The clinical significance of myonecrosis, measured by cardiac troponin, in the context of percutaneous coronary intervention (PCI) is a matter of ongoing debate. The lack of substantial scientific evidence in this domain is apparent from the ever-changing definitions of periprocedural myocardial infarction and the uncertainty regarding its prognostic relevance.Myonecrosis due to PCI is common and occurs in up to 40% of cases, depending on the definition and biomarker used5. In the Third Universal Definition of Myocardial Infarction (MI), the cutoff cardiac troponin level to diagnose myonecrosis increased from 3 to 5 times the upper reference limit (URL). In contrast to previous definitions, troponin elevation needs to be associated with clinical, electrocardiographic, angiographic or cardiac imagingrelated evidence of ischaemia to be classified as a periprocedural MI, or type 4a MI. However, the occurrence of post-PCI chest pain without troponin elevation and troponin elevation without chest pain, angiographic complications or other signs of ischaemia is well documented. The Society of Cardiovascular Angiography and Interventions (SCAI) has proposed an alternative definition of “clinically significant myocardial infarction” requiring troponin levels of ≥70x upper limit of normal (ULN) or ≥35x ULN with electrocardiographic evidence of infarction.
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