Wolff-Parkinson-White syndrome

• Ventricular pre-excitation means that part of the ventricle is activated early through an extra strand of muscle (an accessory pathway) that bypasses the atrioventricular (AV) node. On the electrocardiogram (ECG): a short PR interval, a slurred start to the QRS (the delta wave) and a wide QRS.
• The ECG pattern alone is called the WPW pattern. Wolff-Parkinson-White syndrome is the pattern plus symptomatic tachyarrhythmias.^[3]
• Most people with the pattern never have an arrhythmia. The danger is atrial fibrillation (AF) conducted down the pathway at a very high rate, which can degenerate into ventricular fibrillation (VF). Sudden death can be the first event, especially in the young.^[3][4]
• During pre-excited AF, drugs that block the AV node (adenosine, verapamil, diltiazem, beta-blockers, digoxin, amiodarone) are contraindicated: they can speed conduction down the pathway. Unstable patients get synchronised cardioversion.^[1][2]
• Catheter ablation of the pathway is a cure, with a high success rate and a low complication rate. It is first-line for symptomatic patients and is advised for high-risk asymptomatic patients, including most competitive athletes.^[1][3][4]

By the end of this page you should be able to:

1. Distinguish the WPW pattern from WPW syndrome and say what an accessory pathway is, where it lies and how it is inherited or associated with other disease.
2. Recognise pre-excitation on a 12-lead ECG and explain each feature from the way the ventricle is activated.
3. Compare orthodromic and antidromic atrioventricular re-entrant tachycardia (AVRT) and pre-excited AF, and explain why the last can kill.
4. Choose the acute treatment for each rhythm and say which drugs must be avoided and why.
5. Explain how sudden-death risk is assessed in symptomatic and asymptomatic patients, including the shortest pre-excited RR interval.
6. Counsel on ablation, sport, work, pregnancy and childhood pre-excitation.

Not every pathway shows on the ECG. A pathway that conducts only backwards (ventricle to atrium) is concealed; it gives no delta wave and cannot cause pre-excited AF, but it can still support a re-entry tachycardia. A manifest pathway conducts forwards (and usually both ways) and shows on the resting ECG. A latent pathway conducts forwards but is hidden at rest because normal conduction through the AV node reaches the ventricle first; it can be unmasked by slowing the AV node, by atrial premature beats or by AF.^[4]

Pre-excitation is a spectrum, and the pathway's directions and speed decide the danger (see the section on risk).

• The WPW pattern is found in about 0.15 to 0.25% of the population, and roughly a third of those people develop an arrhythmia over 10 years of follow-up.^[3] A review of athletes puts accessory pathways at about 1 in 300 young people.^[4]
• In most regions only AV nodal re-entry causes paroxysmal supraventricular tachycardia more often than WPW does.^[3]
• Men are affected more often than women, with a reported ratio of about 2 to 1 in adults; the difference is not seen in children.^[16][3]
• Symptoms usually begin in adolescence or early adult life. A long-term study found a mean age of symptom onset of 28 years, and paediatric studies a mean age of 14 years for life-threatening events.^[3]
• Many people are symptom-free, though that can change; the proportion falls from about 90% of children to about 40% of people over 30.^[3]

An accessory pathway is a band of working myocardium that crosses the AV groove and links atrium to ventricle. It is thought to be an embryological remnant: the fibrous ring that separates atria from ventricles did not form completely. The classical name is the bundle of Kent.^[3][16] Most pathways are fast and do not slow down with rapid stimulation, unlike the AV node, because they behave like ordinary atrial or ventricular muscle.^[3]

Pathways can lie anywhere around the AV rings. Left lateral locations are the most common; septal and right-sided pathways are slightly less common.^[4] About a quarter of pathways in one large series were septal, and these matter because ablating near the conduction system risks AV block.^[4] Multiple pathways occur in fewer than 12% of patients overall and in about 50% of those with Ebstein anomaly; they raise the risk of tachycardia, of antidromic re-entry and of very fast conduction during AF.^[3]

About half of pathways conduct in one direction only, most often from ventricle to atrium. Few conduct only forwards.^[4][3]

A small group of pathways have slow, decremental conduction like the AV node itself. They are collectively called Mahaim fibres. The term is conventionally used for decrementally conducting connections between the right atrium or AV node and the right ventricle, near the right bundle branch (atriofascicular pathways). Others connect the AV node to the ventricle (nodoventricular or nodofascicular), and some are fasciculoventricular.^[8][4][10]

Features that distinguish them:

• At rest the ECG is usually normal or shows only subtle clues, such as an rS pattern in lead III or no septal Q waves in leads I and V6, because conduction over the pathway is slow and only the right ventricle is activated early.^[8][9]
• They usually conduct only forwards, so the typical tachycardia is antidromic AVRT with a left bundle branch block shape: the impulse goes down the Mahaim fibre and back up through the AV node.^[8][10]
• During atrial pacing the AH interval lengthens while the QRS widens until a steady value is reached, which shows the decremental behaviour that classical fast pathways lack.^[10][3]
• Mahaim fibres are often found with Ebstein anomaly, reported in 10 to 40% of cases in one review.^[10]

Because they respond differently from fast pathways, they are treated by an electrophysiologist.^[10]

Lown-Ganong-Levine (LGL) syndrome was described as a short PR interval (under 120 ms) without a delta wave plus paroxysmal tachycardia, attributed to a bypass of the AV node. It has no consistent anatomical or electrophysiological correlate, and modern electrophysiology has largely abandoned the label in favour of descriptions: enhanced AV nodal conduction, or an "LGL-phenocopy" pattern.^[11] The finding is often benign, but a short PR interval can still sit alongside dual AV nodal physiology and re-entrant tachycardia; a short PR with palpitations or a family history of sudden death deserves a proper assessment.^[11][12] A short PR in a fit young person without symptoms is often just fast AV nodal conduction.^[4]

• Most people have a structurally normal heart and no family history. About 3.4% of people with WPW syndrome have a first-degree relative with pre-excitation; seen from the other side, pre-excitation is found in about 0.55% of first-degree relatives of people with a pathway, more than twice the rate in the general population.^[3]
• PRKAG2 syndrome is a rare autosomal dominant glycogen storage disease of the heart. Variants in the PRKAG2 gene (the gamma-2 subunit of AMP-activated protein kinase) cause ventricular wall thickening with glycogen deposits, pre-excitation and conduction system disease, and fatal arrhythmias are frequent.^[3][13] Think of it when pre-excitation comes with unexplained hypertrophy or a family history.
• Ebstein anomaly: about 10% of patients with Ebstein anomaly have WPW, and multiple right-sided pathways are common.^[3]
• Other congenital lesions (atrial and ventricular septal defects, corrected transposition), hypertrophic cardiomyopathy and storage diseases such as Danon, Fabry and Pompe disease are also linked.^[3]
• The genetic basis of sporadic pathways is not understood; many genes may contribute to AF risk in WPW.^[3]

In a normal heart the AV node delays the impulse for a moment so that the ventricle can fill, and then the His-Purkinje system activates both ventricles quickly and together. With a manifest pathway there are two routes to the ventricle:

1. The accessory pathway, which conducts at once and starts activating the ventricular muscle early and slowly (muscle to muscle, not along Purkinje fibres).
2. The normal route, which arrives later and activates the rest of the ventricle.

The QRS is therefore a fusion of the two. How much of the ventricle is pre-excited depends on the race between the two routes. A left lateral pathway is far from the sinus node, so the AV node often wins and the pre-excitation is subtle or hidden; the ECG can look normal even when the pathway conducts fast.^[4] During exercise the AV node speeds up and the delta wave can shrink or vanish, which is a trap rather than a reassurance (see risk stratification).^[4]

The pathway's anterograde effective refractory period is the shortest interval at which it can conduct again. If it is short, then during AF (atrial cycle length typically 150 to 250 ms) many impulses pass to the ventricle at an interval that can trigger ventricular fibrillation.^[4] A pathway that conducts only backwards cannot accelerate an atrial rhythm and is less dangerous.^[4]

The same two routes create a re-entry circuit: the impulse goes down one route and up the other. The direction decides the ECG (see the arrhythmia section).^[1]

The three hallmarks in sinus rhythm:

• Short PR interval, under 120 ms.^[4]
• Delta wave: a slurred, slowly rising start to the QRS.
• Broad QRS: sources use cut-offs between 100 and 120 ms.^[3][4][20]

Why each one appears: the PR is short because part of the ventricle is activated before the AV node's delay has elapsed; the delta wave is the early slow muscle-to-muscle spread; the QRS is broad because the ventricle is activated partly by the slow route.

Secondary repolarisation changes follow because the order of ventricular activation is abnormal; the ST-T segments can be discordant to the early QRS forces (Q wave-T wave vector discordance).^[20]

Pseudo-infarct Q waves. If the early activation heads away from a lead, the delta wave is negative and looks like a pathological Q wave. It can occur in the inferior leads with a pathway that pre-excites the inferior wall, and can mimic old inferior infarction. One report describes a true inferior infarct hidden by this pattern until the pathway was ablated.^[20] Think of pre-excitation before diagnosing an old infarct in a young person with a short PR.

Pathway localisation. The polarity of the delta wave and the QRS in different leads allows an estimate of the pathway site. Several algorithms exist; the Arruda algorithm has a reported sensitivity of 90% and specificity of 99%, though accuracy falls with multiple pathways or structural disease and in children.^[3]

Other practical points.

• The pattern can be intermittent. Hours of ambulatory monitoring may show it when slow AV conduction, such as at night, lets the delta wave show.^[4]
• A short PR alone, without a delta wave, is common in young athletes and is usually just fast AV nodal conduction.^[4]
• Intermittent pre-excitation is not a reliable sign of a low-risk pathway: in one review over 20% of such cases had a refractory period under 250 ms.^[4]

The impulse goes down the AV node and His-Purkinje system and up the accessory pathway. The ventricles are activated normally, so the QRS is narrow and there is no delta wave during the tachycardia; the pathway may be concealed. This is the commonest tachycardia in WPW, accounting for 90 to 95% of re-entrant tachycardias in patients with a pathway.^[3][1] It is regular and fast.

The circuit runs the other way: down the accessory pathway and up the AV node (or, rarely, another pathway). The ventricles are activated entirely through the pathway, so the QRS is wide, fully pre-excited and regular. It is documented in only 3 to 8% of patients with WPW, and multiple pathways are found in 30 to 60% of them.^[3][1] It looks like ventricular tachycardia (VT), so wide-complex tachycardia should be treated as VT unless the mechanism is clear.^[1]

AF occurs in about 15% of people with WPW.^[2] It is often triggered by a bout of AVRT, which raises atrial pressure and shortens the filling time, but it can also start by itself.^[3] With a fast pathway the ventricles are activated at the atrial rate, so the ECG shows a fast, irregular, wide-complex tachycardia with varying QRS shapes. Atrial rates can reach 300 beats per minute and can be passed directly to the ventricles to cause VF.^[4]

Why AV-nodal blockers harm in this setting: in AF the AV node acts as a filter, so its slow and variable conduction protects the ventricles. A drug that blocks the node removes competing conduction down the normal route, and more impulses pass down the pathway. In a study of patients receiving verapamil in the electrophysiology laboratory during AF, the shortest pre-excited RR interval fell and two patients deteriorated and needed cardioversion.^[2] A guideline-level contraindication therefore applies to verapamil, diltiazem, amiodarone, digoxin, adenosine and beta-blockers.^[2] Adenosine is a particular worry because it shortens the atrial refractory period and the pause after conversion can start AF.^[3] Amiodarone has been linked to VF in published reports.^[2]

Symptoms. Many people are symptom-free and are found when an ECG is done for another reason. Others report sudden palpitations with abrupt onset and offset, dizziness, breathlessness or chest discomfort. Syncope, pre-syncope and sustained palpitation, particularly during exercise, are the symptoms that most strongly suggest an arrhythmia.^[4] Athletes can under-report symptoms for fear of losing training or career opportunities.^[4] In infants the picture is non-specific: fast breathing, poor feeding, irritability, vomiting and heart failure if the tachycardia persists.^[3]

Examination is usually normal between episodes. During tachycardia, look for adverse features: shock, syncope, ischaemic chest pain or heart failure.^[19]

Reduced exercise capacity. Even overt pre-excitation without symptoms has been linked to dyssynchronous left ventricular contraction, lower exercise capacity in children and a higher risk of heart failure in adults. It is one argument for ablation.^[3][6]

Sudden death in WPW is rare but is "front-loaded" in the young, and it can be the first manifestation.^[3]

• Cardiac arrest or VF risk in WPW is reported at 2.4 per 1000 person-years in the 2019 European Society of Cardiology (ESC) supraventricular tachycardia guideline.^[1] Other sources give 0.15 to 0.39% over 3 to 10 years of follow-up, and life-threatening events in children at 0.8 to 1.9 per 1000 person-years.^[3]
• Pooled case records of 63 adults resuscitated from arrest showed that arrest generally happens at about 20 to 30 years of age, 73% occurred in symptomatic people (especially those with prior AF), and in a mean of 27% of cases it was the first sign.^[3]
• WPW accounts for about 1% of sudden cardiac death in the athletic population in one long-term registry, probably an underestimate because autopsy does not look for pathways.^[4]
• Exercise and emotional stress raise the risk; in one survey two thirds of aborted VF arrests occurred during exercise or emotional stress, and in a more recent Italian registry 36% of events were exercise-related.^[4]

Features raising the risk: male sex, familial WPW, pattern detected in the first two decades, previous AF, syncope, congenital heart disease (especially Ebstein anomaly), multiple or septal pathways, and a short refractory period.^[3]

The question is how fast the pathway can conduct during AF.

• Resting ECG and ambulatory ECG. Sudden complete loss of the delta wave at a particular heart rate suggests a longer refractory period, but this is unreliable.^[4]
• Exercise testing. Abrupt, complete loss of pre-excitation during exercise has been considered low risk, but in a series of 164 patients the low-risk exercise test had a sensitivity of 40% and a negative predictive value of 51% for excluding a high-risk pathway; in 6 of 45 patients with intermittent or sudden loss at exercise the study still found high-risk properties.^[6] The 2019 ESC guideline gives non-invasive assessment in asymptomatic pre-excitation a class IIb recommendation.^[6]
• Drug test. Complete block of the pathway after intravenous ajmaline (1 mg/kg over 3 minutes) or procainamide (10 mg/kg over 5 minutes) suggests a long refractory period (over 270 ms), but this is of limited use.^[3]
• Intermittent pre-excitation does not exclude danger: more than 20% of these cases have a refractory period under 250 ms in an electrophysiology study.^[4] A multicentre cohort recommends ablation when there is documented AVRT, multiple pathways or rapid conduction, defined as a pathway refractory period or a shortest pre-excited RR interval (SPERRI) of 250 ms or less at baseline or during isoprenaline, even when pre-excitation comes and goes.^[15]
• Spontaneous AF on an ECG: a shortest pre-excited RR interval of 250 ms or less clearly shows a high-risk pathway, while a longer interval does not exclude one.^[7]

The electrophysiology study (EPS) is the best-validated way to risk-stratify and is nearly always combined with ablation.^[4] It measures:

• Shortest pre-excited RR interval (SPERRI) during induced AF.
• Accessory pathway effective refractory period (APERP).
• Whether AVRT or AF can be induced, and whether there are multiple pathways.

High-risk features in the ESC framework: SPERRI 250 ms or less, APERP 250 ms or less, multiple pathways or inducible AVRT.^[1][6] Thresholds differ in some sources: one review quotes SPERRI below 250 ms in adults at baseline, below 220 ms in children and below 200 ms during isoprenaline infusion.^[3] For prepubertal children, an Italian protocol considers SPERRI of 210 ms or less at rest high risk.^[14] Isoprenaline (a catecholamine) is often added to mimic exercise.^[3][7]

EPS is imperfect. In one paediatric series, 37% of children with a life-threatening event had no high-risk features on EPS, and anaesthesia and catheter contact may suppress the pathway; EPS under anaesthesia correlates only moderately with the SPERRI recorded during a clinical AF episode.^[3][4] In practice a negative EPS is reassuring but not absolute.

ESC 2019: electrophysiology study with isoprenaline is recommended (class I) for asymptomatic people with high-risk occupations or hobbies and for competitive athletes, and should be considered (class IIa, B) in other asymptomatic people; non-invasive assessment of pathway conduction may be considered (IIb).^[1]

• Old infarction: pseudo-infarct Q waves from a delta wave can mimic it.^[20]
• Bundle branch block: the original 1930 description was of apparent left bundle branch block with tachycardia, but the broad QRS is due to early ventricular activation, not a blocked bundle.^[4]
• Fasciculoventricular pathways give a short PR and a subtle delta wave but do not take part in tachycardia, and the QRS does not change with exercise or adenosine; true WPW pathways can take part in re-entry and can be unmasked.^[16]
• Mahaim fibres, which may give a normal resting ECG or left bundle branch block shape tachycardia.^[8]
• Enhanced AV nodal conduction (short PR only), which is common in young athletes.^[4]
• Other wide-complex tachycardias (VT, SVT with aberrancy): if unsure, treat as VT.^[1]

• Complications are AF with rapid conduction, ventricular fibrillation, cardiac arrest, and (for overt pre-excitation) dyssynchronous contraction with exercise intolerance and heart failure.^[16][3]
• After ablation, mortality is similar to the background population in one cohort of 362 patients, but AF later in life was more common.^[4]
• Successful ablation is associated with lower long-term mortality, from sudden death prevention and a lower risk of heart failure.^[3]

• Unstable (shock, syncope, ischaemia, heart failure): synchronised cardioversion, whatever the rhythm.^[1][2]
• Treat any irregular wide-complex tachycardia in a patient with known or suspected pre-excitation as pre-excited AF.
• If the mechanism is not clear, treat a wide-complex tachycardia as VT.^[1]

Electrical cardioversion is the preferred treatment in the unstable patient.^[19] For AF, the European Resuscitation Council (ERC) 2025 guideline says a first synchronised shock delivered at the machine's highest setting is a reasonable alternative to stepping the energy up; for atrial flutter and regular narrow-complex SVT give an initial shock of 70 to 120 J; for ventricular tachycardia with a pulse 120 to 150 J, with stepwise increases if it fails.^[19] The general unstable-tachycardia algorithms offer amiodarone 300 mg after failed shocks; do not give amiodarone when the rhythm is pre-excited AF, which the ERC lists as a contraindication.^[19] Follow local protocols and the manufacturer's guidance. Case reports describe VF when a shock to pre-excited AF was inappropriately synchronised to the T wave; check where the marker lies before the shock.^[2]

Start with vagal manoeuvres (the ESC summary reports 43% conversion with the modified Valsalva against 17% for the standard one), then adenosine as the first drug.^[1] The ESC advises that adenosine be used with caution in AVRT because it may induce fast AF; place a defibrillator with the patient.^[1][3] Dosing, technique and cautions are on the page about supraventricular tachycardias (the ESC regimen is 6 mg, then 12 mg, then 18 mg if needed, each by rapid bolus).^[1] In known WPW the ESC still allows adenosine for orthodromic AVRT, with a defibrillator at hand, and never when the rhythm is irregular and wide.^[1] Verapamil, diltiazem or a beta-blocker may be used for orthodromic tachycardia only if the resting ECG shows no pre-excitation; if pre-excitation is visible, prefer cardioversion or a pathway-acting drug because AF may follow.^[1][5]

Use a drug that acts on the pathway: ibutilide, procainamide, propafenone or flecainide, because drugs acting on the AV node are ineffective or dangerous here. Amiodarone may be considered for drug-refractory antidromic AVRT, although not in pre-excited AF.^[1]

• Unstable: electrical cardioversion (class 1 in the 2023 American College of Cardiology and American Heart Association, ACC/AHA, guideline).^[2]
• Stable: pharmacological cardioversion with intravenous ibutilide or procainamide is recommended as an alternative to elective cardioversion (ACC/AHA class 1); the ESC guideline lists class IC drugs as a weaker option. Ibutilide prolongs the pathway's refractory period, and in a study cited by the ACC/AHA it terminated AF in 21 of 22 patients.^[2][1]
• Never: verapamil, diltiazem, amiodarone, digoxin, adenosine or beta-blockers.^[2][1]

• Anticoagulation decisions follow the rules for AF; see atrial fibrillation and flutter.

The 2025 American Heart Association (AHA) tachycardia algorithm gives procainamide as 20 to 50 mg per minute until the arrhythmia is suppressed, hypotension develops, the QRS widens by more than 50% or a total of 17 mg/kg has been given, then 1 to 4 mg per minute, and advises avoiding it with a prolonged QT or heart failure. The two regimens differ; follow the local protocol.^[21]

The ACC/AHA algorithm for pharmacological conversion warns that procainamide is best avoided after amiodarone or ibutilide because the QT can lengthen too much.^[2] If neither drug is available, synchronised cardioversion is the safe option; class IC drugs are a weaker option (class IIb) and have accelerated the rhythm in case reports, so use them only on specialist advice.^[1][17] IV flecainide and propafenone are contraindicated in ischaemic or structural heart disease.^[1] Class IC drugs are not risk-free because they have some AV nodal effect.^[17]

Ablation of the pathway (usually radiofrequency, sometimes cryoablation) is the treatment of choice for symptomatic recurrent AVRT or pre-excited AF, and the ESC advises offering it as an initial choice in re-entrant tachycardias.^[1] It cures the pathway in more than 90% of first attempts.^[4] Figures differ by series:

• ESC pooled data for AVRT: acute success 92%, recurrence 8%, complications 1.5%, mortality 0.1%. Septal pathways: cardiac tamponade 0.13 to 1.1% and complete AV block 0.17 to 2.7%.^[1]
• A review citing a meta-analysis: success over 94%, recurrence 6.2%, complications 1%.^[3]
• A US study of WPW ablations over 14 years: tamponade 0.9% and complete heart block 1%.^[4]
• Septal pathways near the AV node and His bundle: cryoablation is often chosen because the effect is partly reversible; in children, AV block risk of 10% with radiofrequency at mid-septal sites has been quoted, against under 1% with cryoablation in more recent literature.^[4]

Ablation reduces long-term mortality, but AF risk may stay raised in WPW even after ablation; the risk is lower if ablation is done before the age of 50.^[3]

About one in five patients develops an arrhythmia related to the pathway during follow-up, most often AVRT (80%), with AF in 20 to 30%.^[1] Management depends on risk:

• High-risk features (SPERRI or APERP 250 ms or less, multiple pathways or an inducible pathway-mediated tachycardia): catheter ablation is recommended (class I, B). Ablation may be considered for a low-risk pathway (IIb, C) and should be considered if there is left ventricular dysfunction attributed to electrical desynchrony (IIa, C).^[1][3]
• Competitive athletes and high-risk occupations, such as pilots: EPS and ablation if the pathway is high risk. Ablation is reasonable when pre-excitation precludes the job.^[3]
• Low risk and willing: observation with follow-up and warning about symptoms, as most never have an event; the decision is shared and an EPS is still reasonable (class IIa).^[1]
• In a randomised trial in asymptomatic patients, arrhythmic events at 5 years occurred in 7% of those ablated and 77% of controls; one control patient had an aborted VF arrest. The trial was small.^[4]
• A review of children reports that restricting sport alone does not make the child safe, and recommends a low threshold for ablation.^[4]

Long-term drugs are a bridge, or for people who decline ablation. Beta-blockers, verapamil and diltiazem are used only if there is no pre-excitation on the resting ECG. Flecainide or propafenone may be considered if there is no ischaemic or structural heart disease.^[1] Drugs do not give reliable blanket protection against dangerous arrhythmias.^[4] In a cohort of 369 symptomatic patients who declined ablation, 1.1% had haemodynamic collapse with pre-excited AF or VF and 6.8% had syncope or pre-syncope, with no deaths.^[4]

After successful ablation most patients need no long-term follow-up. ESC 2019 allows sport 1 month after ablation if there are no recurrences.^[1][4] Because AF risk persists, report palpitations.^[3]

• Blanket advice to avoid vigorous activity has been replaced by risk stratification and ablation; until risk is assessed, avoid competitive exertion.^[4]
• ESC 2019: ablation is mandatory in athletes at high risk, and sport is allowed 1 month after ablation if there are no recurrences. When ablation is undesirable or not feasible, all sports are allowed except those with a high intrinsic risk of loss of consciousness.^[1]
• Competitive athletes with pre-excitation should have EPS for risk stratification, with ablation if high risk. Recreational athletes can start with non-invasive assessment.^[3] For athletes who have had paroxysmal SVT, the ESC generally recommends catheter ablation.^[1]
• A single-centre Italian protocol allows competitive sport when SPERRI and APERP are above 250 ms at baseline and 210 ms or more during exertion or isoprenaline.^[14]
• High-risk occupations such as pilots, bus drivers and athletes get priority for assessment.^[3]
• In a national screening programme of 11,168 elite footballers aged about 16, 26 had pre-excitation; 24 were ablated and returned to play, two with low-risk features continued competing, and no event occurred.^[4]

Sustained SVT occurs in 22 to 24 per 100,000 pregnancies.^[1] Synchronised cardioversion is safe in all stages of pregnancy and is first choice when unstable; the fetal heart rate should be checked afterwards.^[1][18] The usual first-line sequence of vagal manoeuvres, adenosine, beta-blockers and verapamil is set out for pregnancy "in the absence of pre-excitation"; flecainide and propafenone are advised as second-line agents for maternal and fetal SVT with pre-excitation in patients without ischaemic or structural heart disease.^[5] Orthodromic AVRT can be treated with adenosine.^[5] Ablation should be postponed to the second trimester where possible.^[1] Amiodarone causes fetal harm and is reserved for when other measures fail.^[5]

• AVRT may begin in fetal life (most often between 24 and 32 weeks of gestation) and is an important cause of fetal heart failure with hydrops.^[3] It is treated through the mother, with off-label drugs and informed consent.^[14]
• In infants, anterograde conduction is lost in up to 40% in the first year, and tachycardia episodes fall in frequency in about 90%, but recur in about 30% at a mean of 7 to 8 years.^[3]
• In asymptomatic children under 8, risk stratification is not recommended. For asymptomatic children a risk-stratifying EPS is considered at about 8 to 10 years of age and may be repeated after puberty.^[14]
• Avoid verapamil in small children, because it can cause severe hypotension; avoid digoxin in children with WPW.^[1][5]
• Studies in children are mostly done under sedation or general anaesthesia, which can reduce pathway conduction, so a reassuring result must be read with caution.^[3]

Multiple pathways are common in Ebstein anomaly (about 50%), and hypertrophic cardiomyopathy can coexist with WPW, so pre-excitation in these patients needs specialist electrophysiology assessment.^[3]

Whether someone with pre-excitation may drive depends on whether the rhythm has caused, or is likely to cause, sudden incapacity, and on the national licensing authority. Advise the patient not to drive after any episode of collapse or near-collapse until the rhythm is assessed and treated, and tell them to check the rules that apply to them. The UK DVLA rules for arrhythmia are set out in Supraventricular tachycardias (Driving section) and apply in the same way here.

• Any ECG with a delta wave, a short PR with a wide QRS, or unexplained collapse during exercise.
• Any history of sustained palpitations or syncope in a person with pre-excitation.
• Any athlete, pilot or driver with the pattern.
• Anyone with an irregular wide-complex tachycardia: this is an emergency.

Where an electrophysiology laboratory is not available, the main protections are recognition and avoidance of harm: read the ECG for a delta wave before diagnosing "old infarct" or "LBBB" in a young person, keep AV-nodal blockers away from irregular wide-complex tachycardia, and have synchronised cardioversion available. Procainamide and ibutilide may be unobtainable; then use synchronised cardioversion. Refer for ablation when it can be arranged.