Atrial fibrillation induced by mad honey intoxication in a patient with Wolf–Parkinson–White syndrome

To the Editor:

Grayanotoxins, which are extracted by bees from the leaves and flowers of Rhododendron species, are the main compounds responsible for poisoning with honey in the Black Sea region.¹ “Mad honey” intoxication is usually a benign condition and is rarely fatal. In cases of toxication, bradycardia, atrioventricular (AV) block, and hypotension are commonly seen. Adequate fluid replacement and 0.5–1.0 mg of atropine are sufficient to improve the symptoms. We wish to report a case of a patient with Wolf–Parkinson–White syndrome (WPWS), who was admitted to hospital because of atrial fibrillation (AF) after “mad honey” ingestion.

A 46-year-old man was admitted to the emergency department with dizziness and palpitations after eating a few spoonfuls of honey. He had no history of heart disease or drug usage. His blood pressure was 90/60 mmHg and his pulse rate was 172 beats per minute. A 12-lead electrocardiogram (ECG) demonstrated an irregular, wide QRS complex tachycardia (Fig. 1, top). Vital signs improved rapidly after saline infusion and sinus rhythm was restored within the following 20–30 min. A repeated ECG demonstrated a normal sinus rhythm, shortened PR intervals, delta waves, and minimally widened QRS complexes as WPWS (Fig. 1, bottom). All routine biochemical tests and thyroid functions were normal. Both his left atrial size and function were normal, as were his left ventricular size and function. He was monitored for 48 h, and AF did not recur. The patient was discharged with no medical therapy and transferred to an electrophysiology study for radio frequency ablation of the accessory bypass tract. Several cases of honey poisoning with bradyarrhythmia, sinus bradycardia, nodal rhythm, second-degree, or complete AV block were documented in recent literature; however, honey poisoning related to AF with WPWS has not previously been reported.^2–4

Fig. 1. Top. ECG showing irregular, rapid ventricular rate (rate 172) with wide QRS complexes and tachycardia. Bottom. ECG obtained 30 min after admission revealed WPWS including shortened PR interval, slurring, slow rise of the QRS complex (delta wave), and widening of the QRS complex.

WPWS is defined as the presence of an accessory pathway (AP) and has a predisposition for the development of supraventricular tachydysrhythmias. Ventricular pre-excitation is associated with a higher incidence of AF, but if WPWS with AF is treated with drugs that prolong the AV node (AVN) refractory period (e.g. calcium-channel blockers, beta-blockers, digoxin, adenosine), the rate of conduction through the AP may increase and degenerate to ventricular fibrillation.⁵

In our case, the mechanism of enhanced AP conduction was likely due to honey poisoning causing prolonged AVN conduction and resulting in rapid AF. Thus, patients in the Black Sea with honey intoxication who develop new onset wide QRS complex AF should be examined carefully to exclude the possibility of WPWS.

Acknowledgement

A written consent form was obtained from the patient regarding the publication of this interesting case report.