Zaacks S M, Klein L, Tan C D, Rodriguez E R, Leikin J B
Rush Presbyterian St. Luke's Medical Center, Chicago, Illinois 60612, USA.
J Toxicol Clin Toxicol. 1999;37(4):485-9. doi: 10.1081/clt-100102440.
Ephedrine has previously been described as a causative factor of vasculitis but myocarditis has not yet been associated with either ephedrine or its plant derivative ephedra.
A 39-year-old African American male with hypertension presented to Rush Presbyterian St. Luke's Medical Center with a 1-month history of progressive dyspnea on exertion, orthopnea, and dependent edema. He was taking Ma Huang (Herbalife) 1-3 tablets twice daily for 3 months along with other vitamin supplements, pravastatin, and furosemide. Physical examination revealed a male in mild respiratory distress. The lung fields had rales at both bases without audible wheezes. Internal jugular venous pulsations were 5 cm above the sternal notch. Medical therapy with intravenous furosemide and oral enalapril was initiated upon admission. Cardiac catheterization with coronary angiography revealed normal coronary arteries, a dilated left ventricle, moderate pulmonary hypertension, and a pulmonary capillary wedge pressure of 34 mm Hg. The patient had right ventricular biopsy performed demonstrating mild myocyte hypertrophy and an infiltrate consisting predominantly of lymphocytes with eosinophils present in significantly increased numbers. Treatment for myocarditis was initiated with azothioprine 200 mg daily and prednisone 60 mg per day with a tapering course over 6 months. Anticoagulation with warfarin and diuretics was initiated and angiotensin-converting enzyme inhibition was continued. Hydralazine was added later. One month into therapy, an echocardiogram demonstrated improved left ventricular function with only mild global hypokinesis. A repeat right ventricular biopsy 2 months after the first admission showed no evidence of myocarditis. At 6 months, left ventricular ejection fraction was normal (EFN 50%) and the patient asymptomatic.
Ephedra (Ma Huang) is the suspected cause of hypersensitivity myocarditis in this patient due to the temporal course of disease and its propensity to induce vasculitis.
麻黄碱此前被描述为血管炎的一个致病因素，但心肌炎尚未被认为与麻黄碱或其植物衍生物麻黄有关。
一名39岁患有高血压的非裔美国男性因进行性劳力性呼吸困难、端坐呼吸和下肢水肿1个月就诊于拉什长老会圣卢克医疗中心。他每天服用1 - 3片麻黄（康宝莱），持续3个月，同时还服用其他维生素补充剂、普伐他汀和呋塞米。体格检查发现该男性有轻度呼吸窘迫。双肺底部可闻及湿啰音，未闻及哮鸣音。颈内静脉搏动位于胸骨切迹上方5厘米处。入院后开始静脉注射呋塞米和口服依那普利进行药物治疗。冠状动脉造影的心脏导管检查显示冠状动脉正常，左心室扩张，中度肺动脉高压，肺毛细血管楔压为34毫米汞柱。患者接受了右心室活检，结果显示轻度心肌细胞肥大，浸润细胞主要为淋巴细胞，嗜酸性粒细胞数量显著增加。开始用硫唑嘌呤每日200毫克和泼尼松每日60毫克治疗心肌炎，疗程为6个月，逐渐减量。开始使用华法林抗凝和利尿剂，并继续使用血管紧张素转换酶抑制剂。后来加用了肼屈嗪。治疗1个月后，超声心动图显示左心室功能改善，仅存在轻度整体运动减弱。首次入院2个月后再次进行右心室活检，未发现心肌炎迹象。6个月时，左心室射血分数正常（EFN 50%），患者无症状。
由于疾病的时间进程及其诱发血管炎的倾向，麻黄（麻黄）被怀疑是该患者过敏性心肌炎 的病因。
