Ephedrine increases ventricular arrhythmias in conscious dogs after myocardial infarction
Philip B. Adamson, MDFACC*, ,*,
Jennifer Suarez, BS*,
Ethannah Ellis, BS*,
Travis Kanaly, BS* and
Emilio Vanoli, MD*, ,
* Department of Physiology, Cardiovascular Diseases, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
Department of Medicine, Cardiovascular Diseases, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
Dipartimento di Cardiologia, Policlinico San Matteo, IRCCS e Università di Pavia, Pavia, Italy
Manuscript received June 2, 2004;
revised manuscript received July 15, 2004,
accepted July 20, 2004.
* Reprint requests and correspondence: Dr. Philip B. Adamson, University of Oklahoma Health Sciences Center, Department of Medicine, Cardiovascular Diseases Section, 920 S. L. Young Blvd, WP3120, Oklahoma City, Oklahoma 73190 (Email: Philip-adamson{at}ouhsc.edu).
OBJECTIVES: This study examined the hypothesis that the sympathomimetic activity of ephedrine increases the risk of lethal arrhythmias.
BACKGROUND: The sympathomimetic amine, ephedrine, is used to augment physical performance and as a weight loss aid, but little is known about the cardiovascular consequences in individuals with ischemic heart disease.
METHODS: Fifteen dogs at low risk for ventricular fibrillation (VF) during exercise and transient myocardial ischemia 30 days after a small anterior myocardial infarction were retested after five days of ephedrine use (Xenadrine, 0.4 mg/kg/day orally). To assess the effects of ephedrine on cardiac autonomic control, baroreceptor reflex sensitivity (BRS), heart rate (HR) variability, HR response to acute myocardial ischemia, and resting catecholamines were measured before and after ephedrine. Dogs were used as their own control when possible.
RESULTS: Nine of 15 animals had increased ventricular arrhythmias during ephedrine treatment (p = 0.01) and four had VF. Three dogs that had VF could not be resuscitated. Five animals with increased arrhythmias during ephedrine treatment had none during a third exercise and ischemia test after drug washout. Heart rates were higher after 30 s of myocardial ischemia during ephedrine treatment (204 ± 25 beats/min no drug vs. 218 ± 26 beats/min with ephedrine, p = 0.03). All plasma catecholamines increased after ephedrine administration. No changes in BRS, HR variability, or exercise HR were noted.
CONCLUSIONS: Ephedrine increases ischemia-dependent arrhythmias at doses recommended in over-the-counter preparations. Increased arrhythmia risk was associated with augmented ischemia-dependent sympathetic reflex activation.
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Abbreviations and Acronyms
| | BRS = baroreflex sensitivity | | FDA = Food and Drug Administration | | HR = heart rate | | MI = myocardial infarction | | VF = ventricular fibrillation |
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