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心脏导管插入术后血浆肌酸磷酸激酶升高的来源测定。

Determination of the origin of elevated plasma CPK after cardiac catheterization.

作者信息

Roberts R, Sobel B E, Ludbrook P A

出版信息

Cathet Cardiovasc Diagn. 1976;2(4):329-36. doi: 10.1002/ccd.1810020405.

Abstract

Episodes of chest pain are not common in patients undergoing cardiac catheterization. The diagnostic implications of this symptom may be complicated by the occasional appearance of electrocardiographic changes mimicking those seen in acute myocardial infarction, and by the frequent elevation of conventionally measured serum enzymes. Exclusion of infarction is particularly important when coronary revascularization is contemplated. Since the MB CPK isoenzyme is relatively specific to myocardium, we assayed CPK isoenzymes in plasma samples from 184 patients undergoing cardiac catheterization to determine whether CPK elevations accompanying catheterization can be distinguished from those associated with myocardial infarction. Samples were obtained every 2 hr for 24 hr, and CPK isoenzymes quantified by a kinetic fluorometric method. Total plasma CPK increased in all patients (mean peak 0.238 +/- 0.042 (SD) IU/ml) but MB CPK remained normal in 181 patients (less than 0.005 IU/ml). In three remaining patients, MB CPK was elevated and myocardial infarction was confirmed by 99mTc (SN) pyrophosphate scan. Twelve patients after catheterization, in whom no intramuscular premedication was given, exhibited only minimal elevation of total plasma CPK. In contrast, 100 control patients with acute myocardial infarction exhibited peak total CPK activity averaging 0.833 +/- 0.037 (SD), and MB CPK was elevated in all cases (0.078 +/- 0.027 (SD) IU/ml). Thus, CPK elevations after catheterization reflect release of enzyme from noncardiac sources rather than from injured myocardium. Furthermore, increased plasma MB CPK activity may be considered a reliable index of myocardial infarction in patients undergoing cardiac catheterization.

摘要

胸痛发作在接受心导管检查的患者中并不常见。这种症状的诊断意义可能会因偶尔出现类似急性心肌梗死的心电图变化以及常规测量的血清酶频繁升高而变得复杂。当考虑进行冠状动脉血运重建时,排除梗死尤为重要。由于肌酸磷酸激酶(CPK)的MB同工酶对心肌相对特异,我们检测了184例接受心导管检查患者血浆样本中的CPK同工酶,以确定导管检查伴随的CPK升高是否可与心肌梗死相关的升高相区分。每2小时采集样本,共采集24小时,并采用动力学荧光法对CPK同工酶进行定量。所有患者的血浆总CPK均升高(平均峰值为0.238±0.042(标准差)IU/ml),但181例患者的MB CPK仍正常(低于0.005 IU/ml)。其余3例患者的MB CPK升高,99mTc(锝)焦磷酸盐扫描证实为心肌梗死。12例未给予肌肉注射术前用药的导管检查后患者,血浆总CPK仅出现轻微升高。相比之下,100例急性心肌梗死对照患者的总CPK活性峰值平均为0.833±0.037(标准差),所有病例的MB CPK均升高(0.078±0.027(标准差)IU/ml)。因此,导管检查后的CPK升高反映了酶从非心脏来源的释放,而非来自受损心肌。此外,血浆MB CPK活性升高可被视为接受心导管检查患者心肌梗死的可靠指标。

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