Periprocedural myocardial infarction: review and classification

Abstract

Technical 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.

Figure 1

Unadjusted mortality after percutaneous coronary intervention (PCI) through 6 months for increments of periprocedural peak creatine kinase (CK)‐ MB elevation as a multiple of the upper limit of normal (ULN). Reprinted with permission from Elsevier.14

Figure 2

One‐year death among all patients in the ACUITY trial according to the presence or absence of periprocedural myocardial infarction (MI) or spontaneous MI. Abbreviations: PCI, percutaneous coronary intervention. Reprinted with permission from Oxford University Press.8