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Editorial
Ticagrelor in stable coronary disease
  1. Lokien X van Nunen1,
  2. Nils P Johnson2
  1. 1 Department of Cardiology, Radboud University Medical Center, Nijmegen, The Netherlands
  2. 2 Division of Cardiology, Department of Medicine, University of Texas Medical School at Houston, Houston, Texas, USA
  1. Correspondence to Dr Nils P Johnson, Division of Cardiology, Department of Medicine, University of Texas Health Science Center at Houston, Houston, TX 77030, USA; nils.johnson{at}uth.tmc.edu

https://doi.org/10.1136/heartjnl-2023-323034

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    Interventional cardiology luxuriously bathes in a pool of oral P2Y12 antiplatelet medications: ticlopidine, clopidogrel, prasugrel and ticagrelor. In the coming years, all of these agents will be available generically at modest cost to healthcare systems and patients. Once price no longer distinguishes among them, two factors will drive clinical selection. First, logistical practicalities differ such as side effects (hence the near abandonment of ticlopidine), drug interactions (for example, when transitioning off intravenous cangrelor) and administration (two times per day maintenance dosing of ticagrelor instead of once daily for clopidogrel and prasugrel). Second, clinical outcomes favour prasugrel and ticagrelor over clopidogrel but only for acute myocardial infarction.

    For stable patients, clinical advantages for prasugrel and ticagrelor have proven more elusive. However, the current PROMICRO-3 study offers new data regarding the impact of modern P2Y12 agents on surrogate endpoints of myocardial blood flow and injury.1 In brief, 50 stable patients undergoing percutaneous coronary intervention (PCI) almost exclusively of the left anterior descending artery (>90% of all vessels) were randomised to loading doses of either ticagrelor or prasugrel at least 12 hours before the procedure. Coronary physiology and troponin biomarkers were measured before and after intervention. Ticagrelor significantly increased final hyperaemic myocardial blood flow, decreased myocardial resistance, and caused less myocardial injury than prasugrel.

    Ticagrelor and myocardial blood flow

    Approximately 10 years ago, 40 healthy male volunteers underwent a cross-over study of ticagrelor 180 mg versus placebo.2 During a stepwise adenosine infusion (0, 50, 80, 110, and 140 µg/kg/min), transthoracic Doppler velocity in the left anterior descending artery rose more quickly with ticagrelor than placebo but plateaued at the same level when adenosine reached 140 µg/kg/min. Further supporting an effect by ticagrelor on adenosine receptors, an infusion of theophylline (a non-selective antagonist of …

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    Footnotes

    • Contributors Both authors wrote the editorial together.

    • 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 NPJ receives internal funding from the Weatherhead PET Center for Preventing and Reversing Atherosclerosis; significant institutional research support from Neovasc/Shockwave (PET core lab for COSIRA-II, NCT05102019) and CoreAalst (PPG Global, NCT04789317); institutional licensing agreement with Boston Scientific for the smart minimum FFR algorithm commercialised under 510(k) K191008; and patents pending on diagnostic methods for quantifying aortic stenosis and TAVI physiology, and on methods to correct pressure tracings from fluid-filled catheters.

    • Provenance and peer review Commissioned; internally peer reviewed.

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