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Microvascular obstruction: time to bust the clot hypothesis?
  1. Sean Coffey1,
  2. Philip D Adamson2,3
  1. 1 Department of Medicine - HeartOtago, University of Otago, Dunedin, New Zealand
  2. 2 Christchurch Heart Institute, University of Otago, Christchurch, New Zealand
  3. 3 British Heart Foundation Centre for Cardiovascular Science, The University of Edinburgh, Edinburgh, UK
  1. Correspondence to Dr Sean Coffey, Department of Medicine, Otago Medical School - Dunedin Campus, University of Otago, PO Box 56, Dunedin 9054, New Zealand; sean.coffey{at}otago.ac.nz

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Primary percutaneous coronary intervention (PPCI) is a cornerstone of treatment for acute myocardial infarction (AMI). Despite major achievements in the procedure itself and in the infrastructure allowing timely delivery of PPCI, a substantial proportion of patients will suffer significant myocardial injury despite successful treatment of the epicardial coronary artery. Microvascular obstruction (MVO), due to a combination of distal thrombotic embolisation, ischaemia reperfusion injury and related endothelial dysfunction, myocardial oedema and intramyocardial haemorrhage (IMH), is postulated as a mechanism for this residual myocardial injury. When measured by cardiac magnetic resonance (CMR) early after AMI, MVO is predictive of subsequent longer-term outcomes. At the time of PPCI, potential predictors of MVO include AMI characteristics, such as anterior territory AMI, and procedurally assessed characteristics, the most common being reduced or slow intracoronary flow.

T-TIME trial

Many approaches have been proposed to minimise the extent of MVO—thrombus aspiration prior to PCI, glycoprotein IIb/IIIa inhibitors and conventional dose fibrinolysis, with no therapy showing significant clinical efficacy once assessed in randomised trials. On the basis that MVO might be reduced by reducing the overall thrombus burden, low-dose fibrinolytic therapy has been proposed as a potential treatment in this setting. The T-TIME trial examined whether low-dose (one-fifth or one-tenth full dose) intracoronary alteplase would reduce MVO and IMH when administered during PPCI, after reperfusion of the infarct related artery, but before …

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Footnotes

  • Contributors Both authors were responsible for manuscript planning. SC wrote the first draft. Both authors made critical revisions and provided intellectual content to the manuscript, approved the final version to be published and agreed to be accountable for all aspects of the work.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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