What is the recommended rate‑control strategy for a patient with Brugada syndrome who develops rapid atrial fibrillation?

Rate Control for Atrial Fibrillation in Brugada Syndrome

In patients with Brugada syndrome who develop rapid atrial fibrillation, avoid all sodium channel blockers (Class IC and IA agents) for rate or rhythm control, and use beta-blockers or non-dihydropyridine calcium channel blockers (diltiazem, verapamil) as first-line agents for rate control, with pulmonary vein isolation as the definitive treatment for recurrent episodes. 1, 2

Critical Contraindications in Brugada Syndrome

• Sodium channel blocking antiarrhythmic drugs (flecainide, propafenone, quinidine, disopyramide, procainamide) are absolutely contraindicated for rate or rhythm control of atrial fibrillation in Brugada syndrome patients, as these agents can unmask or worsen the Brugada ECG pattern and precipitate ventricular fibrillation. 1

• Before initiating any antiarrhythmic therapy in patients with suspected or confirmed Brugada syndrome, obtain a 12-lead ECG specifically examining right precordial leads (V1-V3) for ST-segment elevation and right bundle-branch block pattern. 1

• The guideline explicitly warns that type I antiarrhythmic drugs have unmasked Brugada syndrome in previously asymptomatic individuals, leading to sudden death from idiopathic ventricular fibrillation. 1

First-Line Rate Control Strategy

For Hemodynamically Stable Patients with Preserved Ejection Fraction

• Administer intravenous beta-blockers (metoprolol 2.5-5 mg IV bolus) or non-dihydropyridine calcium channel blockers (diltiazem 0.25 mg/kg IV over 2 minutes) as first-line therapy to achieve acute rate control, targeting heart rate <110 bpm at rest. 1, 3, 4

• Beta-blockers are preferred over calcium channel blockers because they provide superior control of exercise-induced tachycardia and do not carry the sodium channel blocking properties that could worsen Brugada syndrome. 4

• For maintenance therapy, continue oral beta-blockers or calcium channel blockers, avoiding the combination with any class I antiarrhythmic agents that would normally be used to prevent atrial flutter with 1:1 AV conduction. 1

For Patients with Heart Failure or Reduced Ejection Fraction

• Use intravenous digoxin or intravenous amiodarone for acute rate control in Brugada syndrome patients with heart failure, as beta-blockers and calcium channel blockers should be avoided in decompensated heart failure. 1, 3

• Amiodarone is safe in Brugada syndrome (unlike class IC agents) and can be used when other rate-control measures fail or are contraindicated, though it should be reserved as second-line therapy. 3

• Digoxin controls only resting heart rate and is ineffective during exercise, but remains appropriate for acute management in the setting of volume overload and borderline blood pressure. 3

Management of Hemodynamic Instability

• Proceed immediately to direct-current cardioversion if the patient exhibits symptomatic hypotension, ongoing myocardial ischemia, acute pulmonary edema, or cardiogenic shock from rapid atrial fibrillation. 1, 3, 4

• Do not delay cardioversion for pharmacologic attempts when hemodynamic compromise is present, as this is the definitive intervention regardless of underlying cardiac channelopathy. 4

Definitive Treatment for Recurrent Atrial Fibrillation

• Pulmonary vein isolation using radiofrequency energy or cryoballoon ablation is the treatment of choice for Brugada syndrome patients with recurrent paroxysmal atrial fibrillation, particularly those with ICDs who experience inappropriate shocks from rapid ventricular response. 2

• At 2-year follow-up, 67% of Brugada syndrome patients who underwent pulmonary vein isolation remained free of atrial fibrillation without antiarrhythmic drugs, and none of the patients with prior inappropriate ICD shocks experienced further shocks after ablation. 2

• Catheter ablation should be strongly considered early in the treatment algorithm for Brugada syndrome patients, as pharmacological options are severely limited by the contraindication of sodium channel blockers. 2

Special Considerations and Common Pitfalls

• Never use class IC agents (flecainide, propafenone) or class IA agents (quinidine, procainamide, disopyramide) for rate or rhythm control in Brugada syndrome, even though these drugs are standard therapy for atrial fibrillation in other populations. 1

• The guideline specifically warns that before therapy with class IC agents is begun in any patient, a beta-blocker or calcium channel antagonist should be given to prevent rapid AV conduction if atrial flutter develops—but in Brugada syndrome, class IC agents should never be initiated at all. 1

• Monitor for bradycardia and heart block as unwanted effects of beta-blockers, digoxin, or calcium channel antagonists, particularly in elderly patients with paroxysmal atrial fibrillation. 1, 4

• Assess rate control during physical activity, not just at rest, as the ventricular rate may accelerate excessively during exercise even when well-controlled at rest. 1, 4

Algorithm for Rate Control in Brugada Syndrome with Rapid AF

1. Immediate assessment: Check hemodynamic stability and obtain 12-lead ECG
2. If unstable: Proceed directly to electrical cardioversion 1, 3
3. If stable with preserved EF: IV beta-blocker (metoprolol) or IV calcium channel blocker (diltiazem) 1, 3, 4
4. If stable with reduced EF/HF: IV digoxin or IV amiodarone 1, 3
5. For recurrent episodes: Refer for pulmonary vein isolation 2
6. Never use: Class IC or IA antiarrhythmic drugs 1

Context: Quinidine in Brugada Syndrome

• While quinidine is highly effective for preventing ventricular arrhythmias in Brugada syndrome (including ventricular fibrillation and supraventricular arrhythmias), its use specifically for rate control of atrial fibrillation is contraindicated due to its sodium channel blocking properties that can worsen the Brugada ECG pattern. 5, 6, 7

• The distinction is critical: quinidine may be used in Brugada syndrome to prevent arrhythmias when guided by electrophysiological testing, but it should not be used for acute rate control of rapid atrial fibrillation. 5, 6, 7