Pre-Excited Atrial Fibrillation: What Not to Give
A 26-year-old man is brought to the emergency department after 40 minutes of rapid palpitations, presyncope and chest discomfort. He has had two similar but briefer episodes in the past year and one episode of syncope while playing football. He takes no medication. Blood pressure is 88/60 mmHg, the pulse is irregular at about 240/min, respiratory rate 26/min and oxygen saturation 96%. He is anxious but orientated; the lungs are clear and there is no oedema. The ECG shows an irregularly irregular wide-complex tachycardia with varying QRS width (110–160 ms) and rates up to 300/min, with no discernible P waves. A nurse has drawn adenosine and verapamil and asks you to approve them while the defibrillator is being brought.
1. What is the rhythm and its mechanism? Do you approve the adenosine and verapamil? Justify your answer and outline the immediate management.
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Diagnosis: pre-excited atrial fibrillation in Wolff–Parkinson–White syndrome. The rhythm is irregularly irregular, wide and varying in width, with rates up to 300/min. The accessory pathway conducts antegradely and bypasses the AV node, and because it has no decremental conduction properties the ventricular rate can become dangerously fast.
Do not approve either drug. Adenosine, verapamil, diltiazem, digoxin and beta-blockers block the AV node. In pre-excited AF this removes the competing normal conduction and pushes more impulses down the accessory pathway; the ventricular rate can accelerate into ventricular fibrillation, and some of these drugs also shorten the pathway's refractory period. Ibutilide and amiodarone should also be avoided in this setting because amiodarone can accelerate accessory pathway conduction.
Immediate management. He is hypotensive at 88/60 mmHg with presyncope, so he is unstable: perform synchronized cardioversion with 100–200 J biphasic, with sedation if there is time and airway support available. If he were haemodynamically stable, IV procainamide 10–15 mg/kg at no more than 50 mg/min (maximum 17 mg/kg) or ibutilide would be a reasonable way to block the pathway, with continuous ECG and BP monitoring and a defibrillator at the bedside. Never give AV-nodal-blocking drugs while the rhythm is pre-excited.
2. After successful cardioversion, how will you evaluate and treat him definitively, and what risk stratification matters?
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Definitive treatment: electrophysiology study and catheter ablation. After sinus rhythm is restored, document pre-excitation on a 12-lead ECG and refer for mapping and radiofrequency or cryoablation of the accessory pathway. Success exceeds 95%, recurrence is 5–8%, and the main risk is AV block with septal pathways, which should be part of the consent discussion. Ablation is indicated in symptomatic patients and in asymptomatic patients with high-risk features.
Risk stratification. Sudden death in WPW is rare but unpredictable. Recognised markers include a shortest pre-excited RR interval below 250 ms during AF, multiple accessory pathways, a septal pathway location and a short effective refractory period of the pathway. These markers are most useful for counselling the asymptomatic patient; they do not change management in a man who has already had syncope and rapid pre-excited AF, because he needs ablation regardless.
Interim advice. Give him a written list of drugs to avoid, including over-the-counter products containing verapamil or diltiazem and any 'rate control' tablet. Advise no competitive sport until ablation is complete and pre-excitation has disappeared from the ECG. Warn him that recurrent palpitations with a fast, irregular rate require emergency assessment and cardioversion, not a home pill. Screen first-degree relatives only if there is a family history of sudden death or a suspected inherited accessory pathway syndrome.
3. What would you do if ablation failed or the pathway were deemed high-risk for AV block, and how does this change his long-term follow-up?
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If ablation fails or is judged too risky.
- Repeat ablation at an experienced centre. A second procedure after an initially failed ablation has a high success rate; refer rather than abandoning the strategy.
- Antiarrhythmic suppression. If ablation is not possible, use a drug that slows accessory pathway conduction, such as flecainide or propafenone in a structurally normal heart, or amiodarone in selected cases, with the explicit understanding that AV-nodal-blocking drugs remain forbidden if pre-excitation persists.
- Cryoablation for septal pathways. Cryomapping allows testing for AV conduction before permanent injury and lowers the risk of heart block when the pathway is close to the His bundle.
- Rate control strategy is not acceptable in a patient with inducible pre-excited AF; if AV block occurs as a complication, pacing is required and the pathway must still be addressed.
Follow-up. After successful ablation, perform an ECG at 1–3 months and consider ambulatory monitoring if symptoms recur; loss of pre-excitation and non-inducibility at EPS define success. If pre-excitation persists, he remains at risk and must continue to avoid AV-nodal-blocking drugs. Counsel about athletic participation according to current recommendations, and document the advice in the record. Also address modifiable triggers such as alcohol, stimulants and sleep deprivation, which commonly precipitate AF in young patients.