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September 2026 Br J Cardiol 2026;33:119 doi:10.5837/bjc.2026.044

Has the required heparin dose increased in PCI? A single-centre experience

Mohamed Kira, Mohamed Abouelasaad, Ahmed Elshafey, Mohamed Darwish, Roopa Jairaj Patil, Zaynah Zubair, Alison Calver, Simon Corbett, Richard Jabbour, Michael Mahmoudi, John Rawlins, Rohit Sirohi, James Wilkinson, Jonathan Hinton, Nick Curzen

Abstract

Introduction Unfractionated heparin (UFH) is a naturally occurring anticoagulant released from mast cells.1 It works by reversibly binding to antithrombin III (AT III) and accelerating the rate at which AT III inactivates the coagulation enzymes thrombin (factor IIa) and factor Xa. Since its discovery in 1916,2 UFH has been the most widely used anticoagulant for procedural or therapeutic indications.3 Percutaneous coronary intervention (PCI) inevitably causes vessel wall injury, which leads to activation of platelets and a localised vascular inflammatory reaction, which is prothrombotic and associated with an increased risk of acute or subacu

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