Sykes A P, Lawson N, Finnegan J A, Ayres J G
Chest Research Institute, East Birmingham Hospital.
Thorax. 1991 Aug;46(8):580-3. doi: 10.1136/thx.46.8.580.
Infused beta 2 agonists have been shown to cause focal myocardial necrosis. Serum creatine kinase activity was compared in 13 patients with brittle asthma currently being treated with subcutaneous terbutaline and an age and sex matched control group of patients with moderate asthma having inhaled treatment only. The median serum total creatine kinase activity for patients receiving subcutaneous terbutaline (211 units/l) was greater than that for the control group (120 units/l). The cardiac specific isoenzyme component of creatine kinase was not raised in either group, and the electrocardiograms and serum aspartate aminotransferase activity were normal. Electromyograms in five patients receiving subcutaneous terbutaline with high creatine kinase activity showed changes consistent with myositis in two, one of whom was subsequently shown to have a metabolic myopathy, which is thought to be long standing. No pathological changes were seen in the myocardium at necropsy in a patient who died from an acute attack of asthma while taking subcutaneous terbutaline. These results suggest that the raised creatine kinase activity seen in patients receiving this treatment is unlikely to be myocardial in origin.
已证实静脉输注β2激动剂可导致局灶性心肌坏死。对13例正在接受皮下注射特布他林治疗的脆性哮喘患者与仅接受吸入治疗的年龄和性别匹配的中度哮喘对照组患者的血清肌酸激酶活性进行了比较。接受皮下注射特布他林的患者血清总肌酸激酶活性中位数（211单位/升）高于对照组（120单位/升）。两组患者的肌酸激酶心脏特异性同工酶成分均未升高，心电图和血清天冬氨酸转氨酶活性均正常。5例接受皮下注射特布他林且肌酸激酶活性高的患者的肌电图显示，其中2例有与肌炎一致的变化，其中1例随后被证实患有代谢性肌病，据认为该病病程较长。1例在服用皮下注射特布他林时死于哮喘急性发作的患者尸检时心肌未见病理改变。这些结果表明，接受该治疗的患者中肌酸激酶活性升高不太可能源于心肌。
