Why the study?
Oral P2Y12 inhibitors have significant limitations in acute and high-risk PCIs due to impaired drug absorption, highlighting the need to examine intravenous cangrelor.
Cangrelor provides an attractive intravenous antiplatelet strategy to guarantee adequate periprocedural platelet inhibition in acute and high-risk PCI settings where oral P2Y12 inhibitor absorption may be impaired.
May warrant cautious use in select high-risk PCI; leaves open need for dedicated RCTs.
Dual antiplatelet therapy with acetylsalicylic acid (ASA) and an oral P2Y12 inhibitor is the standard of care to prevent thrombotic complications in patients with acute coronary syndromes undergoing percutaneous coronary intervention (PCI). However, the oral administration of P2Y12 inhibitors bears significant limitations in acute and high-risk PCIs, particularly in ST-elevation myocardial infarction (STEMI) patients, especially those presenting with cardiogenic shock (CS) and cardiac arrest (CA). In these cases, factors such as active vomiting, altered physiology, sedatives, mechanical ventilation, and therapeutic hypothermia can impair drug absorption, reducing the intended antiplatelet effect and increasing ischaemic risk. In these cases, intravenous antiplatelet strategies with ASA and cangrelor could guarantee adequate periprocedural platelet inhibition. Here, we discuss the role of cangrelor in acute and high-risk PCI settings. The pharmacokinetic and pharmacodynamic attributes of cangrelor are discussed first, underscoring the distinctive features that make cangrelor an attractive antiplatelet agent in acute PCI settings. The second part of the review summarizes the evidence from real-world studies that illustrate how cangrelor has been adopted in contemporary practice. Finally, we provide a practical guide to cangrelor use, including recommendations for transitioning from cangrelor to oral P2Y12 inhibitors after PCI.
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Zeymer et al. (2025) studied this question.
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