AbstractTechnical and pharmacologic advances have reduced the occurrence of large periprocedural myocardial infarction (PMI) after percutaneous coronary interventions (PCI), but PMI still occurs in 6% to 18% of the cases and is associated with impaired short‐ and long‐term survival. PMI might be due to side branch closure or flow‐limiting dissection, but is most often diagnosed after apparently uncomplicated PCI and is due to atheroembolization into the microcirculation. Various definitions of PMI are used in clinical trials, but a rise in creatine kinase‐MB greater than 3 to 8 times the upper limit of normal is consistently associated with worse prognosis, particularly as it reflects a more extensive and unstable atherosclerotic burden. On the other hand, data regarding the independent prognostic value of periprocedural troponin increase are conflicting. Some data suggest that PMI has a better prognosis than a spontaneously occurring myocardial infarction, and that its incidence is reduced with aggressive antiplatelet and statin therapy. Copyright © 2010 Wiley Periodicals, Inc.The authors have no funding, financial relationships, or conflicts of interest to disclose.
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