Ehsani A, Ewy G A, Sobel B E
Am J Cardiol. 1976 Jan;37(1):12-8. doi: 10.1016/0002-9149(76)90492-6.
Total and MB serum creatine phosphokinase (CPK) activity levels were measured serially in 30 patients treated with direct current electrical countershock, 17 patients with acute myocardial infarction and 25 normal subjects. In addition, serial determinations of total and MB CPK in serum were performed in 11 closed chest anesthetized dogs subjected to 10 repetitive countershocks at 15 second intervals with a delivered energy of 240 joules per countershock. Less than 4 milli-international units (mlU)/ml of MB CPK was found in the serum of normal subjects. Patients with myocardial infarction whose elevated total CPK levels were comparable with those of patients treated with cardioversion had a usbstantial rise in MB CPK activity, with peak values averaging 39 +/- 6 mlU/ml (mean +/- standard error). Fifteen of the 30 patients treated with countershock had elevated total CPK activity that peaked within 4 hours. In this group, MM CPK elevations accounted for the overall rise in CPK activity. In two patients, modest elevations of MB CPK (11 and 13 mlU/ml, respectively) were observed after cardioversion. In all 11 dogs total CPK increased after countershock, peaking to 1,888 +/- 410 MLU/ml within 6 hours. Six dogs had increased MB CPK activity (52+/- 6 mlU/ml) and myocardial necrosis demonstrable histologically 4 days later. The results indicate that (1) myocardial damage in dogs produced by intense, repetitive countershock is associated with increased serum MB CPK; and (2) countershock as conventionally used in patients does not generally produce myocardial damage and serum MB CPK elevation. Although release of MB CPK into serum occasionally occurs after countershock, perhaps reflecting myocardial damage, the elevations appear to be modest. Thus, electrical countershock does not obscure the diagnosis of myocardial infarction or impair quantitative assessment of the extent of myocardial damage based on analysis of serum MB CPK activity.
对30例接受直流电击除颤治疗的患者、17例急性心肌梗死患者和25名正常受试者连续测定血清总肌酸磷酸激酶(CPK)和MB型CPK活性水平。此外,对11只闭胸麻醉犬每隔15秒进行10次重复电击除颤,每次电击能量为240焦耳,连续测定血清总CPK和MB型CPK。正常受试者血清中MB型CPK低于4毫国际单位(mIU)/毫升。心肌梗死患者总CPK水平升高程度与接受心脏复律治疗的患者相当,其MB型CPK活性显著升高,峰值平均为39±6 mIU/毫升(均值±标准误)。30例接受除颤治疗的患者中有15例总CPK活性升高,在4小时内达到峰值。在该组中,MM型CPK升高是CPK活性总体升高的原因。两名患者在心脏复律后观察到MB型CPK有适度升高(分别为11和13 mIU/毫升)。所有11只犬在除颤后总CPK均升高,在6小时内峰值达到1888±410 mIU/毫升。6只犬MB型CPK活性升高(52±6 mIU/毫升),4天后组织学检查显示有心肌坏死。结果表明:(1)强烈、重复的电击除颤对犬造成的心肌损伤与血清MB型CPK升高有关;(2)患者常规使用的除颤一般不会造成心肌损伤和血清MB型CPK升高。虽然除颤后偶尔会出现MB型CPK释放到血清中,这可能反映心肌损伤,但升高幅度似乎较小。因此,电击除颤不会掩盖心肌梗死的诊断,也不会影响基于血清MB型CPK活性分析对心肌损伤程度的定量评估。