Details

Autor(en) / Beteiligte

• Mayer, Katharina
• Ndrepepa, Gjin
• Schroeter, Mira
• Emmer, Christopher
• Bernlochner, Isabell
• Schüpke, Stefanie
• Gewalt, Senta
• Hilz, Raphaela
• Coughlan, John Joseph
• Aytekin, Alp
• Heyken, Clarissa
• Morath, Tanja
• Schunkert, Heribert
• Laugwitz, Karl-Ludwig
• Sibbing, Dirk
• Kastrati, Adnan

Titel

High on-aspirin treatment platelet reactivity and restenosis after percutaneous coronary intervention: results of the Intracoronary Stenting and Antithrombotic Regimen-ASpirin and Platelet Inhibition (ISAR-ASPI) Registry

Ist Teil von

• Clinical research in cardiology, 2023-09, Vol.112 (9), p.1231-1239

Ort / Verlag

Berlin/Heidelberg: Springer Berlin Heidelberg

Erscheinungsjahr

2023

Link zum Volltext

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• Objective The aim of this study was to assess the association between high on-aspirin treatment platelet reactivity (HAPR) and the subsequent risk of restenosis after percutaneous coronary intervention (PCI) with predominantly drug-eluting stents. Background The association between HAPR and subsequent risk of restenosis after PCI is unclear. Methods This study included 4839 patients undergoing PCI (02/2007–12/2011) in the setting of the Intracoronary Stenting and Antithrombotic Regimen-ASpirin and Platelet Inhibition (ISAR-ASPI) registry. Platelet function was assessed with impedance aggregometry using the multi-plate analyzer immediately before PCI and after intravenous administration of aspirin (500 mg). The primary outcome was clinical restenosis, defined as target lesion revascularization at 1 year. Secondary outcomes included binary angiographic restenosis and late lumen loss at 6- to 8-month angiography. Results The upper quintile cut-off of platelet reactivity measurements (191 AU × min) was used to categorize patients into a group with HAPR (platelet reactivity > 191 AU × min; n =  952) and a group without HAPR (platelet reactivity ≤ 191 AU × min; n =  3887). The primary outcome occurred in 94 patients in the HAPR group and 405 patients without HAPR (cumulative incidence, 9.9% and 10.4%; HR = 0.96, 95% CI 0.77–1.19; P =  0.70). Follow-up angiography was performed in 73.2% of patients. There was no difference in binary restenosis (15.2% vs. 14.9%; P =  0.79) or late lumen loss (0.32 ± 0.57 vs. 0.32 ± 0.59 mm; P =  0.93) between patients with HAPR versus those without HAPR. Conclusions This study did not find an association between HAPR, measured at the time of PCI, and clinical restenosis at 1 year after PCI. Graphical abstract