Wolff–Parkinson–White and ventricular pre-excitation: risk stratification and pathways

This page covers ventricular pre-excitation and the Wolff–Parkinson–White (WPW) syndrome: the pathway, the tachycardias it carries, pre-excited atrial fibrillation (AF), ablation, drugs, and risk stratification when there are no symptoms. ESC 2019 calls sudden cardiac death from pre-excited AF that conducts rapidly over the AP and degenerates into ventricular fibrillation the most feared manifestation of WPW syndrome.^[1] Drug classes and proarrhythmia in general are covered in Antiarrhythmic drugs: class actions and proarrhythmia. AF without an accessory pathway is covered in Atrial fibrillation, and ablation for AF itself in AF ablation: indications, technique and anticoagulation.

Pre-excitation and WPW syndrome: two different labels

Start with the ECG in sinus rhythm.^[1] ESC 2019 describes the typical resting pattern as a short PR interval (≤120 ms), a slurred upstroke (or downstroke) of the QRS complex (the delta wave) and a wide QRS complex (>120 ms).^[1] That pattern means an AP is conducting from atrium to ventricle: ESC 2020 sports cardiology says ventricular pre-excitation on the resting ECG is due to an AP with antegrade conduction.^[8]

The 2009 AHA/ACCF/HRS ECG standardization statement (part III, a scientific statement) says the surface ECG cannot show whether pre-excitation is full, and lists criteria suggestive of full WPW-type pre-excitation.^[17] The first is a PR interval less than 120 ms during sinus rhythm in adults and less than 90 ms in children, assuming no intra-atrial or interatrial conduction block.^[17] The second is a slurred initial QRS (delta wave) that interrupts the P wave or arises immediately after it ends.^[17] The other two are a QRS duration greater than 120 ms in adults and greater than 90 ms in children, and secondary ST and T wave changes.^[17]

The syndrome needs arrhythmia as well as the pattern. ESC 2019 says WPW syndrome refers to the presence of an overt (manifest) AP, resulting in pre-excitation, in combination with usually recurrent tachyarrhythmias.^[1] ACC/AHA/HRS 2015 says the diagnosis of WPW syndrome is reserved for patients who demonstrate ventricular pre-excitation on their resting ECG that participates in arrhythmias.^[2] That is the corrected wording: a December 2016 JACC correction replaced "and have associated SVT" with "that participates in arrhythmias".^[3] ESC 2020 sports cardiology defines WPW syndrome as the presence of paroxysmal arrhythmias in a patient with pre-excitation.^[8]

^{[8] [1] [2] [1] [2] [8]}

The accessory pathway: anatomy and conduction

ESC 2019 says APs are single or multiple strands of myocardial cells that bypass the physiological conduction system and directly connect atrial and ventricular myocardium.^[1] These AV connections are due to incomplete embryological development of the AV annuli, without complete separation of the atria and ventricles.^[1] Approximately 60% lie along the mitral valve (left free wall APs), 25% insert along the septal aspect of the mitral or tricuspid annulus, and about 15% insert along the right free wall.^[1]

Why does an AP behave differently from the AV node?^[1] ESC 2019 says APs typically exhibit fast conduction (with the exception of atypical pathways), dependent on a sodium current similar to that of myocardial cells.^[1] ACC/AHA 2023 says such APs are comprised of atrial tissue, and that the faster conduction properties of atrial tissue compared with the atrioventricular node allow for rapid rates in preexcited AF.^[5]

Pathway vocabulary

^{[1] [2]}

The degree of pre-excitation varies.^[1] ESC 2019 says various degrees of pre-excitation are possible depending on the location of the AP and on AV-nodal conduction properties.^[1] In most cases, APs giving rise to the WPW pattern are seen in structurally normal hearts.^[1] ESC 2019 adds that rare familial forms of pre-excitation associated with LV hypertrophy and multisystem disease (PRKAG2 mutations, Danon and Fabry disease, and others) have also been described.^[1]

How common it is

• ESC 2019: the prevalence of a WPW pattern on the surface ECG in the general population ranges from 0.15–0.25%, increasing to 0.55% among first-degree relatives of affected patients.^[1]
• ACC/AHA/HRS 2015: the incidence of manifest pre-excitation or WPW pattern on ECG tracings in the general population is 0.1% to 0.3%, but not all patients with manifest ventricular pre-excitation develop PSVT.^[2]
• ESC 2019: compared with the remaining population, the pre-excitation population is generally younger, predominantly male, and has less comorbidity.^[1]
• ACC/AHA/HRS 2015: pre-excitation is present in 20% to 35% of children with SVT.^[2]

How often AF occurs depends on which guideline you read, and on the population it describes. ESC 2019 says paroxysmal AF has been found in 50% of patients with WPW and may be the presenting arrhythmia.^[1] In its section on the asymptomatic patient, ESC 2019 says the most common arrhythmia in WPW syndrome is AVRT (80%), followed by a 20–30% incidence of AF.^[1] ACC/AHA 2023 says AF occurs in approximately 15% of persons with WPW, and ESC 2020 sports cardiology estimates that one third of patients with WPW syndrome may develop AF.^[5][8]

Mechanisms: the tachycardias an accessory pathway can carry

An AP plus the AV node makes a circuit with two limbs.^[1] ESC 2019 says AVRT is the most common tachycardia associated with APs, and that two mechanisms of re-entry are possible according to the antegrade or retrograde conduction over the AV node–His–Purkinje system: orthodromic and antidromic AVRT.^[1]

^{[1] [2]}

Two more patterns use the same pathway. ESC 2019 says that in focal atrial tachycardia (AT), atrial flutter, AF or AVNRT, the QRS complexes can be pre-excited when the AP is a bystander, not a critical part of the re-entry circuit.^[1] Pre-excited AF is the dangerous one.^[1] ESC 2019 says AF with fast ventricular response over an overt AP with a short anterograde refractory period is a potentially life-threatening arrhythmia in WPW syndrome, due to potential degeneration into VF.^[1] ESC 2019 says conduction can occur preferentially via the AP "due to its shorter RP compared with the AVN".^[1] ACC/AHA/HRS 2015 says that when AF occurs with ventricular pre-excitation, an AP with a short refractory period may allow rapid pre-excited AV conduction; the resulting fast, often irregular, broad-complex tachycardia is often unstable and may lead to VF.^[2] ESC 2019 adds that these patients are typically young with no structural heart disease, and that high-rate AVRT may potentially initiate AF.^[1]

ACC/AHA/HRS 2015 describes the same sequence: AF in patients with APs may result in extremely rapid conduction to the ventricle over a manifest pathway, which increases the risk of inducing ventricular fibrillation and sudden cardiac death (SCD).^[2] ACC/AHA 2023 says the risk of preexcited AF is higher for those with multiple pathways and a short antegrade pathway refractory period (<250 ms), which allows rapid conduction and predisposes to VF and sudden death.^[5] Concealed pathways are different: ESC 2019 says they are not associated with an increased risk of sudden cardiac death.^[1]

^[1]

Presentation and the ECG

In a patient with regular paroxysmal palpitations, ESC 2019 says pre-excitation on the resting ECG is generally suggestive of AVRT.^[1] Its absence does not rule AVRT out, because the AP may be concealed (conducting only retrogradely) or an atypical (Mahaim) pathway that is latent in sinus rhythm.^[1]

Sudden death can be the first event.^[2] ACC/AHA/HRS 2015 says SCD may be the first presentation of patients with undiagnosed WPW.^[2] In children, it says the absence of prior symptoms does not preclude risk, because cardiac arrest may be the initial manifestation of pre-excitation.^[2]

What each AP rhythm looks like

^[1]

ESC 2019 adds that the ventricular rate in pre-excited AF tends to be higher than in non-pre-excited AF.^[1]

Latent pre-excitation can be unmasked.^[8] ESC 2020 sports cardiology says minimal or latent pre-excitation can be unmasked on a 12-lead ECG during sinus rhythm by vagal manoeuvres or intravenous adenosine; PR prolongation without a change in QRS morphology, or transient AV block, excludes non-intermittent latent pre-excitation.^[8] ESC 2022 ventricular arrhythmia guideline Table 6 (Intravenous provocative diagnostic tests; selected row) lists adenosine to exclude latent pre-excitation, given as 6, 12, 18 mg boluses up to a maximum dose of 24 mg or until AV block or pre-excitation occurs.^[6] The same row lists asthma, sinus node disease and allergy to adenosine as contraindications, and bronchospasm, bradycardia, asystole, AF and seizure as side effects, with theophylline as antagonist.^[6]

Differential diagnosis: the wide, irregular tachycardia

ESC 2019 says wide QRS tachycardias can be VT, SVT conducting with BBB aberration, or antegrade conduction over an AP, with reported proportions of 80, 15 and 5%, respectively.^[1] Its rule is that the default diagnosis should be VT until proven otherwise.^[1] Pre-excited SVT is SVT with antegrade conduction over an AP, which participates in the circuit (antidromic AVRT) or is a bystander during AF, focal AT or atrial flutter, or AVNRT.^[1]

ESC 2019 Table 6 (Differential diagnosis of narrow and wide QRS tachycardias): the wide QRS rows

^[1]

In its narrative, ESC 2019 says the differential diagnosis of an irregular wide QRS tachycardia is either pre-excited AF or polymorphic VT, or AT with variable block in the context of aberrancy.^[1] ANZCOR Guideline 11.9 says an irregular broad-complex tachycardia is most likely AF with BBB, that AF with ventricular pre-excitation (in WPW syndrome) and polymorphic VT are other possible causes, and that expert help should be sought.^[9]

ESC 2019 also warns that the standard wide-QRS criteria are not helpful for separating VT from SVT in settings such as pre-excited SVT, or when class IC or class IA antiarrhythmic drugs are given.^[1]

Investigations: invasive and non-invasive risk markers

Risk stratification looks for several markers, among them an AP capable of rapid conduction to the ventricles.^[1] ESC 2019 says the clinical and electrophysiological features associated with an increased risk of SCD include younger age, inducibility of AV-reciprocating tachycardia during EPS, multiple APs, and a demonstrated capability of the AP to allow rapid conduction to the ventricles.^[1] Those rapid-conduction variables include the shortest pre-excited RR interval during AF (SPERRI) of ≤250 ms at baseline or a short antegrade effective refractory period (ERP) of the AP (≤250 ms).^[1]

^[1]

ESC 2019 lists an inducible AP-mediated tachycardia, in the baseline state or during isoproterenol infusion (which should always be tried), among the EPS variables that identify a high-risk AP.^[1] ACC/AHA/HRS 2015 says that in the absence of symptoms a clinical priority is identifying APs at increased risk of arrhythmic events.^[2] It lists the most useful findings as an R-R interval <250 ms between 2 pre-excited complexes during induced AF, multiple APs, the ability to induce sustained AVRT, AVRT precipitating pre-excited AF, and an AP refractory period <240 ms.^[2] It says malignant arrhythmias correlate more with the EP properties of the AP than with the presence or absence of symptoms.^[2]

How good are the non-invasive markers?

• ESC 2019: an abrupt and complete normalization of the PR interval with loss of the delta wave during exercise testing, or after procainamide, propafenone or disopyramide, has been considered a marker of low risk.^[1]
• ESC 2019: intermittent loss of pre-excitation on a resting ECG or ambulatory monitoring has been associated with APs with longer ERPs and has been accepted as a credible risk-stratification tool, but studies that included both symptomatic and asymptomatic patients found that more than one-fifth of patients with intermittent pre-excitation have AP ERPs <250 ms, so it is now recognized as an imperfect marker of a low-risk AP.^[1]
• ESC 2019: catecholamine sensitivity is a major limiting factor of all tests, invasive and non-invasive, including exercise testing.^[1]
• ACC/AHA/HRS 2015: non-invasive tests have an approximately 90% positive predictive value and 30% negative predictive value for identifying pathways with life-threatening properties.^[2]
• ACC/AHA/HRS 2015: the ECG should be evaluated closely to make certain the delta wave is truly absent, as APs, especially left lateral pathways, may show varying degrees of pre-excitation because of fusion, which may look like loss of pre-excitation if a subtle delta wave is missed.^[2]
• ACC/AHA/HRS 2015: rapid conduction in AF has been described even in the setting of intermittent anterograde conduction.^[2]
• ESC 2020 sports cardiology: in recreational athletes with asymptomatic pre-excitation, risk assessment may first be pursued via non-invasive testing; it says the sensitivity of non-invasive screening for AP properties that facilitate a fast ventricular response to AF or atrial flutter is good, but its specificity is low.^[8]

Symptomatic patients with a manifest pathway (ACC/AHA/HRS 2015, Section 6.3)

ACC/AHA/HRS 2015 Section 6.3: risk stratification of symptomatic patients with manifest accessory pathways (both rows)

^[2]

Its supportive text adds that if non-invasive evaluation suggests poor anterograde conduction, the EP study still may be useful because of patient symptoms, although the risk of life-threatening events is likely lower.^[2]

Acute management of AVRT

Start with the circuit.^[1] ESC 2019 says that during orthodromic and antidromic AVRT, drug therapy could be directed at the AV node (beta-blockers, diltiazem, verapamil or etripamil) or at the AP (ibutilide, procainamide, propafenone or flecainide).^[1] In antidromic AVRT, drugs acting mainly on the AP should be preferred, and where APs form both the anterograde and retrograde limbs, drugs acting on the AV node are ineffective.^[1] ESC 2019 says adenosine should be used with caution in AVRT because of potential induction of fast AF, which could induce VF, so electrical cardioversion should always be available.^[1]

ESC 2019: Recommendations for the therapy of AVRT due to manifest or concealed accessory pathways (acute therapy rows; chronic therapy rows are given under long-term therapy below)

^[1]

• Table notes (ESC 2019): i.v. verapamil and diltiazem are contraindicated in the presence of hypotension or HFrEF; i.v. beta-blockers are contraindicated in decompensated heart failure.^[1]
• Table notes (ESC 2019): i.v. ibutilide is contraindicated with a prolonged QTc interval; i.v. procainamide prolongs the QTc interval but much less than class III agents; i.v. amiodarone prolongs the QTc but torsades de pointes is rare.^[1]
• Table notes (ESC 2019): i.v. flecainide and propafenone are contraindicated in ischaemic or structural heart disease, and also prolong the QTc interval but much less than class III agents.^[1]

ACC/AHA/HRS 2015 rows for acute orthodromic AVRT

The 2015 US guideline, the newest ACC/AHA SVT guideline found in the October 2026 PubMed census for this topic, gives these rows under Section 6.1.1 (acute treatment), within its section on the management of patients with symptomatic manifest or concealed APs.^[2]

ACC/AHA/HRS 2015 Section 6.1.1 (selected rows: the orthodromic AVRT rows; its three pre-excited AF rows are given as history below)

^[2]

Its supportive text says adenosine may precipitate AF that may then conduct rapidly to the ventricle and even cause VF, so electrical cardioversion should be available.^[2] For the COR IIb row, it says intravenous beta blockers, diltiazem and verapamil carry a risk of enhancing conduction over the AP if the AVRT converts to AF during administration.^[2] It adds that the ability to promptly perform electrical cardioversion must be available should AF with rapid ventricular conduction occur.^[2]

Acute management of pre-excited AF

This is the emergency of the topic.^[1] ESC 2019 says urgent cardioversion is usually required in patients presenting with pre-excited AF, and the threshold for electrical cardioversion is lower.^[1] ESC 2024 AF says immediate electrical cardioversion is needed for haemodynamically compromised patients with pre-excited AF, and AV node-modulating drugs should be avoided.^[4] ESC 2019 also says electrical cardioversion is the acute treatment of choice in irregular pre-excited tachycardias associated with haemodynamic instability.^[1]

ESC 2019: Recommendations for the acute therapy of pre-excited atrial fibrillation (all rows)

^[1]

• Table notes (ESC 2019): i.v. ibutilide is contraindicated in patients with a prolonged QTc interval; i.v. procainamide prolongs the QTc interval but much less than class III agents.^[1]
• Table notes (ESC 2019): i.v. flecainide and propafenone are contraindicated in ischaemic or structural heart disease, and also prolong the QTc interval but much less than class III agents.^[1]

ACC/AHA/ACCP/HRS 2023 AF, Section 10.6: Recommendations for WPW and Preexcitation Syndromes (all rows)

^[5]

Why ibutilide and procainamide?^[5] ACC/AHA 2023 says drugs that increase the refractory period of atrial tissue (ibutilide or procainamide) can slow AP conduction and terminate AF, and that hemodynamically stable patients with preexcited AF, with or without rapid ventricular rates, can be managed pharmacologically with such agents.^[5] ESC 2019 says ibutilide can achieve pharmacological cardioversion of pre-excited AF or delayed AP conduction, and that procainamide, propafenone or flecainide, which affect conduction over the AP, may also be used even if they may not restore sinus rhythm.^[1] It cautions that class Ic drugs should be used with caution because they do exert an effect on the AV node, and, having said that i.v. amiodarone may not be as safe as previously thought, that procainamide appears to be safer in this setting.^[1] ESC 2024 AF says pharmacological cardioversion can be attempted using ibutilide or flecainide, while propafenone should be used with caution due to effects on the AV node (no class or level given).^[4]

^{[5] [1]}

Drugs to avoid in pre-excited AF

The AV node is the brake you must not press.^[1] ESC 2019 says any AV node-modulating agents (adenosine, verapamil, diltiazem, beta-blockers or digoxin) should be avoided in pre-excited AF, as they may contribute to a risk of VF.^[1] ACC/AHA 2023 says AP conduction can accelerate with AV-nodal block, and that drugs blocking AV-nodal conduction can increase the risk of VF.^[5]

Drugs to avoid in pre-excited AF, by source

^{[1] [5] [4] [9]}

Two mechanisms are given for the harm.^[2] ACC/AHA/HRS 2015 says digoxin increases the ventricular rate by shortening the refractoriness of the AP, whereas amiodarone, beta blockers, diltiazem and verapamil may increase it through drug-induced hypotension with increased catecholamines.^[2] It adds that these drugs may enhance AP conduction by slowing or blocking AV-nodal conduction, preventing competitive concealed retrograde conduction into the AP.^[2] On amiodarone, ESC 2019 says that in pre-excited AF, i.v. amiodarone may not be as safe as previously thought, because enhanced pathway conduction and VF have been reported, and it should not be considered.^[1] ACC/AHA 2023 says one small series that reviewed intravenous amiodarone for this indication raised significant concerns, in view of several published reports of VF precipitated by amiodarone.^[5]

Two more warnings, on adenosine and on i.v. verapamil or diltiazem, apply beyond AF.^[1] In wide QRS tachycardia, ESC 2019 says adenosine must be avoided if pre-excitation on the resting ECG suggests a pre-excited tachycardia, because in antidromic re-entry adenosine may precipitate cardiac arrest if it induces AF, as may occasionally occur.^[1] Its table for wide QRS tachycardia without an established diagnosis says that, in haemodynamically stable patients, adenosine should be considered if vagal manoeuvres fail and there is no pre-excitation on a resting ECG (Class IIa, Level C).^[1] In its acute SVT drug text, ESC 2019 says i.v. verapamil or diltiazem should be avoided in haemodynamic instability, HF with reduced LVEF (<40%), suspected VT or pre-excited AF.^[1] In the same paragraph it says beta-blockers are contraindicated in decompensated HF.^[1] For long-term therapy, ACC/AHA/HRS 2015 says oral digoxin is potentially harmful in patients with AVRT or AF and pre-excitation on the resting ECG (COR III: Harm, LOE C-LD), because digoxin shortens the AP refractory period so that AF may induce VF.^[2]

^{[5] [1] [9]}

Catheter ablation

ESC 2019 says the treatment of choice for patients with symptomatic and recurrent AVRT, or pre-excited AF, is catheter ablation.^[1] For other patients with asymptomatic and infrequent episodes, it says decisions should be balanced between the risks and benefits of the invasive nature of ablation and a long-term commitment to drug therapy.^[1]

Ablation rows for symptomatic patients

^{[1] [5] [2]}

Two populations have newer rows of their own.^[5][14] For pre-excited AF, the ACC/AHA 2023 row above is the newer US row; the 2015 row still covers AVRT.^[5][2] Adults with congenital heart disease have ESC 2020 rows of their own.^[14] Among them, adults with Ebstein anomaly also have a newer 2025 ACC/AHA/HRS/ISACHD/SCAI row recommending catheter ablation for high-risk accessory pathway conduction or multiple accessory pathways to reduce the risk for SCD.^[15] These rows and the 2025 US Ebstein rows on electrophysiological study are under special populations below.^[14][15] In mild CHD, catheter ablation is recommended over long-term medical therapy for symptomatic, sustained recurrent SVT (AVNRT, AVRT, AT and IART), or if SVT is potentially related to SCD (Class I, Level C).^[14] In moderate and severe CHD, catheter ablation should be considered for symptomatic, sustained recurrent SVT, or if SVT is potentially related to SCD, provided that the procedure is performed in experienced centres (Class IIa, Level C).^[14]

• ESC 2019: ablation of an AP, when performed by an experienced operator, is associated with a high cure rate (>95%) and a low risk (<0.5%) of major complications.^[1]
• ESC 2019: major complications include cardiac tamponade (0.13–1.1%) and complete AV block (0.17–2.7%) in patients in whom ablation of septal APs is attempted.^[1]
• ACC/AHA/HRS 2015: large series report a success rate of approximately 93% to 95% and a 3% risk of major complications over 6 months to 8 years of follow-up; ACC/AHA 2023 cites a high success rate (93%-95%) with low risk of major short- and long-term complications.^[2][5]
• ESC 2019 notes that the 2015 ACC/AHA/HRS guideline reported major complication rates after radiofrequency ablation of 3.0% for AVNRT and 2.8% for AVRT, much higher than those reported by experienced electrophysiologists in the current era, but that the procedure still carries a very small, non-negligible mortality risk.^[1]
• ACC/AHA 2023: pathway ablation has well-established efficacy and safety for preexcited AF for prevention of VF, and EP study with AP ablation can be offered as first-line therapy.^[5]

Technique points

• Septal pathways: ESC 2019 says that with cryoenergy the incidence of AV block is lower than with radiofrequency energy, but recurrence of previously blocked pathways has been reported to be significantly higher.^[1]
• Septal pathway ECG: ESC 2019 says that with septal APs close to the AV node, the ECG typically shows a positive delta wave in aVF and aVL and a narrow positive delta wave in V1 with a prominently negative QRS complex.^[1]
• Left-sided pathways: ESC 2019 says the two approaches are antegrade transseptal and retrograde aortic, and that the transseptal approach, in experienced hands, results in reduced radiation and procedure times.^[1]
• AF after ablation: ACC/AHA/HRS 2015 says AF in younger patients is usually associated with the AP and unlikely to recur after ablation, whereas older patients may have recurrent AF from causes unrelated to the AP; ACC/AHA 2023 says pathway ablation is definitive therapy for AF and SVT in young persons without comorbid conditions whose AF is associated with an AP.^[2][5]

Long-term drug therapy when ablation is not chosen

Choose the target by whether the resting ECG is pre-excited.^[1][2] ACC/AHA 2023 says that for those who cannot undergo ablation, preventive pharmacological therapy is directed to slowing pathway conduction.^[5] ESC 2019 says that if ablation is not desirable or feasible in pre-excitation with symptomatic antidromic AVRT, and structural or ischaemic heart disease has been excluded, class IC drugs act mainly on the AP and can be used.^[1] In pre-excited AF, it warns that caution should be taken not to transform the AF into atrial flutter and induce 1:1 conduction.^[1]

ESC 2019 AVRT therapy table: chronic therapy rows (all four)

^[1]

ACC/AHA/HRS 2015 Section 6.1.2: ongoing management rows (all eight)

^{[2] [5]}

For pre-excited AF, three rows of this table have newer ACC/AHA rows.^[5][2] ACC/AHA 2023 Section 10.6 gives the newer US rows for pre-excited AF: catheter ablation of APs is recommended (COR 1, LOE B-NR), and AV-nodal blocking agents, amiodarone and digoxin among them, are contraindicated (COR 3: Harm, LOE B-NR).^[5] The 2023 COR 3: Harm row names amiodarone and digoxin without a route limit, and the 2023 ablation row covers preexcited AF.^[5] For AVRT, the 2015 rows remain the newest ACC/AHA rows naming AVRT or accessory pathways among the guidelines checked for this topic, except where the 2025 Ebstein anomaly rows on electrophysiological study and ablation apply.^[2][15] Those 2025 ACC/AHA/HRS/ISACHD/SCAI rows are newer than the 2015 rows on the same questions and are set out under special populations below.^[15] Section 10.6 has no row recommending a long-term antiarrhythmic drug in pre-excited AF; its COR 3: Harm row names amiodarone among the AV-nodal blocking agents it contraindicates.^[5]

For the COR IIb row on AV-nodal drugs with pre-excitation, ACC/AHA/HRS 2015 says patients may develop AF during AVRT and be exposed to rapid AP conduction while on beta blockers, diltiazem or verapamil, so these agents must be used with caution.^[2]

The asymptomatic patient with pre-excitation

Most will never have an event related to their pre-excitation.^[1] ESC 2019 says most patients with an asymptomatic WPW pattern will go through life without any clinical events related to their pre-excitation, and approximately one in five will develop an arrhythmia related to their AP during follow-up.^[1] The feared event is SCD from pre-excited AF that conducts rapidly over the AP and degenerates into VF.^[1]

ESC 2019: Recommendations for the management of patients with asymptomatic pre-excitation (all rows)

^[1]

ESC 2019 text treats two groups differently.^[1] ESC 2019 says invasive screening with an EPS should be performed in people with asymptomatic pre-excitation who have high-risk occupations or are competitive athletes.^[1] For everyone else, it says the screening options include an EPS as a risk-stratifying tool, or non-invasive screening with exercise testing, drug testing and ambulatory monitoring.^[1] If an EPS finds an AP with high-risk characteristics, ESC 2019 says catheter ablation should be performed.^[1]

When the EPS shows no high-risk features, ESC 2019 says the approach depends on the experience and expertise of the electrophysiologist and on the preferences and values of the patient.^[1] It says ablation of an asymptomatic low-risk AP also appears reasonable in appropriately experienced centres according to informed patient choice.^[1] Ablation of APs in the anteroseptal or mid-septal region carries a small risk of AV block, and that risk may preclude ablation of such an AP in an asymptomatic patient.^[1] ESC 2019 says it seems reasonable to recommend an EPS and consider ablation if a link between pre-excitation and LV dysfunction can be made, citing evidence of LV dysfunction related to electrical asynchrony in patients, especially children, with asymptomatic pre-excitation.^[1]

^[1]

ACC/AHA/HRS 2015 rows on asymptomatic pre-excitation

These rows rest on a commissioned evidence review; ACC/AHA/HRS 2015 marks them SR to emphasize the rigor of support from that systematic review.^[2]

ACC/AHA/HRS 2015 Section 6.2.2: Asymptomatic Patients With Pre-Excitation (all rows)

^[2]

Its supportive text says most observational cohorts suggest the great majority of adults with asymptomatic pre-excitation who do not undergo ablation have a benign course, with the small SCD risk seen mainly in children.^[2] It says the choice to observe should be preceded by informing the patient of the small risk of life-threatening arrhythmias without treatment, and of the success rate and complications of ablation.^[2] It also says the risks and benefits of ablating pathways found not to have high-risk characteristics should be discussed thoroughly before the EP procedure.^[2] For adults with Ebstein anomaly, the EP-study, ablation-if-high-risk and observation rows in this table are partly superseded by population.^[2][15] The 2025 ACC/AHA/HRS/ISACHD/SCAI ACHD guideline recommends an electrophysiological study in adults with Ebstein anomaly and asymptomatic ventricular preexcitation, to assess for substrates for ablation, including multiple or high-risk accessory pathways (COR 1, LOE B-NR).^[15] It also recommends catheter ablation in adults with Ebstein anomaly and high-risk accessory pathway conduction or multiple accessory pathways, to reduce the risk for SCD (COR 1, LOE B-NR).^[15] These 2015 rows call an EP study to risk-stratify for arrhythmic events, or observation without further evaluation or treatment, reasonable in asymptomatic pre-excitation (COR IIa, LOE B-NR).^[2] They also call catheter ablation of the AP reasonable in asymptomatic pre-excitation if an EP study identifies a high risk of arrhythmic events (COR IIa, LOE B-NR).^[2]

The evidence behind the rows

^[10]

The randomised evidence is reported with different numbers.^[1][2][10] ESC 2019 describes one prospective RCT of catheter ablation (37 patients) versus clinical follow-up without treatment (35 patients), with arrhythmic events in 7 vs. 77% over 5 years.^[1] ACC/AHA/HRS 2015 says 1 RCT of ablation in high-risk patients enrolled 76 patients, with arrhythmic events (symptomatic SVT, AF and VF in that study) in 7% with ablation versus 77% without.^[2] Its systematic review describes a dual-design study: an RCT of ablation versus no ablation in 76 patients plus an uncontrolled prospective cohort of 148 more.^[13] The Pappone 2003 abstract reports 37 and 35 patients randomly assigned, among 224 eligible asymptomatic patients.^[10]

^{[11] [12]}

ESC 2019 cites that study right after warning that even invasive studies do not confer absolute certainty about risk assessment.^[1] The 2015 ACC/AHA/HRS evidence review (9 studies) concluded that EPS risk stratification of asymptomatic pre-excitation may be beneficial, with consideration of AP ablation in those deemed at high risk, and that well-designed studies are needed.^[13]

Atypical pathways and PJRT

ESC 2019 says atypical APs (Mahaim fibres) are connections between the right atrium or the AV node and the right ventricle, into or close to the right bundle branch.^[1] They usually contain accessory nodal tissue, which results in decremental properties, and cross the lateral aspect of the tricuspid annulus, although posteroseptal locations can be found in rare cases.^[1] ESC 2019 says catheter ablation is therefore recommended for all patients with recurrent symptomatic tachycardia from these pathways (narrative; no class or level given).^[1] Preventive ablation for prognostic reasons is not routinely recommended, even with pre-excitation or BBB on the surface ECG, because fast AP conduction is unlikely given the decremental properties.^[1] The 2009 AHA/ACCF/HRS ECG statement says the term Mahaim-type preexcitation is not recommended, because the diagnosis cannot be made with certainty on the basis of the surface ECG.^[17]

ESC 2019 says permanent junctional reciprocating tachycardia (PJRT) is a rare form of AV reciprocating tachycardia using a concealed AP.^[1] Concealed APs, it says, are predominantly localized along the left free wall (64%), and less frequently at septal (31%) and right free wall locations.^[1]

Special populations

Pregnancy

ESC 2025 pregnancy says that in pregnant women with AVRT and WPW syndrome, arrhythmia episodes can be prevented with oral flecainide, or propafenone when flecainide is not available.^[7] It warns that when AV-nodal blocking agents are used in WPW syndrome and AF occurs, the risk of rapid ventricular rates is increased.^[7] In pregnant women without documented AF, with known orthodromic AVRT and with intermittent pre-excitation, it says long-term AV blockade is acceptable for prevention.^[7] If catheter ablation is necessary, it should be performed by experienced operators in a centre equipped with non-fluoroscopic mapping techniques.^[7]

ESC 2025 pregnancy, Recommendation Table 14 (Recommendations for supraventricular tachycardia and pregnancy): selected rows

^[7]

ESC 2024 AF Recommendation Table 28 adds that immediate electrical cardioversion is recommended in patients with AF during pregnancy and haemodynamic instability or pre-excited AF, to improve maternal and foetal outcomes (Class I, Level C).^[4] ESC 2025 pregnancy, the newer of the two, has no row in Recommendation Table 14 that names pre-excited AF; its text says that in all cases with haemodynamic instability caused by any SVT including AF and AFL, synchronized DC cardioversion is indicated.^[7]

Adult congenital heart disease and Ebstein anomaly

Pre-excitation also matters in Ebstein anomaly.^[1][14] ESC 2019 says multiple APs occur in up to 12% of patients with pre-excitation, and in up to 50% of patients with Ebstein’s anomaly.^[1] ESC 2020 adult congenital heart disease (ACHD) lists pre-excitation and multiple pathways (AVRT) among the ECG findings in Ebstein anomaly.^[14] It says symptomatic rhythm disorders can be treated conservatively or, preferably, with EP intervention.^[14] Tricuspid valve surgery may hinder transcatheter access to right-sided APs and to the slow pathway in AV node re-entry, so it may be reasonable to assess for arrhythmia substrates and proceed with catheter ablation, if identified, before surgery.^[14] Its Table 4 (classification of congenital heart disease complexity) places Ebstein anomaly in the moderate group.^[14]

ESC 2020 ACHD: rows on SVT ablation and on arrhythmias in Ebstein anomaly

^[14]

Both the moderate-CHD row and the Ebstein row apply to an adult with Ebstein anomaly and symptomatic, sustained recurrent AVRT.^[14] The Ebstein row also covers pre-excitation on the ECG without symptoms.^[14] These ESC 2020 rows are newer than the ESC 2019 SVT rows and apply to adults with congenital heart disease.^[14]

The 2025 ACC/AHA/HRS/ISACHD/SCAI adult congenital heart disease guideline gives the US rows for the same patient.^[15]

ACC/AHA/HRS/ISACHD/SCAI 2025 ACHD, Recommendations for Ebstein Anomaly: the rows on electrophysiological study and catheter ablation (3 of its 10 rows)

^[15]

Its Table 1 (What Is New) marks the electrophysiological study row as revised.^[15] The 2018 recommendation it replaced was COR 2a: an electrophysiological study with or without catheter ablation can be useful in the diagnostic evaluation of adults with Ebstein anomaly and ventricular preexcitation but without SVT.^[15] Its supportive text says approximately one-third of adults with Ebstein anomaly and ventricular preexcitation have multiple accessory pathways, associated with a high risk for SCD.^[15] It adds that concealed APs are common in Ebstein anomaly and may coexist with manifest APs.^[15] Pre-excitation may also be present but difficult to appreciate on the surface ECG.^[15] Adults with Ebstein anomaly and ventricular preexcitation often have multiple APs, associated with a higher risk for SCD, and generally can undergo ablation successfully.^[15] Surgical interruption of APs is largely reserved for patients in whom multiple attempts at catheter ablation have not succeeded.^[15]

Both bodies therefore recommend electrophysiological testing in Ebstein anomaly with pre-excitation on the ECG, with or without symptoms.^[14][15] For Ebstein anomaly with symptomatic arrhythmias or pre-excitation on the ECG, ESC 2020 recommends electrophysiologic testing followed by ablation therapy, if feasible, or surgical treatment of the arrhythmias in the case of planned heart surgery (Class I, Level C).^[14] For adults with Ebstein anomaly and symptomatic arrhythmia or asymptomatic ventricular preexcitation, ACC/AHA/HRS/ISACHD/SCAI 2025 recommends an electrophysiological study to assess for substrates for ablation, including multiple or high-risk accessory pathways (COR 1, LOE B-NR).^[15] ESC 2020 says in its text that it may be reasonable to assess for arrhythmia substrates and proceed with catheter ablation, if identified, before tricuspid valve surgery.^[14] The 2025 US guideline gives this a row: in adults with Ebstein anomaly, electrophysiological study (and catheter ablation, if needed) can be useful before tricuspid valve surgery to improve clinical outcomes (COR 2a, LOE B-NR).^[15]

For competitive athletes with Ebstein anomaly, Table 8 of the 2025 AHA/ACC competitive sports statement lists ambulatory cardiac rhythm monitoring as the added evaluation.^[16] A footnote on the additional-evaluations column and on the Ebstein row’s participation cell covers all competitive athletes with diagnosed congenital heart abnormalities.^[16] It says they should have a 12-lead ECG, echocardiography, oxygen saturation, BP, symptom assessment and the listed testing assessed within 1 year of initial competitive sports participation, depending on the lesion (no class or level given).^[16] The same footnote says patients with moderate or greater complexity, or with inconsistent diagnostic findings, should undergo a specific congenital heart disease or ACHD cardiology evaluation before starting competitive sports participation (no class or level given).^[16] Table 8 gives no WPW or residual WPW, with normal RV and LV function, as reassuring findings, and RV dysfunction or complex arrhythmias at rest or stress as concerning ones.^[16] A Table 8 footnote on complex arrhythmias says tachyarrhythmias and bradyarrhythmias in congenital heart disease may portend increased risk and may require additional monitoring and treatment (no class or level given).^[16] A Table 8 footnote on RV dysfunction refers to the most recent available guidelines or recommendation statements for imaging definitions of the severity of valve or ventricular dysfunction.^[16] It says these definitions also must be contextualized with the effects of exercise-induced cardiac remodelling on ventricular function in athletes (no class or level given).^[16] Without concerning findings, the statement says it is reasonable to consider competitive sports participation after shared decision-making with the athlete and family (no class or level given).^[16] A Table 8 footnote on the concerning-findings and participation columns says these considerations assume no concerning clinical findings, including no concerning symptoms with exercise.^[16] If concerning clinical findings are present, it says further clinical assessment is necessary before considering competitive sports participation in a shared decision-making process (no class or level given).^[16] It adds that certain findings may suggest a different diagnosis or risk classification or merit consideration for intervention before participation in competitive sports.^[16] A footnote on the Ebstein row’s participation cell says that if haemodynamically significant residual or postintervention lesions are found, the reader is referred to the appropriate sections.^[16]

Children

• ACC/AHA/HRS 2015 is aimed at adults (18 years or older) and gives no specific paediatric recommendations; ESC 2019 says detailed paediatric recommendations are beyond its scope.^[2][1]
• ACC/AHA/HRS 2015: the risk of VF or SCD related to WPW in childhood is 1.3% to 1.6% and is highest in the first 2 decades of life; cardiac arrest risk is higher with AVRT precipitating AF, short AP refractory periods and posteroseptal APs.^[2]
• ACC/AHA/HRS 2015: risk stratification, such as with ambulatory 24-hour monitoring or treadmill exercise testing, is often considered for children with pre-excitation to assess persistence of pre-excitation.^[2]
• ACC/AHA/HRS 2015: digoxin is avoided in the presence of pre-excitation because its use in infancy has been associated with SCD or VF.^[2]
• ESC 2019: AVRT due to WPW that begins in infancy may resolve in about 90% of patients but may recur in later childhood in 30–50%; if tachycardia is present after the age of 5, it persists in more than 75%.^[1]
• ESC 2019: avoidance of radiofrequency ablation, if at all possible, in the first 2 years of life is prudent.^[1]
• ESC 2022 ventricular arrhythmias: SVT due to WPW in children can usually be managed pharmacologically, APs often lose antegrade conduction in the first years of life, and in children with asymptomatic APs risk stratification is not recommended before the age of 8 years (text; no class or level given).^[6]
• ESC 2020 sports cardiology: in children younger than 12 years, the risk of AF-induced VF and sudden death is very low, and a conservative approach is generally recommended in this age group.^[8]

Athletes and high-risk occupations

ESC 2020 sports cardiology says that because AF is more common in athletes, pre-excitation is a prognostic concern in athletes.^[8] Evaluation should exclude associated structural disease such as HCM or Ebstein anomaly.^[8] Its recommendation table on paroxysmal SVT and pre-excitation, and its Table 15 of high-risk EPS findings, are images in the held text and are not quoted here.^[8] Its text says ablation of the AP is recommended in competitive and recreational athletes with pre-excitation and documented arrhythmias.^[8] In competitive athletes with asymptomatic pre-excitation, an EP study is warranted to evaluate the risk of sudden death, and in the event of a high-risk finding, ablation of the AP is recommended.^[8] In recreational athletes with asymptomatic pre-excitation, risk assessment may first be pursued via non-invasive testing.^[8]

• ESC 2020 sports: intermittent pre-excitation usually indicates low-risk pathway properties, but some APs may be potentiated by adrenergic stimuli, so exercise testing excluding pre-excitation at peak exercise is recommended before clearance for sports.^[8]
• ESC 2020 sports: with a long refractory period and hence low risk of sudden death, sport may continue without ablation, on the understanding that it stops if palpitations recur.^[8]
• ESC 2020 sports: for athletes who refuse ablation, or when the procedure carries high risk (such as an anteroseptal AP), competitive sport can be discussed case by case, including drug therapy, although there are currently no data about its efficacy; sports in which loss of consciousness could be fatal should be discouraged.^[8]
• ESC 2020 sports: leisure-time and low- to medium-intensity exercise can generally resume 1 week after ablation if there is no particular risk of recurrence; competitive sport is possible after 1–3 months, with ECG follow-up at 6 months and 1 year.^[8]
• Occupations: ESC 2019 gives pilots and professional drivers as examples of high-risk occupations in its Class I, Level B row on EPS for asymptomatic pre-excitation; ACC/AHA/HRS 2015 says ablation of the AP is reasonable in asymptomatic patients if pre-excitation precludes specific employment, such as with pilots (COR IIa, LOE B-NR).^[1][2]

The 2025 AHA/ACC scientific statement on competitive sports participation is newer than ESC 2020 and gives clinical considerations (no class or level given).^[16] Its Table 1 says "should" means that clinicians should proceed with practices that are accepted standards of medical care.^[16] Its Table 11 gives clinical considerations for competitive athletes with arrhythmias, implantable cardioverter defibrillators or pacemakers, syncope, and asymptomatic abnormal ECG interpretation.^[16] Table 11 says competitive athletes with a WPW pattern on ECG should undergo a cardiac evaluation including physical examination, personal and family history, and echocardiogram.^[16] Competitive athletes with WPW syndrome, which includes symptoms suggestive of arrhythmias or documented arrhythmias, should be evaluated by an electrophysiologist to discuss treatment options to reduce the risk of life-threatening events.^[16]

The statement says asymptomatic competitive athletes with a WPW pattern should be seen by sports cardiology and electrophysiology to discuss non-invasive (exercise stress testing) or invasive risk stratification (EP study with or without catheter ablation).^[16] That discussion uses shared decision-making, which includes the athlete’s age and the risks, benefits and limitations of each modality.^[16] Competitive athletes with an asymptomatic WPW pattern should not be restricted from competitive sports participation during the clinical evaluation process.^[16] After WPW ablation, competitive sports participation can resume after vascular access site healing, taking into consideration the risk assessment of the pathway and the success of the procedure.^[16] ESC 2020 instead says competitive sport is possible 1–3 months after ablation.^[8]

The statement’s text says increasing data, particularly in young individuals, show that non-invasive exercise testing lacks sensitivity and may not exclude the risk of rapidly conducted AF or sudden cardiac arrest.^[16] It says an EP study to identify high-risk pathways, and ablation of those pathways, may be beneficial.^[16] It adds that invasive versus non-invasive risk stratification for an asymptomatic WPW pattern remains controversial among competitive athletes and requires shared decision-making, particularly given the difference in SCD risk with age.^[16] The two documents part company on the asymptomatic competitive athlete: ESC 2020 says an EP study is warranted, while the AHA/ACC statement leaves the choice between non-invasive and invasive risk stratification to shared decision-making.^[8][16]

Prognosis

Sudden death risk with pre-excitation: the numbers each source gives

^{[1] [6] [2] [8]}

ACC/AHA/HRS 2015 links increased SCD risk to a history of symptomatic tachycardia, multiple APs and a shortest pre-excited R-R interval of <250 ms during AF.^[2] Its evidence review found that, in observational cohorts of asymptomatic patients not ablated (883 patients, followed 8 to 96 months), malignant AF (shortest RR ≤250 ms) developed in 0% to 9% and VF in 0% to 2%, most of the latter in children.^[13]

Complications and pitfalls

Evidence, guidelines and regional differences

• EPS for all asymptomatic patients. ESC 2019 says an EPS to risk stratify individuals with asymptomatic pre-excitation should be considered (Class IIa, Level B); ACC/AHA/HRS 2015 says an EP study is reasonable in asymptomatic patients with pre-excitation to risk-stratify for arrhythmic events (COR IIa, LOE B-NR).^[1][2]
• Watchful waiting. ACC/AHA/HRS 2015 says observation without further evaluation or treatment is reasonable in asymptomatic pre-excitation (COR IIa, LOE B-NR); ESC 2019 says clinical follow-up should be considered once invasive risk stratification shows a low-risk AP (Class IIa, Level C).^[2][1]
• Stable pre-excited AF. ESC 2019 gives i.v. ibutilide or procainamide Class IIa, Level B and i.v. flecainide or propafenone Class IIb, Level B; ACC/AHA 2023 recommends i.v. ibutilide or i.v. procainamide as an alternative to elective cardioversion (COR 1, LOE C-LD) and its Section 10.6 has no flecainide or propafenone row; ESC 2024 AF text says pharmacological cardioversion can be attempted using ibutilide or flecainide, and that propafenone should be used with caution.^[1][5][4]
• History. Before ACC/AHA 2023, ACC/AHA/HRS 2015 gave the US rows for acute treatment of pre-excited AF: synchronized cardioversion in haemodynamically unstable patients (COR I, LOE B-NR), ibutilide or i.v. procainamide in haemodynamically stable patients (COR I, LOE C-LD), and intravenous digoxin, intravenous amiodarone, intravenous or oral beta blockers, diltiazem and verapamil potentially harmful for acute treatment (COR III: Harm, LOE C-LD).^[2]
• Evidence gaps. ESC 2019 says both invasive and non-invasive risk tests have limitations, being dependent on autonomic tone, that more accurate risk-stratification models are needed, and that the proper management of asymptomatic pre-excitation and strict ablation indications have not been established.^[1]

ANZ practice: ANZCOR Guideline 11.9 says that if pre-excited AF (or atrial flutter) is suspected, adenosine, digoxin, verapamil and diltiazem should be avoided, and that electrical cardioversion is usually the safest treatment option.^[9] Its rate-control list, which it references to the 2006 ACC/AHA/ESC AF guideline, says intravenous digoxin or nondihydropyridine calcium channel antagonists in AF with a preexcitation syndrome may paradoxically accelerate the ventricular response and are not recommended (Level of Evidence IV).^[9] The same list, under a Class C heading, says amiodarone may be considered for hemodynamically stable patients with AF involving conduction over an AP (Level of Evidence III-2).^[9] By contrast, ESC 2019 says i.v. amiodarone is not recommended in haemodynamically stable patients with pre-excited AF (Class III, Level B), and ACC/AHA 2023 lists amiodarone among the AV-nodal blocking agents it calls contraindicated in preexcited AF (COR 3: Harm, LOE B-NR).^[1][5] No NHFA/CSANZ guideline on SVT or pre-excitation was found among the guidelines checked for this topic. The NHFA/CSANZ Australian Clinical Guidelines for the Diagnosis and Management of Atrial Fibrillation 2018 (PMID 30077228) are not held as text in their version of record, so they were not checked for this topic.

ESC 2022 says the management of WPW patients was reviewed in the 2019 ESC SVT guideline and updated with a particular focus on athletes in 2020.^[6] Guidelines used for this topic: 2019 ESC SVT; 2015 ACC/AHA/HRS SVT (JACC text with its 2016 correction); 2024 ESC AF; and 2023 ACC/AHA/ACCP/HRS AF. Also used: 2022 ESC ventricular arrhythmias; 2025 ESC cardiovascular disease and pregnancy; 2020 ESC sports cardiology; the 2009 AHA/ACCF/HRS ECG standardization statement (part III); and ANZCOR Guideline 11.9. Also used for adults with congenital heart disease and for athletes: the 2020 ESC and 2025 ACC/AHA/HRS/ISACHD/SCAI adult congenital heart disease guidelines, and the 2025 AHA/ACC scientific statement on competitive sports participation. No ESC SVT guideline newer than 2019 was found in the PubMed census for this topic, run in October 2026. No ACC/AHA SVT guideline newer than 2015 was found in that PubMed census for this topic. For each guideline row used that carries a class or COR, the guidelines in the evidence pack’s currency-sweep list published in the same month or later were swept. The sweep searched them for recommendations on pre-excitation, WPW, accessory pathways, AVRT or pre-excited AF. That list holds the guidelines and the sports statement used here, apart from the 2009 ECG statement. It also holds the held guidelines the pack lists as checked and not used. These include the 2017 AHA/ACC/HRS ventricular arrhythmia guideline and Part 10 of the 2025 AHA resuscitation guidelines, both checked and not used. The Part 11: Post-Cardiac Arrest Care: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (PMID 41122894) are not held as text in their version of record, so they were not checked for this topic; only their PubMed abstract is quotable. Held only as PubMed abstracts for this topic, and not used: the HRS athlete (2024) and pregnancy (2023) statements and the 2025 EHRA provocation-testing statement. Also held only as PubMed abstracts, and not used: the 2021 EAPC and EHRA recommendations on sport with supraventricular arrhythmias, and the 2026 HRS/PACES statement on antiarrhythmic drugs in understudied clinical scenarios. Not held as text for this topic, and not used: the 2012 PACES/HRS young-WPW statement (its PubMed record has no abstract) and the 2016 PACES/HRS paediatric ablation statement. Also not held as text, and not used: the 2014 PACES/HRS statement on arrhythmias in adult congenital heart disease and the 2026 ACC/AHA tactical athlete statement. Also not held as text, and not used: the 2020 EAPC/ESC/AEPC statement on sport in congenital heart disease and the 2026 HRS/ISACHD/PACES statement on ACHD electrophysiology programs. Found in the census but not held, and not used: the 2026 EAPC/ACNAP/AEPC statement on sport in children with cardiovascular disease. Also found in the census but not held, and not used: the 2026 EAPC/ACC statement on masters athletes. Found in the census, not held as text, so not checked: the 2026 EAPC consensus statement on abnormal electrocardiogram findings in athletes. Also found in the census, not held as text, so not checked: the 2026 EAPC/AEPC clinical consensus document on cardiac evaluation of paediatric athletes. Also found in the census, not held as text, so not checked: the 2026 ACC report opposing legislative mandates for ECG screening in competitive athletes. Also checked and not used: the 2024 EHRA/HRS/APHRS/LAHRS expert consensus statement on catheter and surgical ablation of AF. Its AVRT text concerns SVTs that may trigger AF. It names no pre-excitation, WPW or accessory pathway outside its reference list.

Exam pearls

^[1]

References17ShowHide

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16. [16]Kim JH, et al. Clinical Considerations for Competitive Sports Participation for Athletes With Cardiovascular Abnormalities: A Scientific Statement From the American Heart Association and American College of Cardiology. J Am Coll Cardiol, 2025.PMID 39976316
17. [17]Surawicz B, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part III: intraventricular conduction disturbances: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol, 2009.PMID 19281930