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International Journal of Arrhythmia 2015;16(1): 55-58.
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Introduction
Ephedra alkaloids are a group of sympathomimetic compounds
derived from the shrubs of the Ephedra genus. These alkaloids are
structurally similar to amphetamines and catecholamines, and
possess both α- and β-adrenergic activity.1 Ephedra alkaloids have
been used in traditional folk remedies, particularly in China, for
millennia. The principle alkaloid ephedrine was first isolated in
1885, and has been used in modern medicine as a bronchodilator,
decongestant, and vasopressor.2 Ephedra extracts are also
commonly taken to enhance weight loss and athletic performance.
Ephedra-containing dietary supplements were banned by the
American Food and Drug Administration in 2004 because of
significant adverse effects.3 Between 1995 and 1997, 37 cases of
adverse effects were reported and predominantly involved serious
cardiovascular events (e.g., stroke, myocardial infarction, sudden
cardiac death), despite no underlying cardiovascular disease.3
Here, I report a case of ventricular tachycardia (VT) with two
distinct morphologies caused by the consumption of herbal medicine containing Ephedra sinica (Ma Huang).
Case
A 77-year-old man presented to the emergency department
with a fluttering sensation in the chest and sudden onset dyspnea.
On initial presentation, the vital signs were as follows: heart rate,
208 beats per minute (bpm); respiratory rate, 22 breaths per
minute; and body temperature, 36.6°C. Although the patient had
weak femoral pulses and a blood pressure of 60/40 mmHg, he
seems to be mentally alert when in a supine position. Breath
sounds were clear, and no evidence of wheezing or crackling.
However, the heart sound was distorted because of tachycardia.
Twelve-lead electrocardiography (ECG; Figure. 1A) initially
showed sustained monomorphic VT (208 bpm), a right bundle
branch block (RBBB) pattern in the precordial leads, and left axis
deviation. Biphasic electrical cardioversion (200 J) successfully
terminated the VT through conversion to atrial fibrillation
(Figure. 1B). After 1 hour, a further sustained monomorphic VT (210 bpm) developed spontaneously, with a QRS morphology
that was indicative of left BBB (LBBB) and superior axis
deviation (Figure. 1C). Biphasic electrical cardioversion (200 J)
was reattempted, and sinus rhythm was successfully restored
(Figure. 1D).
After the treatment, the possible causes of the VT were
considered, including anemia, electrolyte imbalance, hypoxemia,
coronary artery disease, cardiomyopathy, congenital heart disease,
or drug effects. Laboratory result revealed normal serum
creatinine levels, electrolyte levels, and arterial blood gases.
Similarly, ECG showed a normal left ventricular ejection fraction
(65%) with no significant valve degeneration or structural
abnormalities. Although coronary angiography revealed a stenosis
of 70% in both the proximal part of the left circumflex coronary
artery and the posterior descending artery, I decided to administer
pharmacologic treatment based on the presence of normal blood
flow and absence of angina.
The patient had been diagnosed with chronic obstructive
pulmonary disease 30 years prior to admission. He had a history
of smoking (one half-pack per day for 50 years) but had ceased
this habit one year previously. The current medication included
methylprednisolone (2 mg/day) and the β2-agonist fenoterol (2.5
mg/day). The patient reported no history of alcohol or
intravenous drug abuse, and had no remarkable family history of
cardiovascular disease or sudden cardiac death. He reported
taking herbal medicine containing E. sinica over the course of two
days (total four doses) for abdominal discomfort and indigestion.
I concluded that the consumption of the herbal medicine was the
cause of the VT with two distinct QRS morphologies.
The patient was prescribed clopidogrel, warfarin, an
angiotensin-converting enzyme inhibitor, a β-blocker, and a statin,
and was advised against resuming the herbal medication prior to
discharge. No recurrences of VT occurred during more than 6
months of follow-up.
Discussion
Ephedrine and related alkaloids have been associated with
numerous adverse cardiovascular events, including acute
myocardial infarction, severe hypertension, myocarditis,4,5 and
lethal cardiac arrhythmias.6,7 This development of adverse cardiovascular events is largely attributable to the
sympathomimetic activity of these alkaloids.1 That is, these
compounds directly stimulate α1, β1, and β2 adrenergic receptors
and can thereby result in vasoconstriction, bronchodilation,
increased heart rate, enhanced myocardial contractility, and
increased automaticity. Such compounds also shorten cardiac
refractory periods and can therefore facilitate the development of
cardiac arrhythmogenesis.8 The long-term use of ephedrine may
lead to the cardiomyopathy typically observed during
catecholamine excess.7
To date, there has been no report of VT with two distinct QRS
morphologies (RBBB and LBBB) caused by E. sinica in patients.
The present case is also distinct from previously reported cases of
VT6,7 in several additional respects: 1) the sustained distinct
monomorphic VTs originated from different ventricles; 2) the
patient had taken unknown but small doses of E. sinica (four in
total); and 3) the ingestion of the herbal medication had been of a
relatively short duration (two days).
Recently, the molecular mechanisms underlying E. sinica
activity have been demonstrated, in vivo, to involve the activation
of the slowly activating KCNQ1 potassium channel and other
members of the KCNE protein family.9 Although this activation
could be expected to precipitate ventricular arrhythmia, further
investigation is required to confirm this. Nonetheless, because
even short-term, low-dose intake of E. sinica is associated with the
risk of life-threatening ventricular arrhythmias, its use should be
closely monitored and tightly regulated.
References
- Dulloo AG. Herbal simulation of ephedrine and caffein in treatment of obesity.
Int J Obes Relat metab Disord.
2002;26:590-592.
- Haller CA, Benowitz NL. Adverse cardiovascular and central nervous system events associated with dietary supplements containing ephedra alkaloids.
N Engl J Med.
2000;343:1833-1838.
- Greenway FL. The safety and efficacy of pharmaceutical and herbal caffein and ephedrine use as a weight loss agent.
Obes Rev.
2001;2:199-211.
- Mark PB, Watkins S, Dargie HJ. Cardiomyopathy by performance enhancing drugs in a competitive bodybuilder.
Heart.
2005;91:888.
- Samenuk D, Link MS, Homoud MK, Contreras R, Theoharides TC, Wang PJ, Estes NA 3rd. Adverse cardiovascular events temporally associated with ma huang, an herbal source of ephedrine.
Mayo Clin Proc.
2002;77:12-16.
- Makaryus JN, Makaryus AN. Cardiac arrest in the setting of diet pill consumption.
Am J Emerg Med.
2008;26:732.e1-3.
- Casella M, Dello Russo A, Izzo G, Pieroni M, Andreini D, Russo E, Colombo D, Bologna F, Bolognese L, Zeppilli P, Tondo C. Ventricular arrhythmias induced by long-term use of ephedrine in two competitive athletes.
Heart Vessels.
2015;30:280-283.
- Maughan RJ. Contamination of dietary supplements and positive drug tests in sport.
J Sports Sci.
2005;23:883-889.
- Jing H, Luo L, Li H, Sun J, Yi H, Wu Y, Wang C, He G. Ephedrine controls heart rhythms by activating cardiac I (IKs) currents.
J Cardiovasc Pharmacol.
2010;55:145-152.
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