Sax H, Contesse J, Dubach P, Reinhart W H
Kantonsspital, Chur, Switzerland.
Acta Cardiol. 1997;52(5):423-30.
Creatine kinase (CK) and its isoenzyme CK-MB are important tools for the diagnosis of acute myocardial infarction. The content of CK-MB relative to total CK in myocardial cells is variable; it is low in normal myocardium and increased several-fold in hypoxic myocardium. We tested the hypothesis that CK-MB mass (CK-MBm) could be related to cardiovascular history, preinfarctional medication and clinical course during myocardial infarction. In a prospective study CK and CK-MBm were measured 0, 6, 12, 18, 24, 36, 48 and 72 h after the admission to the coronary care unit. Peak values and areas under the curve (AUC) were determined and normalized for total CK activity (CK-MBm/CK). Of 185 patients with acute chest pain, 70 patients had 71 acute myocardial infarctions and were enrolled in the study. A history of chronic angina pectoris or hypertension had no influence on CK-MBm/CK levels. In contrast, treatment with beta-blockers before infarction resulted in a lower relative CK-MBm peak value (CK-MBm/CK 6.0 (median value), range 3.1-15.3, versus 7.0, range 0.5-17.3: p < 0.05). Other drugs had no influence. Patients with persistent pain on admission tended to have higher relative CK-MBm values (peak CK-MBm/CK: 6.8, range 0.5-17.3, versus 5.3, range 1.4-7.9, p = 0.08; AUC CK-MBm/CK: 0.05, range 0.01-0.10, versus 0.03, range 0.01-0.06, p < 0.05). Three vessel disease on coronary angiography was associated with higher peak CK-MBm/CK values during the acute phase of myocardial infarction than those with 1-2 vessel disease (Peak CK-MBm/CK: 7.9, range 5.5-17.3, versus 6.4, range 3.1-10.2, p < 0.05; AUC CK-MBm/CK: 0.06, range 0.02-0.11, versus 0.04, range 0.02-0.07, p < 0.05). We conclude that relative CK-MBm/CK levels reflect to a certain degree the extent of the coronary disease and that preinfarctional beta-blockade may result in lower CK-MBm levels.
肌酸激酶(CK)及其同工酶CK-MB是诊断急性心肌梗死的重要工具。心肌细胞中CK-MB相对于总CK的含量是可变的;在正常心肌中含量较低,而在缺氧心肌中会增加几倍。我们检验了这样一个假设,即CK-MB质量(CK-MBm)可能与心血管病史、心肌梗死前用药及心肌梗死期间的临床病程有关。在一项前瞻性研究中,于冠心病监护病房入院后0、6、12、18、24、36、48和72小时测定CK和CK-MBm。确定峰值和曲线下面积(AUC),并根据总CK活性进行标准化(CK-MBm/CK)。在185例急性胸痛患者中,70例发生了71次急性心肌梗死并纳入研究。慢性心绞痛或高血压病史对CK-MBm/CK水平无影响。相比之下,梗死前使用β受体阻滞剂导致相对CK-MBm峰值较低(CK-MBm/CK中位数为6.0,范围3.1 - 15.3,而未使用β受体阻滞剂者中位数为7.0,范围0.5 - 17.3:p < 0.05)。其他药物无影响。入院时持续疼痛的患者往往具有较高的相对CK-MBm值(峰值CK-MBm/CK:6.8,范围0.5 - 17.3,而无痛者为5.3,范围1.4 - 7.9,p = 0.08;AUC CK-MBm/CK:0.05,范围0.01 - 0.10,而无痛者为0.03,范围0.01 - 0.06,p < 0.05)。冠状动脉造影显示三支血管病变的患者在心肌梗死急性期的CK-MBm/CK峰值高于单支或两支血管病变的患者(峰值CK-MBm/CK:7.9,范围5.5 - 17.3,而单支或两支血管病变者为6.4,范围3.1 - 10.2,p < 0.05;AUC CK-MBm/CK:0.06,范围0.02 - 0.11,而单支或两支血管病变者为0.04,范围0.02 - 0.07,p < 0.05)。我们得出结论,相对CK-MBm/CK水平在一定程度上反映了冠状动脉疾病的程度,且梗死前使用β受体阻滞剂可能导致较低的CK-MBm水平。