Does flecainide need to be stopped if it prolongs the PR interval?

Flecainide and PR Interval Prolongation: When to Stop

PR interval prolongation alone is an expected pharmacologic effect of flecainide and does not require discontinuation; however, the drug must be stopped or dose-reduced if QRS duration increases by ≥25% from baseline, which signals proarrhythmic risk. 1

Expected vs. Dangerous Conduction Changes

Normal Pharmacologic Effects (Continue Drug)

• PR interval prolongation is an anticipated effect of flecainide's sodium channel blockade and should be monitored but does not mandate discontinuation. 1
• Flecainide prolongs the PR interval as part of its therapeutic mechanism, affecting all major cardiac conduction pathways 1, 2
• The PR interval should be measured at baseline and monitored during therapy, but prolongation itself is not a stopping criterion 1

Dangerous Changes Requiring Action (Stop or Reduce Dose)

• QRS duration increase of ≥25% compared to baseline is the critical threshold that signals potential proarrhythmia risk and mandates either dose reduction or drug discontinuation. 1, 3
• QRS widening should not exceed 150% of pretreatment duration 3
• Development of new bundle branch block, particularly left bundle branch block, requires precautions 1

Monitoring Algorithm During Flecainide Therapy

At Initiation

• Obtain baseline 12-lead ECG measuring PR interval, QRS duration, and QT interval 3
• Perform echocardiogram to exclude structural heart disease and assess LVEF 3
• Check serum electrolytes (potassium, magnesium) 3

During Dose Titration

• Obtain ECG after each dose change 1
• Weekly ECG monitoring during dose adjustments 3
• Calculate percentage change in QRS duration from baseline 1

Ongoing Maintenance

• Regular ECG monitoring to assess QRS duration, PR interval, and QT/QTc interval 3
• Monitor for development of atrial flutter with rapid ventricular conduction 3

Absolute Contraindications to Continuation

Stop flecainide immediately if any of these develop:

• QRS widening ≥25% from baseline 1, 3
• Development of sustained monomorphic ventricular tachycardia 1, 4
• Polymorphous ventricular tachycardia or ventricular fibrillation 2, 5
• New structural heart disease or reduction in LVEF 1
• Symptomatic bradycardia or high-grade AV block 1

Common Clinical Pitfalls

Mistake: Stopping for PR prolongation alone

• PR prolongation without excessive QRS widening is expected and therapeutic 1
• Focus monitoring on QRS duration changes, not PR interval changes 1, 3

Mistake: Inadequate baseline assessment

• Failing to obtain baseline ECG makes it impossible to calculate the critical 25% QRS increase threshold 3
• Missing undiagnosed structural heart disease at baseline increases proarrhythmic risk 1

Mistake: Ignoring concomitant AV nodal blockade

• Flecainide can convert atrial fibrillation to atrial flutter with rapid ventricular conduction 1, 3
• Beta-blockers or calcium channel antagonists should be given concomitantly to prevent 1:1 AV conduction 1

Mistake: Outpatient initiation in high-risk patients

• Avoid outpatient initiation in patients with symptomatic sick sinus syndrome, AV conduction disturbances, or bundle branch block 1
• Initial conversion should be undertaken in hospital before declaring patients fit for outpatient use 1

Drug Interactions Affecting Conduction

• CYP2D6 inhibitors increase flecainide levels and may worsen conduction abnormalities 6, 3
• Digoxin levels rise with flecainide; monitor and reduce digoxin dose 3
• Combining with other QT-prolonging agents increases arrhythmic risk 6