What does the abbreviation "WRL" on an ECG refer to, and how should WPW syndrome be managed in asymptomatic versus symptomatic patients?

WPW on ECG: Definition and Management

"WPW" (Wolff-Parkinson-White) on an ECG refers to a ventricular pre-excitation pattern characterized by a PR interval <120 ms, a delta wave (slurred initial QRS upstroke), and QRS duration >120 ms; asymptomatic patients require risk stratification with exercise testing or electrophysiological study, while symptomatic patients should undergo catheter ablation as first-line definitive therapy. 1, 2

Diagnostic ECG Criteria

• The delta wave is the defining feature and must be present to diagnose WPW pattern—it represents the slurred upstroke of the QRS complex caused by ventricular pre-excitation via the accessory pathway bypassing the AV node 1, 2, 3
• The complete triad includes: PR interval <120 ms, delta wave, and QRS duration >120 ms 1, 3
• A short PR interval alone without delta waves does NOT constitute WPW and may represent enhanced AV nodal conduction or a normal variant 2
• Left lateral accessory pathways may show minimal delta waves due to fusion with normal AV nodal conduction, potentially appearing intermittent when actually continuously present 2, 4

Critical Distinction: Pattern vs. Syndrome

• WPW pattern = electrocardiographic finding of pre-excitation only 2, 4
• WPW syndrome = pre-excitation PLUS documented symptomatic tachyarrhythmias (palpitations, syncope, atrial fibrillation) 2, 4, 5
• This distinction drives management decisions—asymptomatic pattern requires risk stratification, while syndrome requires intervention 2

Management Algorithm for Asymptomatic Patients

Initial Risk Stratification (Non-Invasive)

• Exercise stress testing is the first-line non-invasive approach: abrupt, complete loss of pre-excitation at higher heart rates indicates a low-risk accessory pathway with long refractory period 1
• Intermittent pre-excitation on resting ECG or 24-hour Holter monitoring has 90% positive predictive value for low risk, making observation without further testing reasonable 1, 2
• Echocardiography is mandatory to exclude associated structural heart disease, particularly Ebstein's anomaly, hypertrophic cardiomyopathy, or PRKAG2-related familial WPW 1, 2, 4

When to Proceed to Electrophysiological Study

• High-risk clinical features warrant EP study even if asymptomatic: young age, competitive athletes, family history of sudden cardiac death, high-risk professions (pilots, heavy equipment operators), or multiple accessory pathways 1, 2
• Inconclusive non-invasive testing should prompt EP study to determine the shortest pre-excited RR interval during induced atrial fibrillation 1
• EP study findings that mandate ablation: shortest pre-excited RR interval <250 ms during AF, accessory pathway refractory period <240 ms, inducible sustained AVRT, or multiple pathways 1, 2

Common Pitfall in Asymptomatic Management

• Non-invasive tests have only 30% negative predictive value—a "negative" exercise test does NOT exclude high-risk pathways because sympathetic stimulation during intense competition may shorten the accessory pathway refractory period in ways that cannot be reproduced in laboratory testing 1, 2
• Some physicians recommend EP study for ALL competitive athletes in moderate/high-intensity sports regardless of non-invasive results, given this limitation 1

Management Algorithm for Symptomatic Patients

Acute Management of Pre-Excited Atrial Fibrillation (Wide QRS ≥120 ms)

Hemodynamically unstable:

• Immediate synchronized electrical cardioversion is the only appropriate intervention (Class I recommendation) 2

Hemodynamically stable:

• Intravenous procainamide is first-line pharmacologic therapy to block accessory pathway conduction 2, 5
• Intravenous ibutilide is an equally effective alternative 2
• ABSOLUTELY CONTRAINDICATED: digoxin, β-blockers, diltiazem, verapamil, adenosine—these AV nodal blocking agents can precipitate ventricular fibrillation by blocking the AV node while allowing unopposed rapid conduction through the accessory pathway 1, 2, 5

Acute Management of Orthodromic AVRT (Narrow QRS)

• Vagal maneuvers should be attempted first 2
• Intravenous adenosine is safe and effective for narrow-complex tachycardia (Class I) 2
• Critical caveat: ALWAYS verify QRS width before administering adenosine or AV nodal blockers—they are contraindicated if QRS ≥120 ms 2

Definitive Therapy: Catheter Ablation

• Catheter ablation is Class I recommendation (first-line) for ALL symptomatic patients with documented tachyarrhythmias, syncope, or atrial fibrillation 1, 2
• Success rate is approximately 95% with major complication risk of only 0.1-0.9% (complete heart block, bundle branch block) 1, 2
• Long-term outcomes: no malignant arrhythmias or ventricular fibrillation observed during 8-year follow-up after successful ablation 2
• Ablation is also reasonable (Class IIa) for high-risk asymptomatic patients, particularly young athletes or those with family history of sudden cardiac death 1, 2

High-Risk Features Requiring Urgent Intervention

• Shortest pre-excited RR interval <250 ms during atrial fibrillation is the strongest predictor of sudden cardiac death risk 1, 2, 4
• History of syncope is particularly concerning and may indicate rapid conduction with hemodynamic compromise 1, 2
• Multiple accessory pathways or posteroseptal location increase risk 1, 2
• Associated Ebstein's anomaly significantly elevates sudden death risk 1, 2

Long-Term Pharmacologic Therapy (When Ablation Declined)

• Class IC agents (flecainide, propafenone) are first-line for patients with rapid anterograde conduction through the accessory pathway, blocking accessory pathway conduction with high efficacy 2, 6
• Class IA agents (procainamide, quinidine) prolong accessory pathway refractory period for pre-excited AF prevention 2
• AV nodal blockers (β-blockers) may be used ONLY for orthodromic AVRT prevention if EP study confirms the accessory pathway cannot conduct rapidly anterogradely 2, 6
• Class III agents (amiodarone, sotalol) are reserved for refractory cases 2

Sudden Cardiac Death Risk

• Population-based risk: 0.15-0.39% over 3-10 years in all WPW patients 1, 2, 4
• Symptomatic WPW syndrome: lifetime risk approaches 4% 2, 4
• Death occurs when atrial fibrillation conducts rapidly over the accessory pathway (RR <250 ms) and degenerates into ventricular fibrillation 1, 2
• Sudden death may be the first manifestation in approximately 50% of cardiac arrest cases in WPW patients, emphasizing the importance of risk stratification even in asymptomatic individuals 1, 2