Michal Droppa1, Pascal Spahn2, Khalid Takhgiriev3, Karin A L Müller4, Ahmed Alboji5, Andreas Straub6, Dominik Rath7, Young-Hoon Jeong8, Meinrad Gawaz9, Tobias Geisler10. 1. Department of Cardiology and Cardiovascular Medicine, University Hospital of Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany. Electronic address: mdroppa@gmail.com. 2. Department of Cardiology and Cardiovascular Medicine, University Hospital of Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany. Electronic address: Pascal.Spahn@med.uni-tuebingen.de. 3. Department of Cardiology and Cardiovascular Medicine, University Hospital of Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany. Electronic address: khalidtakhgiriev@gmail.com. 4. Department of Cardiology and Cardiovascular Medicine, University Hospital of Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany. Electronic address: k.mueller@med.uni-tuebingen.de. 5. Department of Cardiology and Cardiovascular Medicine, University Hospital of Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany. Electronic address: Ahmed.Alboji@med.uni-tuebingen.de. 6. Department of Anesthesiology and Intensive Care Medicine, University Hospital of Tübingen, Hoppe-Seyler-Strasse 3, 72076 Tübingen, Germany. Electronic address: Andreas.Straub@med.uni-tuebingen.de. 7. Department of Cardiology and Cardiovascular Medicine, University Hospital of Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany. Electronic address: Dominik.Rath@med.uni-tuebingen.de. 8. Department of Internal Medicine, Gyeongsang National University, School of Medicine and Cardiovascular Center, Changwon Gyeongsang National University Hospital, Changwon-si, Gyeongsangnam-do, Republic of Korea. Electronic address: goodoctor@naver.com. 9. Department of Cardiology and Cardiovascular Medicine, University Hospital of Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany. Electronic address: Meinrad.Gawaz@med.uni-tuebingen.de. 10. Department of Cardiology and Cardiovascular Medicine, University Hospital of Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany. Electronic address: tobias.geisler@email.de.
Abstract
BACKGROUND: Effective inhibition of platelet aggregation during PCI in high risk patients with ACS is of utmost importance. The new intravenous short acting P2Y12-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 P2Y12-receptor inhibitors in patients with acute coronary syndromes (ACS). METHODS: Cangrelor was administered during PCI to 21 P2Y12-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 P2Y12-inibitors only. RESULTS: 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). CONCLUSION: We demonstrate significantly improved platelet inhibition during PCI in ACS patients treated with cangrelor in comparison to early treatment with potent oral P2Y12-inhibitors. Cangrelor should be considered for periprocedural treatment of high risk patients with acute coronary syndrome.
BACKGROUND: Effective inhibition of platelet aggregation during PCI in high risk patients with ACS is of utmost importance. The new intravenous short acting P2Y12-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 P2Y12-receptor inhibitors in patients with acute coronary syndromes (ACS). METHODS: Cangrelor was administered during PCI to 21 P2Y12-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 P2Y12-inibitors only. RESULTS: 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). CONCLUSION: We demonstrate significantly improved platelet inhibition during PCI in ACS patients treated with cangrelor in comparison to early treatment with potent oral P2Y12-inhibitors. Cangrelor should be considered for periprocedural treatment of high risk patients with acute coronary syndrome.
Authors: Leonardo De Luca; Paolo Calabrò; Fabio Chirillo; Cristina Rolfo; Alberto Menozzi; Piera Capranzano; Maurizio Menichelli; Elisa Nicolini; Ciro Mauro; Carlo Trani; Francesco Versaci; Fabrizio Tomai; Giuseppe Musumeci; Carlo Di Mario; Martino Pepe; Sergio Berti; Carlo Cernetti; Plinio Cirillo; Diego Maffeo; Giuseppe Talanas; Marco Ferlini; Marco Contarini; Valerio Lanzilotti; Marino Scherillo; Giuseppe Tarantini; Simone Muraglia; Roberta Rossini; Leonardo Bolognese Journal: Clin Cardiol Date: 2022-06-22 Impact factor: 3.287