Angiographic complications and post‐PCI myocardial enzyme elevation: Brave new world revisited

Periprocedural elevation of creatine kinase-MB isoenzyme (CK-MB) may occur in about 25% of patients who undergo percutaneous coronary intervention (PCI) [1]. Our current understanding of post-intervention CK-MB elevation is that a ‘‘threshold’’ relationship may exist between the degree of myocardial injury (as measured by CK-MB level) and adverse short and long-term outcomes [2]. Very high levels of CK-MB elevation (>83 upper limit of normal [ULN]) are associated with worse outcomes and have an additive effect to other known negative prognosticators (e.g., periprocedural Q-wave myocardial infarction [MI]) [3–5]. However, while CK-MB elevation >33 ULN is generally accepted as pathophysiologically meaningful, there are data that patients with intermediate post-PCI CK-MB levels may not require inhospital monitoring and the relation of CK-MB to other sequelae have been debatable; often this laboratory finding can be considered as a marker rather than a cause of subsequent prognosis [2,6]. In any case, CK-MB measurement after successful or uncomplicated PCI is still recommended practice [7]. In previous reports, CK-MB elevation after PCI: (i) correlates with diffuse atherosclerosis as assessed by intravascular ultrasound of the lesion as well as the ‘‘normal’’ reference segment [8], (ii) can be the trade-off for optimal stent expansion and ‘‘superior restenosis protection’’ [9], (iii) has important adverse prognosis only when is it is combined with a Q-wave development or at a level >83 ULN [5] and (iv) should not affect patient management at intermediate levels of elevation [6]. In this issue of ‘‘Catheterization and Cardiovascular Interventions’’ Fefer et al., explore the hypothesis that in patients with post-PCI elevation of CK-MB >23 ULN, visible angiographic complications predict adverse outcomes. This hypothesis indeed provides a simple way to risk stratify patients with post-procedural CK-MB elevations and has implications for shortening hospital lengthof-stay. In a retrospective study of 2,849 patients, who underwent PCI over a 2-year period at a single hospital in Canada, the authors identified 438 patients (15% of total patients) with CK-MB levels >23 ULN measured 6–24 hours post-procedure. Patients were excluded if they underwent PCI for acute ST elevation MI, had postprocedure CK-MB values that were <150% of the preprocedure value, or, in the majority of cases, because of ‘‘incomplete procedural or follow-up data. ’’ The remaining 265 patients with elevated CK-MB levels (9% of the total original patient pool) were then separated into two groups according to whether two blinded observers identified visible angiographic complications on their cineangiograms. Angiographic complications were overwhelmingly side-branch occlusions (75.7%), a known risk factor for periprocedural CK-MB elevation [2]. The third group was the control arm, comprised of 250 randomlyselected patients without post-PCI CK-MB elevation whose cineangiograms were not reviewed. Overall, the limited data available for the three groups suggests that they were well matched with respect to age, gender distribution, and use of dual anti-platelet therapy. Patients with elevated CK-MB post-PCI were more likely to present with unstable angina or non-ST elevation MI and had a greater number of vessels treated and stents deployed, in agreement with prior studies correlating atherosclerotic plaque burden with post-procedure CK-MB elevation [6,8]. Shortand long-term major adverse cardiac event (MACE) incidence was significantly greater in the group with angiographic complications compared with the group with CK-MB elevation alone (i.e., without any angiographic adverse event) or the control group (26 vs 11 vs 11% at 1 year, respectively, P 5 0.002). Indeed, most patients with identifiable angiographic