III antiarrhythmic medication
  • Patients with recurrent symptomatic paroxysmal AF, as an initial rhythm control strategy before therapeutic trials of antiarrhythmic drug therapy, after weighing the risks and outcomes of drug and ablation therapy

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

  • Patients with symptomatic long-standing (> 12 months) persistent AF refractory or intolerant to at least 1 class I or III antiarrhythmic medication
  • Patients with symptomatic persistent AF before initiation of antiarrhythmic drug therapy with a class I or III antiarrhythmic medication

AF catheter ablation should not be performed (recommendation class III: harm):

  • In patients who cannot be treated with anticoagulant therapy during and after the procedure
  • For the sole intent of obviating the need for anticoagulation

The incidence of major periprocedural complications of AF ablation is estimated at 4-5%, and the risk of all-cause death at 0.1-0.2%. 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].)

LeftAtrialAppendageThrombus

Preventing thromboembolism

Thromboembolism and thromboembolic stroke occur due to detachment of a left atrial thrombus into the systemic circulation. In atrial fibrillation, 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 current ACC/AHA Guidelines recommend chronic oral anticoagulation for patients with AF and a CHA2DS2 score of 2 and higher for men or 3 and higher for women. (January CT, et al. J Am Coll Cardiol. 2019[6a(e130)].) 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 Guidelines, the selection of anticoagulant therapy depends “on the risk of thromboembolism, irrespective of whether the AF pattern is paroxysmal, persistent, or permanent”. (January CT, et al. J Am Coll Cardiol. 2019[7a(e131)].)

All AF patterns are associated with greatly increased risk of thromboembolic ischemic stroke. (January CT, et al. J Am Coll Cardiol. 2014[14a(e212)].)

The choice of anticoagulation should be individualized. Options include warfarin and novel 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 atrial fibrillation. 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 ACC/AHA Guidelines state 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. (January CT, et al. J Am Coll Cardiol. 2019[7a(e131), 8a(e132)].)

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. (January CT, et al. J Am Coll Cardiol. 2019[7a(e131), 8a(e132)].)

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 (patients with “valvular” AF). Warfarin is the recommended option for patients with mechanical heart valves. (January CT, et al. J Am Coll Cardiol. 2019[6a(e130)].)

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 by the ACC/AHA Guidelines “for the reversal of dabigatran in the event of life-threatening bleeding or an urgent procedure” (recommendation class I). (January CT, et al. J Am Coll Cardiol.  2019[6a(e130)].) 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 ACC/AHA Guidelines state that it “can be useful for the reversal of rivaroxaban and apixaban in the event of life-threatening or uncontrolled bleeding” (recommendation class IIb). (January CT, et al. J Am Coll Cardiol. 2019[6a(e130)].)

Direct surgical occlusion of the left atrial appendage during cardiac surgery for patients with atrial fibrillation who continue chronic oral anticoagulation post operatively 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. However, these data do not provide any assurance that LA appendage occlusion is effective for thromboprophylaxis without chronic oral anticoagulation. (Page RL. N Engl J Med. 2021[2a].)

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 Lariat device (SentreHeart) is used in a complex minimally invasive procedure requiring trans-septal 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 non-surgical 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 post-discharge 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 [Effient, Daiichi Sankyo/Eli Lilly] and ticagrelor [Brilinta, AstraZeneca] because of a lower risk of bleeding) is continued for up to 12 months. To lower the risk of 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 – Atrial Fibrillation

Atrioventricular Nodal (AVN) Ablation and Permanent Pacing

When high doses of AV blocking drugs do not control the ventricular response rate in atrial fibrillation, 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 beats per minute resulting in severe bradycardia after the AV node ablation, and a permanent pacemaker is required.

Vagally-mediated Atrial Fibrillation

Atrial fibrillation 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 atrial fibrillation, even with a structurally normal heart. Clinicians refer to the familiar association of excessive alcohol intake and acute atrial fibrillation as “holiday heart.”

Atrial Fibrillation in Hypertrophic Obstructive Cardiomyopathy (HOCM)

Patients with hypertrophic obstructive cardiomyopathy (HOCM) do not tolerate the loss of atrial contraction and rapid ventricular rates that occur with acute atrial fibrillation. Effective atrial contraction is required to fill the non-compliant hypertrophied ventricle, and tachycardia shortens the available time for diastolic filling. These factors may result in severe hemodynamic compromise in HOCM patients with acute atrial fibrillation (similar hemodynamic compromise may occur when atrial fibrillation 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 atrial fibrillation in patients with HOCM, although sotalol is more attractive. (Miller CAS, et al. Am J Cardiol. 2019[1a].)

Atrial fibrillation in Wolff-Parkinson-White (WPW)

Atrial fibrillation may be fatal in patients with Wolff-Parkinson-White 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 atrial fibrillation with WPW syndrome on ECG is crucial. The ECG below was recorded on a patient with atrial fibrillation 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 atrial fibrillation with WPW.

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

Patients with Wolff-Parkinson-White syndrome and atrial fibrillation should be evaluated for accessory pathway ablation.

References: