Herbal Aconite Tea and Refractory Ventricular Tachycardia
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《新英格兰医药杂志》
To the Editor: Recently, a patient presented to our emergency department with severe poisoning after ingesting an aconite-containing tea with therapeutic intent. Her course highlights the potentially great danger of ingesting such a preparation. The patient, a 66-year-old woman without known cardiac disease, obtained the herb for treatment of her osteoarthritis from a local herbalist, who instructed her to prepare it by making a tea. Approximately 90 minutes after ingestion of the tea, facial and extremity paresthesias developed, after which nausea, generalized weakness, and chest pressure rapidly developed. On arrival at our emergency department, she was found to have a hemodynamically compromising supraventricular tachycardia that was refractive to both administration of adenosine and electrical cardioversion. Subsequently, ventricular tachycardia developed; it had varying morphologic features (monomorphic, polymorphic, and bidirectional), was associated with periods of pulselessness, and was refractory to both electrical and various pharmacologic interventions. After approximately four hours, there was conversion to sinus rhythm, which continued until the patient was discharged as neurologically normal four days later.
The results of routine blood chemical tests were normal, the presence of digoxin was ruled out, and a myocardial perfusion scan was normal. A sample of the herb was determined on gas chromatography to contain aconitine. Aconitine binds with high affinity and causes persistent activation of sodium channels. It is one of various alkaloids responsible for the clinical effects of aconite.1 Aconitine is used in Chinese and Japanese medicine as an analgesic or antirheumatic agent and to treat neurologic indications, and it has a well-documented association with life-threatening ventricular dysrhythmias.2 Incorrect preparation and a narrow therapeutic index have been implicated in the toxic effects. The combination of paresthesias, muscle weakness, and ventricular tachycardia is typical in poisoning.3 There remains no consistently effective treatment, although class I antiarrhythmic drugs (particularly flecainide) and beta-blockers have decreased mortality in a rat model.4 Although reports of poisonings with aconite have been extremely rare in North America, this could change with the increasing popularity of herbal medicines.
Lisa Lowe, M.D.
Michael J. Matteucci, M.D.
Aaron B. Schneir, M.D.
University of California, San Diego, Medical Center
San Diego, CA 92103
aschneir@ucsd.edu
References
Friese J, Gleitz J, Gutser UT, et al. Aconitum sp. alkaloids: the modulation of voltage-dependent Na+ channels, toxicity and antinociceptive properties. Eur J Pharmacol 1997;337:165-174.
Ameri A. The effects of Aconitum alkaloids on the central nervous system. Prog Neurobiol 1998;56:211-235.
Lin CC, Chan TY, Deng JF. Clinical features and management of herb-induced aconitine poisoning. Ann Emerg Med 2004;43:574-579.
Gutierrez B, Vilumara A, Farre AJ. Inhibition of aconitine-induced mortality in the conscious rat: a screening test for antiarrhythmic drugs. Methods Find Exp Clin Pharmacol 1987;9:307-310.
The results of routine blood chemical tests were normal, the presence of digoxin was ruled out, and a myocardial perfusion scan was normal. A sample of the herb was determined on gas chromatography to contain aconitine. Aconitine binds with high affinity and causes persistent activation of sodium channels. It is one of various alkaloids responsible for the clinical effects of aconite.1 Aconitine is used in Chinese and Japanese medicine as an analgesic or antirheumatic agent and to treat neurologic indications, and it has a well-documented association with life-threatening ventricular dysrhythmias.2 Incorrect preparation and a narrow therapeutic index have been implicated in the toxic effects. The combination of paresthesias, muscle weakness, and ventricular tachycardia is typical in poisoning.3 There remains no consistently effective treatment, although class I antiarrhythmic drugs (particularly flecainide) and beta-blockers have decreased mortality in a rat model.4 Although reports of poisonings with aconite have been extremely rare in North America, this could change with the increasing popularity of herbal medicines.
Lisa Lowe, M.D.
Michael J. Matteucci, M.D.
Aaron B. Schneir, M.D.
University of California, San Diego, Medical Center
San Diego, CA 92103
aschneir@ucsd.edu
References
Friese J, Gleitz J, Gutser UT, et al. Aconitum sp. alkaloids: the modulation of voltage-dependent Na+ channels, toxicity and antinociceptive properties. Eur J Pharmacol 1997;337:165-174.
Ameri A. The effects of Aconitum alkaloids on the central nervous system. Prog Neurobiol 1998;56:211-235.
Lin CC, Chan TY, Deng JF. Clinical features and management of herb-induced aconitine poisoning. Ann Emerg Med 2004;43:574-579.
Gutierrez B, Vilumara A, Farre AJ. Inhibition of aconitine-induced mortality in the conscious rat: a screening test for antiarrhythmic drugs. Methods Find Exp Clin Pharmacol 1987;9:307-310.