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Periprocedural type IVa myocardial infarction and the importance of platelet inhibition
  1. Anoop S V Shah,
  2. Nicholas L Mills,
  3. David E Newby
  1. BHF/University Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK
  1. Correspondence to Professor David E Newby, BHF/University Centre for Cardiovascular Science, Chancellor's Building, Royal Infirmary, Little France, Edinburgh EH16 4SB, UK;

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More than two million percutaneous coronary intervention (PCI) procedures are performed worldwide each year.1 Periprocedural myocardial infarction is one of the most common complications with evidence of myonecrosis in almost half of all PCI procedures.2 Defining periprocedural myocardial infarction is, however, not straightforward. The latest expert consensus on the Universal Definition of Myocardial Infarction defines PCI-related myocardial infarction (type IVa) as either an increase in cardiac troponin 5-fold greater than the 99th percentile upper reference limit (URL) in patients with normal baseline values (≤99th percentile URL), or a more than 20% increase in patients with already elevated but stable or falling baseline troponin concentrations.3 In addition to this, the definition further stipulates that clinical evidence of myocardial ischaemia, angiographic loss of patency of a major or minor coronary artery patency or imaging evidence of new loss of viable myocardium or new regional wall motion abnormality is necessary for a diagnosis of type IVa myocardial infarction.3

Leonardi and colleagues, in this issue of Heart,4 reclassified patients originally recruited in the CHAMPION PLATFORM trial4 as having periprocedural myocardial infarction using 3-fold to 10-fold increases in cardiac biomarkers above the 99th percentile of the URL. The authors used creatine kinase(CK)-MB, and not troponin, in the adjudication of periprocedural myocardial infarction. Several important observations arise from Leonardi's study. First, with the adoption of a 3-fold increase in CK-MB, they showed a more than 30% relative reduction in the number of …

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  • Contributors All authors contributed to writing the manuscript.

  • Funding British Heart Foundation Chair (CH/09/002), Intermediate Fellowship (FS/10/024/28266) and Clinical Research Scholarship (SS/CH/09/002).

  • Competing interests NLM has received honoraria from Abbott Diagnostics and acted as a consultant for Beckman-Coultar and Abbott Diagnostics. All other authors have no competing interests or financial disclosures to declare.

  • Provenance and peer review Commissioned; internally peer reviewed.

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