Case Report - Consequences Of Ephedra Use In An Athlete

A right-handed African-American man with no significant medical history was admitted to our hospital in May, 2003, aged 37 years. He presented with a 1-day history of progressive headache and blurred vision in his left visual field. He reported decreased exercise tolerance and palpitations during the previous 2 weeks. He was a body builder employed as a personal fitness trainer, and denied use of prescribed medications, tobacco, alcohol, or illicit drugs. He had a family history of myocardial infarction and stroke, but none of dilated cardiomyopathy. He had an irregular heartbeat of 76 beats per minute. Neurological examination showed moderate left hemineglect, dense left homonomous hemianoppia, and left hemisensory loss. Laboratory investigations, including hypercoaguability profile, were unremarkable and blood cultures were negative. Urine toxicology was negative for cocaine and amphetamines. Electrocardiogram showed atrial fibrillation. MRI scan with gadolinium confirmed a right middle cerebral artery (MCA) territorial infarction with minor haemorrhagic transformation. A small left parietal infarction was also identified suggestive of an embolic source. No significant extracranial carotid stenosis was identified on duplex or magnetic resonance angiography (MRA). Intracranial MRA revealed decreased flow within the distal aspect of the right MCA branches. Transthoracic and transoesophageal echocardiography showed severe left-ventricular dilation and hypokinesis with an estimated ejection fraction of 20–25%. No patent foramen ovale, intracardiac masses, thrombi, or vegetations were noted, and there was no significant atherosclerotic disease in the aorta. Cardiac catheterisation showed normal coronary arteries. We treated our patient with digoxin, β blockers, and an angiotensin-converting enzyme inhibitor. He was not considered a candidate for cardioversion. A few days after admission, the patient revealed that he had taken an ephedra-containing nutritional supplement (Hydroxycut, MuscleTech, http://www.muscletech.com) daily for the past 3 years. He later also admitted weekly intravenous use of nandrolone and intermittent use of intravenous stanazol 1 year before onset of symptoms. Despite administration of intravenous heparin, his recovery was complicated by two additional left cerebellar infarcts. He was discharged 10 days after admission and subsequently lost to follow-up. Hydroxycut is a herbal supplement that contains ephedra (banned by the US Food and Drug Administration in April, 2004), caffeine, and aspirin; it is often used by bodybuilders and athletes to aid weight loss and to improve performance. Potential side-effects of ephedra-containing compounds include complications associated with the cardiovascular—eg, hypertension, palpitations, tachycardia, arrhythmia, myocardial infarction, and sudden cardiac death—and the central nervous systems—eg, stroke, transient ischaemic attack, and seizure. Ephedra acts on both α adrenergic and β adrenergic receptors and stimulates release of endogenous catecholamine, resulting in vasoconstriction and, possibly, altering myocardial refractory time. Ephedra use is also temporally related to left-ventricular systolic dysfunction because of its sympathomimetic effects on repetitive stimulation of the myocardium. In our patient, ephedra use might have either caused a tachyarrhythmia-induced dilated cardiomyopathy or acted as a direct toxin to the myocardium, resulting in a tachyarrhythmia. About 25–50% of patients with atrial fibrillation associated with left-ventricular systolic dysfunction have some degree of tachycardic-induced cardiomyopathy, and in cardiomyopathy induced by atrial fibrillation, haemodynamic improvements are seen with heart rate or rhythm control. As such, a follow-up echocardiogram and Holter studies after intervention might have been diagnostic. Ephedra seems to predispose to both ischaemic and haemorrhagic stroke. Haemorrhagic stroke might result from catecholamine-induced hypertension or cerebral vasculitis, and ischaemic stroke has been linked to vasoconstriction and sympathomimetic platelet activation, resulting in local thrombosis. We believe our patient probably had a cardioembolic stroke, resulting from ephedra-induced cardiomyopathy and atrial fibrillation, caused by direct cardiac toxicity, catecholamine excess, or possibly hypersensitivity myocarditis. Our patient's use of anabolic steroids probably contributed to his symptoms. Although vasculitis remains a possible cause of stroke in our patient, the multiple territorial ischaemic lesions in the setting of atrial fibrillation and cardiomyopathy make embolism more likely. A cerebral angiogram, which would have indicated segmental narrowing characteristic of vasculitis or vasospasm, was not done.