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Ticagrelor versus prasugrel for PCI-managed myocardial infarction: the battle of the giants continues
  1. Robert F Storey1,2
  1. 1Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK
  2. 2Directorate of Cardiology and Cardiothoracic Surgery, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK
  1. Correspondence to Professor Robert F Storey, Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield S10 2RX, UK; r.f.storey{at}sheffield.ac.uk

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Pharmacodynamic data and large phase III clinical trials have clearly established ticagrelor and prasugrel as first-line therapies in acute coronary syndrome (ACS) in preference to clopidogrel, which is unreliable as a platelet inhibitor due to interindividual variability in the efficiency of metabolising this prodrug to its active form. However, debate and controversy continue to surround the choice of ticagrelor versus prasugrel as the preferred oral P2Y12 receptor antagonist (‘P2Y12 inhibitor’) for acute management of patients with myocardial infarction (MI) who are managed with percutaneous coronary intervention (PCI). In this issue of Heart, Venetsanos and colleagues present analyses from the SWEDEHEART (Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies) registry that compare the clinical outcomes associated with ticagrelor and prasugrel in 37 990 PCI-managed patients with MI.1 Such observational comparisons are inevitably impeded by the select nature of the prasugrel-treated population who tend to be younger and at lower risk than the broader population selected for treatment with ticagrelor in view of regulatory restrictions on the use of the standard regimen of prasugrel. However, SWEDEHEART benefits from a very large population with a high usage of ticagrelor over recent years that allows for a fair adjustment of HRs according to differences between the ticagrelor-treated and prasugrel-treated populations, as well as the opportunity to perform propensity-score matching analysis. The findings show no …

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Footnotes

  • Contributors RFS is the sole contributing author.

  • 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 RFS reports institutional research grants/support from AstraZeneca, Cytosorbents, GlyCardial Diagnostics and Thromboserin; consultancy fees from Amgen, AstraZeneca, Bayer, Bristol Myers Squibb/Pfizer, Cytosorbents, GlyCardial Diagnostics, Haemonetics, HengRui, Idorsia, PhaseBio, Portola, Sanofi Aventis and Thromboserin; and honoraria from AstraZeneca, Bayer, Bristol Myers Squibb/Pfizer, Intas Pharmaceuticals and Medscape.

  • 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; externally peer reviewed.

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