Jochen Wöhrle1, Julia Seeger2, Shqipdona Lahu3, Katharina Mayer3, Isabell Bernlochner4, Senta Gewalt3, Maurizio Menichelli5, Bernhard Witzenbichler6, Willibald Hochholzer7, Dirk Sibbing8, Salvatore Cassese3, Dominick J Angiolillo9, Rayyan Hemetsberger10, Christian Valina7, Sebastian Kufner3, Erion Xhepa3, Alexander Hapfelmeier11, Hendrik B Sager12, Michael Joner12, Gert Richardt10, Karl-Ludwig Laugwitz4, Franz Josef Neumann7, Heribert Schunkert12, Stefanie Schüpke12, Adnan Kastrati12, Gjin Ndrepepa3. 1. Department of Cardiology and Intensive Care, Medical Campus Lake Constance, Friedrichshafen, Germany. Electronic address: jochen.wohrle@t-online.de. 2. Department of Cardiology and Intensive Care, Medical Campus Lake Constance, Friedrichshafen, Germany. 3. Deutsches Herzzentrum München, Cardiology, and Technische Universität München, Munich, Germany. 4. Medizinische Klinik und Poliklinik Innere Medizin I (Kardiologie, Angiologie, Pneumologie), Klinikum rechts der Isar, Munich, Germany; German Center for Cardiovascular Research, Partner Site Munich Heart Alliance, Munich, Germany. 5. Ospedale Fabrizio Spaziani, Cardiology, Frosinone, Italy. 6. Helios Amper-Klinikum Dachau, Cardiology & Pneumology, Dachau, Germany. 7. Department of Cardiology and Angiology II, University Heart Center Freiburg Bad Krozingen, Bad Krozingen, Germany. 8. German Center for Cardiovascular Research, Partner Site Munich Heart Alliance, Munich, Germany; Klinik der Universität München, Ludwig-Maximilians-University, Cardiology, Munich, Germany. 9. Division of Cardiology, University of Florida College of Medicine, Jacksonville, Florida, USA. 10. Heart Center Bad Segeberg, Bad Segeberg, Germany. 11. Technical University of Munich, School of Medicine, Institute of General Practice and Health Services Research, Munich, Germany. 12. Deutsches Herzzentrum München, Cardiology, and Technische Universität München, Munich, Germany; German Center for Cardiovascular Research, Partner Site Munich Heart Alliance, Munich, Germany.
Abstract
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 m2), intermediate eGFR (≥60 and <90 mL/min/1.73 m2), and high eGFR (≥90 mL/min/1.73 m2). 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).
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 m2), intermediate eGFR (≥60 and <90 mL/min/1.73 m2), and high eGFR (≥90 mL/min/1.73 m2). 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).