Slow but steady progress towards understanding peri-procedural myocardial infarction.

Despite over two decades of research, the clinical significance and optimal management of peri-procedural myocardial infarction (PMI) remains a matter of considerable controversy. The topic is important because percutaneous coronary intervention (PCI) is the dominant method for revascularization, with over a million patients around the world receiving the therapy each year. The large body of data correlating PMI with adverse clinical outcomes provides compelling evidence that it may be a clinically meaningful complication of PCI. However, our knowledge of this entity is limited by the fact that virtually all data published to date are retrospective, demonstrate an association with outcomes but not a causal relationship, pre-date the use of contemporary cardiac troponin (cTn) assays with the recommended 99th percentile cut-off value for the upper reference limit (URL), and do not provide an explanation for the fact that even a trivial elevation in a biomarker is associated with an unfavourable outcome. From a clinician’s perspective, the unanswered questions are—whether one should routinely screen for PMI, which patients need to be observed in hospital for a longer duration after PMI, what are the therapeutic implications, what should we tell patients who sustained a PMI despite an otherwise successful procedure, and is PMI prognostically equivalent to spontaneous myocardial infarction (MI). The recently published third universal definition of MI attempts to provide some guidance by defining PMI in patients with normal (,99th percentile URL) baseline cTn concentrations as an elevation of .5× URL within 48 h of the procedure together with either (i) evidence of prolonged (.20 min) ischaemia as demonstrated by chest pain; (ii) ischaemic ST changes or new pathological Q waves; (iii) angiographic evidence of a flow-limiting complication, such as of loss of patency of a side branch, persistent slow-flow or no-reflow, embolization; or (iv) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. The key changes from the second universal definition are that cTn is now the only biomarker recommended, the threshold has been increased from 3× URL to 5× URL, and clinical criteria have been added for defining PMI. Nevertheless, even this revised definition is far from perfect, with the authors of the document acknowledging that it remains arbitrary.