Rosenblum A M, Ludbrook P A, Jaffe A S
Cathet Cardiovasc Diagn. 1984;10(6):547-52. doi: 10.1002/ccd.1810100604.
To clarify the etiology of elevations in plasma MB creatine kinase (CK) in patients after cardiac catheterization, we studied 32 consecutive patients undergoing cardiac catheterization and coronary arteriography. Total CK and MB CK were within the normal range in all patients prior to catheterization. Total CK activity rose from a mean of 61.46 +/- 33.8 IU/1 (SD) to 141 +/- 105 in the first sample after catheterization (p less than .005) and 121.6 +/- 92.4 in the second catheterization sample (p less than .0005). The MB CK activity also rose from a mean of 3.2 +/- 1.6 IU/1 prior to catheterization to a maximum value of 5.0 +/- 2.9. The mean increase in MB CK, though statistically significant (p less than .005), was only 1.8 IU/1. Only one patient's value for MB CK rose to outside of the normal range (greater than 12) likely due to cardiac injury. Thus, our data document that marked elevations in MB CK after cardiac catheterization are unusual. They likely represent cardiac muscle injury rather than MB CK released due to skeletal muscle injury induced by the catheterization itself.
为了阐明心脏导管插入术后患者血浆肌酸激酶同工酶(CK)升高的病因,我们研究了32例连续接受心脏导管插入术和冠状动脉造影的患者。在导管插入术前,所有患者的总CK和肌酸激酶同工酶均在正常范围内。总CK活性从导管插入术前的平均61.46±33.8 IU/1(标准差)升至导管插入术后第一个样本中的141±105(p<0.005),以及第二个导管插入术样本中的121.6±92.4(p<0.0005)。肌酸激酶同工酶活性也从导管插入术前的平均3.2±1.6 IU/1升至最大值5.0±2.9。肌酸激酶同工酶的平均升高虽具有统计学意义(p<0.005),但仅为1.8 IU/1。只有1例患者的肌酸激酶同工酶值升至正常范围之外(大于12),可能是由于心脏损伤。因此,我们的数据表明,心脏导管插入术后肌酸激酶同工酶的显著升高并不常见。它们可能代表心肌损伤,而非因导管插入术本身引起的骨骼肌损伤而释放的肌酸激酶同工酶。