Wolff-Parkinson-White Creates an Accessory Pathway That Bypasses Normal Conduction. Ablation Is Curative.

The Scene

Note: The following is a HIPAA-clean composite constructed from published case series and clinical patterns. It does not represent a single identifiable patient.

The 19-year-old had been having episodes since she was 14. Her heart would start racing and then stop. The pediatrician called it “anxiety.” The school nurse called it “panic attacks.” She learned to sit down, breathe, splash cold water on her face. The episodes always ended.

The one in the airport did not end the same way.

She was running to catch a connection, bag over one shoulder, heart hammering from the sprint. Then it started, and it was different. Not the usual tight percussion in her chest. Something faster, more chaotic. By the time she reached the gate, she was on the floor.

The flight crew retrieved the AED. One shock. Sinus rhythm. She was 19 years old and had never had a formal cardiac evaluation.

The ECG in the emergency department showed a short PR interval. There was a slurred upstroke on every QRS complex: the delta wave. Wolff-Parkinson-White syndrome. Her cardiologist would later explain that she had been carrying an extra electrical wire in her heart since birth, and that the night the wire sent atrial fibrillation directly to her ventricles at 300 beats per minute, the outcome had been fifty-fifty.

She had the ablation eight weeks later. The procedure took ninety minutes. She has had no episodes in the three years since.

WPW is, in most patients, a nuisance arrhythmia. In a subset, it is a sudden death risk. The skill of the clinician is knowing which patient is which, and the guidelines are explicit: once WPW is identified, the question of electrophysiology referral is not optional. Watchful waiting without EP evaluation is no longer the standard.

What It Is

Wolff-Parkinson-White (WPW) syndrome is a clinical entity defined by two simultaneous features: ventricular pre-excitation on the ECG (the delta wave and associated short PR interval) and symptomatic arrhythmias attributable to the accessory pathway. It was first formally described in 1930 by Louis Wolff, John Parkinson, and Paul Dudley White in a case series of patients with short PR intervals, bundle-branch-block-like QRS morphology, and paroxysmal tachycardia (Wolff L, Parkinson J, White PD, Am Heart J 1930; DOI: 10.1016/S0002-8703(30)90086-5).

The terms require careful distinction:

Ventricular pre-excitation is the ECG phenomenon: a short PR interval (less than 120 ms) and a delta wave (a slurred upstroke of the initial QRS) caused by conduction over an accessory pathway that bypasses the normal delay in the AV node. The ventricle begins to depolarize earlier than it would through the His-Purkinje system.

WPW pattern refers to the ECG finding of pre-excitation without any documented arrhythmia.

WPW syndrome requires the ECG pattern plus symptomatic arrhythmias (palpitations, syncope, cardiac arrest, or documented tachycardia).

This distinction matters for risk management and treatment discussions. The patient with an incidentally found delta wave on a pre-employment physical has a different risk profile from the patient with recurrent tachycardia episodes, and a completely different profile from the patient who has survived pre-excited atrial fibrillation.

Epidemiology

WPW pattern occurs in approximately 1 to 3 per 1,000 people in the general population 5 / Solid . Men are affected approximately twice as often as women in symptomatic series. The prevalence is slightly higher in first-degree relatives of affected individuals, consistent with a genetic predisposition. Most cases are sporadic. Familial WPW is associated with mutations in PRKAG2, the gene encoding a regulatory subunit of AMP-activated protein kinase, and can coexist with hypertrophic cardiomyopathy in some kindreds 4 / Promising .

The risk of sudden cardiac death in the overall WPW population is low, estimated at 0.1 to 0.2 percent per decade of follow-up in asymptomatic individuals 5 / Solid . In symptomatic patients with high-risk accessory pathway properties, the risk is substantially higher.

The Mechanism

The Accessory Pathway

During normal fetal cardiac development, the fibrous ring separating the atria from the ventricles (the annulus fibrosus) forms a complete electrical insulator. Conduction from atrium to ventricle passes through only one channel: the AV node, which imposes a physiological delay of 100 to 200 milliseconds, then continues through the His-Purkinje system. This delay is essential for coordinated ventricular filling.

In WPW, a strand of myocardial tissue (the accessory pathway, also called the bundle of Kent after the anatomist who described it) persists across the annulus fibrosus and forms a second conduction route from atrium to ventricle. This pathway has none of the rate-limiting properties of the AV node. It conducts faster, it does not slow down as heart rate increases, and it does not protect the ventricle from rapid atrial rates.

Accessory pathways are named by their anatomical location around the mitral or tricuspid annulus. The most common location is the left free wall (approximately 50 to 60 percent of cases), followed by posteroseptal (20 to 30 percent), right free wall (10 to 15 percent), and anteroseptal (5 to 10 percent) 5 / Solid .

Anterograde Conduction and the Delta Wave

In normal sinus rhythm, electrical activation from the atrium travels down both the AV node and the accessory pathway simultaneously. The accessory pathway is faster. It activates the ventricle earlier than the His-Purkinje system, producing the delta wave: a slow, slurred initial deflection that represents direct myocyte-to-myocyte spread from the pathway insertion point. When the His-Purkinje wavefront arrives, it fuses with the direct spread. The resulting QRS is a fusion of normal and pre-excited activation.

The PR interval is short because the accessory pathway bypasses the AV nodal delay entirely. The total QRS duration is slightly prolonged due to the delta wave, giving the classic triad: short PR, delta wave, wide QRS.

The direction and polarity of the delta wave varies by pathway location and is the basis of ECG-based pathway localization. An electrophysiologist looking at a 12-lead ECG can often identify which anatomical quadrant the pathway occupies before the patient enters the EP lab.

Retrograde Conduction and AVRT

Many accessory pathways can conduct in both directions: from atrium to ventricle (anterograde) and from ventricle to atrium (retrograde). This bidirectional conduction is the substrate for atrioventricular reentrant tachycardia (AVRT), the most common arrhythmia in WPW.

In orthodromic AVRT (accounting for approximately 95 percent of AVRT in WPW), the circus movement runs: atrium down the AV node, through the His-Purkinje system to the ventricle, up the accessory pathway back to the atrium. This produces a narrow-complex tachycardia (because the ventricle is activated via the normal His-Purkinje system) with a short RP interval (because retrograde atrial activation occurs quickly after ventricular activation) 5 / Solid .

In antidromic AVRT (approximately 5 percent of AVRT in WPW), the circuit runs in the opposite direction: down the accessory pathway to the ventricle, up through the His-Purkinje system back to the AV node and atrium. This produces a wide-complex tachycardia with maximally pre-excited QRS complexes, which can be confused with ventricular tachycardia.

The Critical Danger: Pre-excited Atrial Fibrillation

AVRT, while symptomatic and sometimes poorly tolerated, is rarely immediately life-threatening. The pathway for sudden cardiac death in WPW is atrial fibrillation with rapid conduction over the accessory pathway.

In atrial fibrillation, the atria are generating hundreds of chaotic electrical impulses per minute. In a normal heart, the AV node acts as a filter: it can only conduct approximately 140 to 180 of those impulses per minute to the ventricle, even at maximum physiological rates. The ventricles never receive the full atrial barrage.

In WPW, the accessory pathway has no such filtering capacity. If the pathway has a short anterograde refractory period (meaning it can conduct rapid impulses), it will transmit the chaotic atrial fibrillation directly to the ventricle at whatever rate the atrium is producing. Ventricular rates of 250 to 300 beats per minute are documented in WPW patients with pre-excited AFib. At those rates, the ventricle degenerates into ventricular fibrillation 5 / Solid .

The shortest RR interval during pre-excited AFib is the key measurement that predicts VFib risk. An RR interval below 250 ms (250 milliseconds between consecutive conducted beats) during pre-excited AFib indicates an accessory pathway capable of conducting at rates fast enough to cause VFib. This is the electrophysiological danger threshold 5 / Solid .

This is the scenario that killed the 19-year-old runner before the AED arrived in time. The delta wave had been on her ECGs for years. Nobody acted on it.

How We Diagnose

The 12-Lead ECG

The delta wave is visible to any cardiologist and to most cardiologists’ computers, though automated ECG interpretation software misses WPW more often than it should. When reviewing an ECG and noticing a short PR interval (under 120 ms) with a QRS that starts with a broad, slurred initial deflection, the first question is: which lead shows it most clearly?

Several ECG-based algorithms (most notably the Arruda algorithm and the revised Milstein algorithm) allow accessory pathway localization from the 12-lead ECG with reasonable accuracy before EP study 4 / Promising .

Important caveats:

• The delta wave may be small or absent in some leads depending on pathway location. A septal pathway can produce minimal pre-excitation and a subtle delta wave that is easy to miss.
• The degree of pre-excitation (how much delta wave versus normal QRS) varies with sympathetic tone. During exercise or sympathetic activation, increased conduction through the AV node can reduce the relative contribution of the accessory pathway, minimizing the delta wave.
• A “concealed” accessory pathway conducts only retrograde (ventricle to atrium) and produces no delta wave on ECG. These pathways can still cause AVRT but are not visible on a resting ECG.

Electrophysiology Study (EPS)

The EP study is the definitive evaluation for WPW. Under intracardiac catheter guidance, the electrophysiologist can:

1. Confirm the presence and location of the accessory pathway precisely
2. Map the pathway’s anterograde refractory period (the shortest interval at which it conducts to the ventricle)
3. Measure the shortest pre-excited RR interval during induced AFib
4. Assess whether the patient is inducible for AVRT or pre-excited AFib
5. Proceed directly to catheter ablation if the clinical decision has been made

An accessory pathway anterograde effective refractory period (AERP) under 250 ms defines a “high-risk” pathway: capable of conducting at rates sufficient to trigger VFib during AFib 5 / Solid .

Non-Invasive Risk Assessment

Before referring to EP study, two non-invasive findings can offer preliminary risk assessment:

Exercise stress testing: In a low-risk accessory pathway, the delta wave typically disappears abruptly during exercise when the sinus rate increases enough that AV nodal conduction dominates. This “abrupt loss of pre-excitation” during exercise suggests a pathway with a longer AERP that cannot conduct at fast rates and is therefore lower risk. If pre-excitation persists to high heart rates during exercise, the pathway may have a short AERP and higher risk 4 / Promising .

Holter monitor / continuous ECG: Intermittent pre-excitation (the delta wave appears and disappears over the recording) also suggests a longer AERP and lower short-term risk. However, intermittent pre-excitation does not guarantee safety, and it does not eliminate the need for EP evaluation in symptomatic patients.

Neither test has the sensitivity or specificity to replace EP study in symptomatic patients or in athletes who wish to compete.

The Evidence

Ablation: Efficacy and Cure Rates

Catheter ablation of accessory pathways is the definitive treatment for WPW. It uses radiofrequency energy (or cryoenergy in select locations) delivered through a catheter to destroy the small strand of tissue forming the accessory pathway.

Cure rates depend on pathway location:

The anteroseptal and para-Hisian locations carry the highest risk because the His bundle and AV node are adjacent. Damage to the His bundle during ablation can cause complete heart block requiring permanent pacemaker. In these locations, cryoablation is sometimes preferred because it allows “test freezing” before permanent energy delivery, with reversible effect at intermediate temperatures 4 / Promising .

The overall procedural success rate across pathway locations is approximately 93 to 95 percent with experienced operators. Recurrence (pathway recovery) occurs in 5 to 8 percent of successful procedures, most within the first three months. A second ablation resolves most recurrences 5 / Solid .

Complications of accessory pathway ablation include cardiac tamponade (0.5 to 1%), AV block requiring pacemaker (0.3 to 0.5% overall, higher for septal pathways), and vascular access complications. The risk of death attributable to the procedure is below 0.1% at experienced centers 5 / Solid .

The Pappone Studies and Prophylactic Ablation

The question of whether to ablate asymptomatic patients with WPW pattern was addressed in two landmark studies by Carlo Pappone and colleagues.

The first (2003) enrolled 212 asymptomatic patients with WPW pattern and performed EP study. Among the 69 patients with high-risk EP findings (short AERP, multiple pathways, inducible AVRT or pre-excited AFib), 2 had VFib during follow-up versus none among the 143 low-risk patients 5 / Solid .

The second (2012) was a randomized trial of asymptomatic WPW patients with high-risk EP findings, comparing ablation to no ablation. Arrhythmic events occurred in 7.7 percent of the no-ablation group versus 0 percent in the ablation group over 5 years 5 / Solid .

These studies fundamentally changed guidelines. Current ACC/AHA/HRS guidelines (2015) classify accessory pathway ablation in asymptomatic patients with high-risk EP features as Class IIa (benefit outweighs risk; reasonable to perform) 5 / Solid .

For asymptomatic patients with low-risk EP findings (long AERP, non-inducible), watchful waiting without ablation is reasonable (Class IIa for EP study to stratify risk; Class IIb for ablation).

Why AV-Nodal Blocking Agents Are Contraindicated

This is the most dangerous pharmacological error in WPW management. When a patient presents with a wide, irregular tachycardia that represents pre-excited atrial fibrillation, a reflex to give AV-nodal blocking agents (adenosine, beta-blockers, calcium channel blockers, digoxin) can be fatal.

These drugs block the AV node and may actually enhance conduction over the accessory pathway, either by reflex sympathetic activation following adenosine or by preferentially slowing AV nodal conduction relative to accessory pathway conduction. The result is faster ventricular conduction through the accessory pathway and a higher risk of VFib 5 / Solid .

The correct management of pre-excited AFib (wide, irregular tachycardia in a known or suspected WPW patient) is:

• If hemodynamically unstable (hypotension, altered consciousness, chest pain): immediate synchronized cardioversion
• If hemodynamically stable: IV procainamide (which slows accessory pathway conduction) or IV ibutilide 5 / Solid

Adenosine is absolutely contraindicated in pre-excited AFib. Every emergency physician and hospitalist needs this in memory, not just in a reference card.

Pediatric and Congenital Heart Disease Considerations

WPW occurs in association with Ebstein anomaly (a congenital malformation of the tricuspid valve and right ventricle) in approximately 25 percent of Ebstein cases 5 / Solid . Multiple right-sided accessory pathways are common in Ebstein WPW. Ablation in this population is more complex and requires coordination between the EP team and congenital heart disease specialists.

Children with WPW who are diagnosed before adolescence undergo EP study and ablation at most tertiary centers when they are symptomatic. The procedure is technically similar to the adult approach, though catheter sizes and energy delivery are adjusted. Ablation in children is generally not performed before age 5 unless arrhythmia control cannot be achieved with medical therapy 5 / Solid .

The Patient Experience

The Typical Presentation: Years of Dismissal

Most WPW patients who reach cardiology have spent months to years with their symptoms attributed to anxiety, panic disorder, or “stress.” The palpitations are real: sudden-onset, rapid, regular percussion in the chest that starts and stops abruptly. They may last 30 seconds or 30 minutes. They may resolve spontaneously or require vagal maneuvers (the Valsalva, a carotid sinus massage, cold water on the face).

The abrupt onset and offset is the distinguishing feature. Anxiety palpitations build gradually and fade gradually. AVRT starts at full speed in one beat and stops in one beat. Patients who have experienced both can describe the difference precisely, even if they lack the vocabulary.

The typical WPW patient is young: most present in adolescence or young adulthood. Episodes may increase in frequency with caffeine, alcohol, sleep deprivation, or sympathetic activation (exercise, stress). The episodes are frightening even when they are not dangerous.

When the Scenario Turns Dangerous

Pre-excited AFib is a different experience entirely. Patients who have had it and survived describe the sensation as a loss of control: the chest sensation is not just rapid but irregular, and the associated hemodynamic compromise (lightheadedness, near-syncope, or syncope) makes the event qualitatively different from AVRT. Not all patients can describe the arrhythmia that preceded their cardiac arrest. Some have no warning.

Risk factors for a WPW patient’s first presentation being pre-excited AFib:

• Age (AFib becomes more common with age, and WPW patients are not exempt)
• Structural heart disease increasing AF susceptibility
• High sympathetic activation (intense exercise, stimulant use, acute illness)

The 19-year-old runner in the scene above had none of the traditional AFib risk factors. Her AF was triggered by the adrenergic surge of sprinting to catch a flight. The accessory pathway did the rest.

The ICD-vs-Ablation Question Does Not Usually Arise

Unlike Brugada syndrome or Long QT, WPW is a structural problem with a structural fix. An ICD does not address the problem: it does nothing to prevent pre-excited AFib from producing VFib, because the VFib degrades so rapidly that there may not be time for detection and shock. The ICD would respond after collapse, not prevent it.

Ablation prevents the arrhythmia from occurring. This is the reason ablation is the preferred strategy over long-term antiarrhythmic drugs or watchful waiting in any symptomatic WPW patient or any asymptomatic patient with high-risk EP findings.

Antiarrhythmic drugs (flecainide, propafenone, sotalol) can be used to suppress tachycardia in patients who decline ablation or who are awaiting ablation, but they do not eliminate pathway conduction and do not provide the security of ablation 5 / Solid .

The Psychological Arc of WPW

The typical arc for a WPW patient who undergoes successful ablation:

1. Years of unexplained episodes attributed to anxiety
2. Diagnosis established by ECG or event monitor
3. Shock at learning the cause; fear about the dangerous scenario
4. Ablation (often an outpatient or overnight procedure)
5. Follow-up ECG showing loss of delta wave
6. Realization, sometimes gradual, that the problem is gone

Most patients experience a significant psychological benefit after ablation. They no longer live with the low-level vigilance of knowing an episode can start at any moment. The anxiety that had been attributed to a psychological disorder is often resolved because the physiological trigger has been removed.

Post-ablation monitoring: a repeat ECG at 3 months is standard to confirm persistent loss of pre-excitation. A Holter monitor or exercise stress test may be performed to confirm that no pre-excitation recurs at higher heart rates. If symptoms recur, a second ablation is required.

The Athlete Question

This is one of the more contested areas in WPW management. Competitive athletes with WPW pattern, particularly those who have not had EP study, present a specific challenge.

The 2015 ACC/AHA scientific statement on competitive athletes with arrhythmias states that athletes with symptomatic WPW syndrome (documented tachycardia) should not participate in competitive sports until they have undergone EP evaluation and, if indicated, successful ablation 5 / Solid .

For asymptomatic athletes with WPW pattern, the same document recommends EP evaluation before clearing them for high-intensity competitive sports. The rationale is that high sympathetic activity during competition can trigger AFib, and if the pathway has a short AERP, the first symptomatic episode in a competitive sports context could be VFib on the field.

This recommendation is not universally applied. Some sports medicine physicians and some cardiologists have advocated a more permissive approach for asymptomatic athletes with non-high-risk EP findings (long AERP, non-inducible). The Bethesda Conference #36 provides additional detail on specific sport categorization 5 / Solid .

The practical bottom line: an asymptomatic athlete with an incidentally found delta wave on a pre-participation physical needs EP evaluation before the question of sports clearance can be answered. “It looks like a low-risk pattern” is not sufficient. The EP study is the answer.

Decisions and Trade-Offs

Why Electrophysiology Consultation Is Not Optional

This is not a clinical controversy. When WPW is identified, EP referral is the standard of care. The question is not whether to refer but how urgently.

Symptomatic WPW: EP evaluation should be arranged within weeks, not months. The patient should avoid antiarrhythmic triggers (stimulants, large alcohol intake, sleep deprivation, extreme exertion) in the interim. If the arrhythmia is frequent and poorly tolerated, pharmacologic suppression with flecainide or propafenone is reasonable as a bridge, understanding that these agents suppress but do not eliminate pathway conduction.

Asymptomatic WPW pattern: EP evaluation is appropriate and now recommended in guidelines (Class IIa). The timing depends on the clinical context. An asymptomatic 14-year-old starting high school sports gets EP evaluation before the season. An asymptomatic 55-year-old discovered incidentally at a pre-operative evaluation warrants discussion about whether the risk of the syndrome in their age group justifies EP study, weighing their surgical risk and life expectancy.

The two scenarios where observation without EP referral is defensible: an elderly patient with multiple comorbidities where the procedural risk of EP study exceeds the reasonable benefit, or a patient with clear intermittent pre-excitation on exercise testing (abrupt loss of delta wave at low heart rates) who understands the residual uncertainty and declines further evaluation. Both require documented shared decision-making.

Sex Differences

Symptomatic WPW occurs approximately twice as often in men as in women, though the prevalence of the ECG pattern itself (asymptomatic pre-excitation) does not differ significantly by sex 5 / Solid . The reasons for the symptomatic disparity are not fully established; hormonal effects on accessory pathway conduction properties have been proposed but are not confirmed.

Women of childbearing age with WPW warrant specific counseling: AVRT can worsen during pregnancy due to hemodynamic changes and the proarrhythmic effect of high estrogen and progesterone on accessory pathway conduction. Catheter ablation is the preferred strategy before pregnancy in any symptomatic WPW patient to avoid the complications of antiarrhythmic drug therapy during pregnancy 4 / Promising .

The Pre-Excited AFib Recognition Problem in Emergency Departments

The most dangerous clinical encounter in WPW occurs not in a cardiology office but in an emergency department, where a patient presents with rapid palpitations and a wide-complex irregular tachycardia is on the monitor. The differential includes pre-excited AFib, AFib with aberrant conduction (typical wide-complex AFib), and, in some presentations, polymorphic VT.

The features that suggest pre-excited AFib:

• Very rapid ventricular rate (often 200 to 300 bpm)
• Irregular rhythm
• Wide, bizarre QRS complexes with delta wave morphology
• Variability in QRS width beat to beat (reflecting varying degrees of fusion between pathway and AV node conduction)

The management decision must be made before the diagnosis is confirmed. If the patient is hemodynamically unstable (systolic BP under 90, altered mental status, angina): synchronized cardioversion immediately. If stable: procainamide IV, not adenosine, not verapamil, not metoprolol.

A misidentification of pre-excited AFib as regular narrow AVRT and treatment with adenosine can be immediately fatal by accelerating conduction over the pathway. Adenosine transiently blocks the AV node while the accessory pathway conducts unopposed, and the rapid atrial activity reaches the ventricle at higher rates 5 / Solid .

The Concealed Pathway Question

A patient presents with recurrent orthodromic AVRT, documented on event monitor, but the resting ECG shows no delta wave. The pathway is “concealed”: it conducts only retrograde (from ventricle to atrium) and not anterograde. There is no risk of pre-excited AFib because the pathway cannot conduct rapidly from atrium to ventricle. The arrhythmia (AVRT) is the same circuit as in manifest WPW, just without the dangerous anterograde limb.

Concealed pathway AVRT is treated with ablation in the same way as manifest WPW, with the same cure rates by location. The risk stratification conversation is different: the concern about VFib from pre-excited AFib does not apply. Many patients with concealed pathways have spent years with “SVT” diagnosed without awareness of the pathway substrate, because the ECG did not show the delta wave.

When to Choose Medical Management Over Ablation

Ablation is the preferred definitive therapy, but some patients choose medical management:

• Patients with very infrequent, well-tolerated AVRT who are informed of the VFib risk and decline EP evaluation
• Patients with significant comorbidities where procedural risk is high
• Patients in whom the accessory pathway is in a high-risk anatomical location (para-Hisian, midseptal) where the risk of complete heart block is non-trivial and the patient chooses to live with episodic pharmacologic management

Long-term pharmacologic management options:

• Flecainide or propafenone (Class IC): suppress AVRT and slow accessory pathway conduction. Contraindicated in structural heart disease (post-CAST era). Effective for symptom control.
• Sotalol: beta-blocking and Class III effects. Slows both AV node and accessory pathway conduction. Requires QTc monitoring.
• Amiodarone: last-resort pharmacology due to toxicity profile; highly effective at suppressing both AVRT and accessory pathway conduction, but not for long-term use in young patients.

None of these agents provide the 95 percent resolution that ablation provides, and none address the core risk of pre-excited AFib as definitively as ablation.

Clinical Synthesis

Wolff-Parkinson-White syndrome is a congenital electrical anomaly that most patients carry for years without appropriate evaluation. The delta wave sits on the ECG, visible to anyone who knows what to look for, and is ignored, misinterpreted, or not followed up on until something dramatic forces the issue.

The clinical logic is straightforward here: the ECG is the test. The delta wave is the finding. The EP referral is the next step. The ablation, in the right hands, is curative with a 95 percent success rate. There is a clear path from “incidentally found delta wave” to “cured” that does not require a cardiac arrest in the middle.

The failure mode in WPW is not a lack of technology. The technology is mature. Catheter ablation for accessory pathways has been performed for over 30 years with well-characterized outcomes. The failure mode is a gap in recognition, evaluation, and follow-through:

• The primary care physician who sees a short PR on a routine ECG, decides it is a normal variant, and does not refer.
• The urgent care provider who treats a WPW patient’s tachycardia with adenosine without looking at the QRS width or rhythm regularity.
• The sports medicine physician who clears an asymptomatic athlete with a delta wave because “it looks like a low-risk pattern” without EP evaluation.
• The patient whose WPW was diagnosed years ago, who was told to “come back if symptoms worsen,” and who has never had a formal risk stratification.

Every one of these gaps is identifiable and closable.

For the patient with a delta wave on their baseline ECG: EP consultation at a center with a high-volume ablation program is the appropriate routing. Northwestern Medicine (Chicago), University of Chicago Medical Center, and University of Illinois Chicago all have established EP programs. For downstate Illinois patients, Carle Foundation Hospital in Urbana provides evaluation and coordinates referral for ablation procedures.

For the patient with a family history of WPW, unexplained syncope, or unexplained sudden cardiac death in a young family member: the investigation should include a 12-lead ECG with attention to the PR interval and delta wave. Genetic testing for PRKAG2 mutation is appropriate when familial WPW coexists with features of hypertrophic cardiomyopathy.

For the emergency provider who encounters a wide, irregular, rapid tachycardia: the rule is non-negotiable. No AV-nodal blocking agents until pre-excited AFib has been excluded. Cardioversion if unstable. Procainamide if stable.

The pathway is curable. The death from pre-excited AFib is preventable. The ECG is already in the chart.

What happens next is a decision.

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