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Diagnosing procedural myocardial injury following percutaneous coronary intervention: replacing confusion with consensus?
  1. William J van Gaal1,2,
  2. Adrian P Banning3
  1. 1Department of Cardiology, Northern Health, Victoria, Australia
  2. 2Department of Medicine, University of Melbourne, Victoria, Australia
  3. 3Oxford Heart Centre, Oxford University Hospitals, Oxford, UK
  1. Correspondence to Professor Adrian Banning, Consultant Cardiologist, Oxford Heart Centre, Divisional Director, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK; adrian.banning{at}ouh.nhs.uk

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Introduction

Periprocedural myocardial injury can result from clinically relevant procedural complications of percutaneous coronary intervention (PCI) such as distal embolisation, side-branch occlusion and coronary dissection.1 ,2 Measurement of biomarkers, usually either troponin or creatinine phosphokinase myocardial-banding (CK-MB), after such a complicated procedure will usually document myocyte necrosis, and using detailed cardiac magnetic resonance (CMR) with late gadolinium enhancement (LGE) these areas of myocardial injury can be visualised (figure 1). However, myocardial injury can also be diagnosed by measurement of biomarkers after clinically uneventful routine PCI procedures. While few coronary interventionalists would debate the likely adverse consequences of occluding a large diagonal branch during a PCI to the left anterior descending artery, considerable controversy persists about the relevance of elevated troponin levels in isolation following a clinically uneventful PCI.

Figure 1

An example of new late gadolinium enhancement (LGE) in a 66-year-old man following percutaneous coronary intervention for triple vessel disease. Baseline cardiac magnetic resonance (CMR) demonstrates normal, viable myocardium (panel A: short axis, and panel B: vertical long axis). During treatment of a complex lesion in the left anterior descending artery, the vessel dissected with transient slow flow. A total of four stents (total stent length 85 mm) were required to restore patency and TIMI grade III flow. Troponin I peaked at 21.9 ug/l and creatinine kinase MB peaked at 44.9 ng/ml within 24 h. The postprocedure CMR demonstrated an area of LGE (arrows) in the anteroseptal wall (panel A: short axis, and panel D: vertical long axis), indicative of irreversible myocardial necrosis equivalent to 8.3 g of myocardium.

Publication of the ‘Universal definition of Myocardial Infarction’ by the joint ESC/ACCF/AHA/WHF task force was valuable in establishing the importance of periprocedural myocardial infarction (MI) but added to the clinical debate by defining PCI-related MI (MI type …

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