What are the treatment options for a patient with a short PR interval, potentially associated with Wolff-Parkinson-White syndrome, presenting with symptoms such as palpitations, shortness of breath, or chest pain?

Management of Short PR Interval with Symptoms

For symptomatic patients with a short PR interval, the critical first step is determining whether delta waves are present on ECG—if present with symptoms like palpitations, shortness of breath, or chest pain, this confirms Wolff-Parkinson-White syndrome and mandates immediate cardiology referral for risk stratification and consideration of catheter ablation, which is the definitive first-line treatment with 95-98% success rates. 1, 2

Initial Diagnostic Differentiation

The presence or absence of delta waves fundamentally changes management:

• With delta waves (PR <120 ms + slurred QRS upstroke + widened QRS >120 ms): This confirms ventricular pre-excitation via an accessory pathway bypassing the AV node, establishing WPW syndrome when symptoms are present 3, 2, 4

• Without delta waves (isolated short PR <120 ms with normal QRS): This may represent a normal variant in athletes, enhanced AV nodal conduction, Lown-Ganong-Levine syndrome, or underlying structural disease such as hypertrophic cardiomyopathy or Fabry's disease—requires careful evaluation but is not WPW syndrome 3

Risk Stratification for Confirmed Symptomatic WPW

Once WPW syndrome is confirmed, immediate risk stratification is essential:

High-risk features requiring urgent intervention: 1, 5

• Shortest pre-excited RR interval <250 ms during atrial fibrillation
• History of syncope or near-syncope
• Documented atrial fibrillation with pre-excitation
• Multiple accessory pathways or posteroseptal location
• Accessory pathway refractory period <240 ms

Low-risk indicators: 1, 5

• Intermittent loss of pre-excitation on ambulatory monitoring (90% positive predictive value for low risk)
• Abrupt loss of pre-excitation during exercise testing

Mandatory Diagnostic Workup

All symptomatic patients require comprehensive evaluation before definitive treatment: 3, 1

• 12-lead ECG during tachycardia (obtain before cardioversion if hemodynamically stable)
• 24-hour Holter monitoring to detect paroxysmal arrhythmias and assess for intermittent pre-excitation
• Exercise ECG to evaluate if pre-excitation disappears with exercise (suggests low risk)
• Echocardiography to exclude Ebstein anomaly, hypertrophic cardiomyopathy, or glycogen storage cardiomyopathy (PRKAG2-related familial WPW)
• Electrophysiology study for definitive risk stratification and to guide ablation

Definitive Treatment Algorithm

Catheter ablation is the first-line definitive treatment for all symptomatic WPW patients: 1, 5, 6

• Success rates: 95-98.5%
• Major complication rates: 0.1-0.9% (including complete heart block, bundle branch blocks)
• 5-year arrhythmic event rates: 7% in ablated patients versus 77% in non-ablated patients
• Should be performed at experienced centers

Mandatory indications for ablation: 1

• Symptomatic tachyarrhythmias (palpitations, chest pain, shortness of breath)
• History of syncope
• Documented atrial fibrillation with WPW
• High-risk features identified on electrophysiology study

Acute Management of Tachyarrhythmias

For Hemodynamically Unstable Patients:

• Immediate synchronized DC cardioversion to prevent progression to ventricular fibrillation 3, 1

For Hemodynamically Stable Patients with Regular Narrow-Complex Tachycardia (Orthodromic AVRT):

• First-line: Vagal maneuvers followed by IV adenosine 3
• Alternative: IV verapamil or diltiazem (safe in orthodromic AVRT without pre-excitation)

For Hemodynamically Stable Patients with Pre-excited Atrial Fibrillation (Wide, Irregular QRS):

• First-line: IV procainamide 1, 6
• Alternative: IV flecainide or propafenone 7, 8, 6

Critical Medication Contraindications

AV nodal blocking agents are absolutely contraindicated in pre-excited atrial fibrillation: 1, 5

• Never use: Digoxin, diltiazem, verapamil, beta-blockers, adenosine
• Reason: These agents block the AV node preferentially, forcing conduction down the accessory pathway, which can accelerate ventricular rates to >300 bpm and precipitate ventricular fibrillation

This is a common and potentially fatal pitfall—always verify the presence or absence of pre-excitation (delta waves) before administering AV nodal blockers.

Long-Term Medical Management (Bridge to Ablation Only)

If ablation is delayed or declined, antiarrhythmic medications can be used, but are inferior to ablation: 7, 8, 9, 6

• For preventing AVRT: Propranolol or other beta-blockers (safe when no pre-excited AF)
• For preventing rapid conduction in atrial fibrillation: Flecainide (50-300 mg/day), propafenone (600 mg/day), or amiodarone—these prolong accessory pathway refractory periods
• Avoid: Digoxin as monotherapy (may shorten accessory pathway refractory period)

Special Monitoring Considerations

Symptoms requiring urgent evaluation: 1, 5

• Syncope or near-syncope (may indicate rapid accessory pathway conduction)
• New onset palpitations lasting >30 minutes
• Chest pain or dyspnea during palpitations
• Episodes occurring while driving (57% of SVT patients experience episodes while driving)

Family screening: 3

• Obtain ECG in siblings of young patients with WPW or bifascicular block patterns
• Assess family history for pre-excitation, sudden cardiac death in young relatives, or cardiomyopathy

Key Clinical Pitfalls to Avoid

1. Misdiagnosing isolated short PR without delta waves as WPW syndrome—this leads to unnecessary interventions 3

2. Administering AV nodal blockers during pre-excited atrial fibrillation—this can be fatal 1, 5

3. Assuming hemodynamic stability rules out ventricular tachycardia—stable vital signs do not distinguish SVT from VT 3

4. Delaying ablation in symptomatic patients—medical therapy is inferior and carries ongoing risk of sudden death (lifetime risk approaches 4% in symptomatic WPW) 5, 4

5. Missing subtle delta waves in left lateral pathways—these may show minimal pre-excitation due to fusion with normal conduction 5