Ticagrelor or Prasugrel in Patients With Acute Coronary Syndrome in Relation to Estimated Glomerular Filtration Rate.

Objectives: The aim of this study was to assess the safety and efficacy of ticagrelor versus prasugrel for patients with acute coronary syndrome (ACS) according to their estimated glomerular filtration rates (eGFRs).
Background: The outcomes of ticagrelor versus prasugrel in patients with ACS according to eGFR have not been defined.
Methods: Patients (n = 4,012) were categorized into 3 groups: low eGFR (<60 mL/min/1.73 m ² ), intermediate eGFR (≥60 and <90 mL/min/1.73 m ² ), and high eGFR (≥90 mL/min/1.73 m ² ). The primary endpoint was a composite of all-cause death, myocardial infarction, and stroke; the secondary safety endpoint was Bleeding Academic Research Consortium types 3 to 5 bleeding, both at 1 year.
Results: Patients with low eGFRs had a higher risk for the primary endpoint compared with patients with intermediate eGFRs (adjusted HR: 1.89; 95% CI: 1.46-2.46]) and those with high eGFRs (adjusted HR: 2.33; 95% CI: 1.57-3.46). A risk excess for low eGFR was also observed for bleeding (adjusted HR: 1.55 [95% CI: 1.12-2.13] vs intermediate eGFR; adjusted HR: 1.59 [95% CI: 1.01-2.50] vs high eGFR). However, eGFR did not affect the relative efficacy and safety of ticagrelor versus prasugrel. In patients with low eGFR, the primary endpoint occurred in 20.5% with ticagrelor and in 14.7% with prasugrel (HR: 1.47; 95% CI: 1.04-2.08; P = 0.029); there was no significant difference in bleeding.
Conclusions: These results show that among patients with ACS, reduction of eGFR is associated with increased risk for ischemic and bleeding events but has no significant impact on the relative efficacy and safety of ticagrelor versus prasugrel. (Prospective, Randomized Trial of Ticagrelor Versus Prasugrel in Patients With Acute Coronary Syndrome [ISAR-REACT 5]; NCT01944800).
Competing Interests: Funding Support and Author Disclosures This research was supported by a grant (FKZ 81X1600501) from the German Center for Cardiovascular Research and Deutsches Herzzentrum München. Dr Angiolillo has received grants and personal fees from Amgen, Aralez, AstraZeneca, Bayer, Biosensors, Boehringer Ingelheim, Bristol Myers Squibb, Chiesi, Daiichi-Sankyo, Eli Lilly, Janssen, Merck, Sanofi, and CeloNova; has received personal fees from Haemonetics, PhaseBio, PLx Pharma, Pfizer, The Medicines Company, and St. Jude Medical; and has received grants from CSL Behring, Eisai, Gilead, Idorsia Pharmaceuticals, Matsutani Chemical Industry, Novartis, Osprey Medical, Renal Guard Solutions, and the Scott R. MacKenzie Foundation. Dr Hochholzer has received personal fees from Bayer Vital, Boehringer Ingelheim, Bristol Myers Squibb, Daiichi-Sankyo, Novartis, AstraZeneca, and The Medicines Company. Dr Kufner has received personal fees from Bristol Myers Squibb, AstraZeneca, and Translumina. Dr Sager has received grants from the European Research Council, Else-Kröner-Fresenius-Stiftung, Deutsche Herzstiftung, and Deutsche Forschungsgemeinschaft. Dr Neumann has received personal fees from Amgen, Boehringer Ingelheim, Daiichi-Sankyo, Novartis, and Ferrer; has received grants and personal fees from Pfizer, Biotronik, Edwards Lifesciences, Bayer Healthcare, and Boston Scientific; and has received grants from Medtronic and GlaxoSmithKline outside the submitted work. Dr Schüpke has received the Else Kröner memorial grant from Else Kröner-Fresenius Stiftung; has received financial support from the German Center for Cardiovascular Research; has received consulting fees from Bayer Vital; and has received lecture fees from Daiichi-Sankyo and Biopas Laboratories. Dr Sibbing has received personal fees from Daichi-Sankyo, Sanofi, AstraZeneca, Bayer, Pfizer, and Servier. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)