Periprocedural creatine kinase‐mb elevations: Long‐term impact and clinical implications

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Abstract
Since the introduction of percutaneous transluminal coronary angioplasty (PTCA), percutaneous intervention with balloon catheters, stents, and atherectomy devices has become a widely accepted practice. The persistent complication of non‐Q‐wave myocardial infarction (MI), as evidenced by increased cardiac enzyme levels after intervention, has aroused only moderate concern because its incidence was perceived to be small and not clinically relevant. With more systematic assessments of cardiac enzymes—specifically, creatine kinase (CK) and its MB isoform—evidence has begun to clarify both the incidence and the prognosis of periprocedural non‐Q‐wave MI: It appears to occur nearly three times more often than is clinically evident across all device types (8 to 9% of all interventions) and is directly and continuously associated with adverse outcomes, including late death. Although directional and rotational atherectomy improve angiographic outcome compared with PTCA, periprocedural infarction occurs at least twice as often with these newer technologies; the incidence associated with stent placement is comparable to and possibly higher than that of PTCA. Factors that may cause elevated CK‐MB levels include distal embolization, side branch occlusion, thrombus, and coronary spasm. Analyses of the major trials of platelet glycoprotein (GP) IIb/IIIa receptor inhibitors, a class of potent antiplatelet agents, show striking effectiveness of these drugs in reducing the incidence of “enzyme‐only” or “silent” MI and in improving long‐term clinical outcomes. The findings implicate platelet mediation in the occurrence of periprocedural infarction and suggest an important role for antiplatelet therapy, particularly GP IIb/IIIa receptor inhibition, in protecting patients undergoing percutaneous intervention.

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