Abstract

The debate over the importance of periprocedural creatinine kinase-myocardial band (CK-MB) elevation after percutaneous coronary intervention (PCI) has captured the attention of cardiologists since the early days of balloon angioplasty, when the phenomenon was first recognized and reported to have no clear association with adverse clinical sequelae.1,2 These early reports were limited by the small numbers of patients and follow-up that extended only to hospital discharge. Since then there have been numerous published studies documenting the frequency and clinical outcomes of periprocedural CK-MB elevation, most of which have implicated it in a clear relationship to later adverse outcome including increased mortality.3–9 Multiple additional reports of this adverse association have been presented only in abstract form. Moreover, previous controversies about whether these enzyme elevations actually represent myocardial infarction (MI) have been dismissed by clear evidence demonstrating myocardial necrosis in the zones of the target vessel after PCI accompanied by CK-MB elevation.10 The consistency of these findings has led to widespread acceptance of a deleterious role for periprocedural MI,11 and moderate elevations of CK-MB (>3 times the upper limit of normal [ULN]) have been regarded by many as appropriate surrogate end points for studies of coronary interventional devices and antithrombotic drug therapy. Still, some investigators have not found an association or have reported adverse outcomes only after large MI (CK-MB >5 to 10 times the ULN) or with a concurrent procedural complication for which the survival consequences are not debated.12–15 The fact that the debate continues at national meetings and has been included here in this series of controversies in cardiovascular medicine points to a need for a critical reappraisal of this literature to determine a thesis that the available data can support, while providing a clear explanation for the discrepant findings of the opposing view. As …

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