Yew Causes Brugada ECG
A 52-year-old man presented to the emergency department with nausea, abdominal discomfort, and extreme fatigue after ingestion of ≈15 g of yew leaves 20 hours before admission. Physical examination revealed a blood pressure of 85/55 mm Hg and a regular heart rate of 190 bpm. The Glasgow coma scale was 15. Physical examination was otherwise unremarkable. Laboratory investigations showed a white blood cell count of 15×109/L and slightly elevated liver enzymes (alanine aminotransferase 63 U/L; aspartate aminotransferase 76 U/L). Stable monomorphic ventricular tachycardia was documented. Active charcoal was administered, and the patient was transferred to the intensive care unit. A lidocaine bolus of 50 mg was administered, and an infusion was started at a rate of 0.6 mg/kg per hour. After 10 minutes, the rate of ventricular tachycardia slowed to 150 bpm and converted to sinus rhythm. The ECG after termination of ventricular tachycardia revealed sinus rhythm at a rate of 71 bpm, first-degree atrioventricular block (PR 240 ms), significant prolongation of the QRS complex (150 ms) and right bundle-branch block. In addition, a coved-type Brugada ECG pattern with ST-segment elevation of 0.6 and 0.7 mV in leads V1 and V2, respectively, was identified. Serial 12-lead ECGs showed gradual regression of the ST-segment elevation (Figure). The ECG normalized within 26 hours. Because the Brugada phenotype had appeared after the yew leaf ingestion, an intravenous ajmaline challenge was performed 3 days later to exclude “true” Brugada syndrome. The ajmaline challenge was negative without any alteration of the ST segment. During follow-up of 1 year, the patient was asymptomatic.
Yew (Taxus baccata) is a ubiquitous ornamental plant that is highly toxic.1 In most cases, ingestion leads to death from severe cardiac conduction defects, ventricular tachyarrhythmias, or electromechanical dissociation. The diagnosis of yew leaf intoxication is difficult if no anamnestic information is available because no specific symptoms occur. The treatment is mainly symptomatic. The prognosis of yew leaf intoxication depends on the amount of ingested yew tree constituents and on the cardiac involvement. The toxicity of Taxus baccata is based on pseudoalkaloids, which are found in all parts of the tree except for the red flesh of the berry. The major pseudoalkaloid, taxine B, accounts for 30% of the total taxine fraction. Taxine A only represents 1.8% of the taxine fraction.1 The proportion of taxol is very low at 0.01%. Taxine B and A mainly inhibit the cardiac calcium channel (ICa), but also the fast cardiac sodium channel (INa) in a dose-dependent manner. Taxol inhibits INa indirectly by enhancing tubulin polymerization causing a decrease of Nav1.5 expression, reduction of INa amplitude, and modification of the gating properties of the channel.2 Blockade of either INa or ICa causes the electrocardiographic phenotype of Brugada syndrome, an inherited primary electrical disease.3,4 For the first time, we could demonstrate the effect of combined sodium and calcium channel blockade caused by yew leaf intoxication. Fish et al have demonstrated via in vitro experiments that blocking both sodium and calcium channels unmasks the Brugada ECG more effectively than single-channel block alone.5 In the present patient, blockade of INa alone by ajmaline was not able to induce the Brugada phenotype.
Yew leaf intoxication leads to a new form of acquired Brugada syndrome. The underlying mechanisms of cardiac tachyarrhythmias and heart failure after yew leaf ingestion have been discussed, and we have drawn attention to the severity of deliberate or accidental intoxication resulting from the ingestion of this common ornamental plant.
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