Periprocedural platelet inhibition with cangrelor in P2Y 12 -inhibitor naïve patients with acute coronary syndromes - A matched-control pharmacodynamic comparison in real-world patients

• Published in: International journal of cardiology Vol. 223; p. 848
• Main Authors: Droppa, Michal, Spahn, Pascal, Takhgiriev, Khalid, Müller, Karin A L, Alboji, Ahmed, Straub, Andreas, Rath, Dominik, Jeong, Young-Hoon, Gawaz, Meinrad, Geisler, Tobias
• Format: Journal Article
• Language: English
• Published: Netherlands 15.11.2016
• Subjects: Acute Coronary Syndrome - blood; Acute Coronary Syndrome - therapy; Adenosine Monophosphate - administration & dosage; Adenosine Monophosphate - analogs & derivatives; Adenosine Monophosphate - pharmacokinetics; Administration, Intravenous; Aged; Female; Humans; Male; Middle Aged; Percutaneous Coronary Intervention - methods; Perioperative Care - methods; Platelet Aggregation - drug effects; Platelet Function Tests - methods; Purinergic P2Y Receptor Antagonists - administration & dosage; Purinergic P2Y Receptor Antagonists - pharmacokinetics; Treatment Outcome; Multiple electrode aggregometry; Thromboelastography; Cangrelor; Acute coronary syndrome; Platelet inhibition
• ISSN: 1874-1754

Effective inhibition of platelet aggregation during PCI in high risk patients with ACS is of utmost importance. The new intravenous short acting P2Y -receptor inhibitor cangrelor is available for use in PCI-treated patients. We aimed to study platelet inhibition during treatment with cangrelor and transition phase with oral P2Y -receptor inhibitors in patients with acute coronary syndromes (ACS). Cangrelor was administered during PCI to 21 P2Y -inhibitor naïve patients with ACS. Patients received a loading dose of ticagrelor at the time of procedure or prasugrel 30min before end of the cangrelor infusion. Platelet inhibition was measured by multiple electrode aggregometry (MEA) and thromboelastography (TEG), before and after PCI, immediately and 2h after stopping the infusion. Platelet inhibition after PCI was compared to a matched cohort of patients treated with oral P2Y -inibitors only. There was a significant reduction of platelet reactivity measured by MEA-ADP from 46.7U to 17.9U and by TEG MA ADP from 43.1mm to 22.0mm before infusion and after PCI respectively (p<0.001). There was also sustained platelet inhibition after stopping of cangrelor infusion and 2h later. Significant higher platelet inhibition was observed at the end of PCI in comparison to control cohort without cangrelor (MEA 17.9U vs. 54.2U, p=0.001). We demonstrate significantly improved platelet inhibition during PCI in ACS patients treated with cangrelor in comparison to early treatment with potent oral P2Y -inhibitors. Cangrelor should be considered for periprocedural treatment of high risk patients with acute coronary syndrome.