Katharina Mayer1, Isabell Bernlochner2, Siegmund Braun3, Stefanie Schulz3, Martin Orban4, Tanja Morath3, Lisena Cala3, Petra Hoppmann2, Heribert Schunkert5, Karl-Ludwig Laugwitz6, Adnan Kastrati5, Dirk Sibbing7. 1. Deutsches Herzzentrum München, Technische Universität München, Munich, Germany. Electronic address: katharina.mayer.mt@gmx.de. 2. I. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München, Munich, Germany. 3. Deutsches Herzzentrum München, Technische Universität München, Munich, Germany. 4. Department of Cardiology, Ludwig-Maximilians-Universität, Munich, Germany. 5. Deutsches Herzzentrum München, Technische Universität München, Munich, Germany; DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany. 6. I. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München, Munich, Germany; DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany. 7. Department of Cardiology, Ludwig-Maximilians-Universität, Munich, Germany; DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany.
Abstract
BACKGROUND: Aspirin administration, as part of a dual antiplatelet treatment regimen, is essential for patients undergoing percutaneous coronary intervention (PCI). Although the correlation between high on-clopidogrel treatment platelet reactivity (HCPR) and clinical outcome is well established, data for high on-aspirin treatment platelet reactivity (HAPR) are conflicting. OBJECTIVES: The aim of the ISAR-ASPI (Intracoronary Stenting and Antithrombotic Regimen-ASpirin and Platelet Inhibition) registry was to assess the value of HAPR as a possible prognostic biomarker in PCI-treated patients with regard to clinical outcome. METHODS: From February 2007 to May 2013, we identified 7,090 consecutive PCI-treated patients with measured on-aspirin treatment platelet aggregation values directly before PCI. Platelet function was assessed with a Multiplate analyzer. The primary endpoint was death or stent thrombosis (ST) at 1 year. RESULTS: The upper quintile of patients (n = 1,414), according to Multiplate measurements, was defined as the HAPR cohort. Compared with non-HAPR patients (n = 5,676), HAPR patients showed a significantly higher risk of death or ST at 1 year (6.2% vs. 3.7%, respectively; odds ratio [OR]: 1.78; 95% confidence interval [CI]: 1.39 to 2.27; p < 0.0001). HAPR was found to be an independent predictor of the primary outcome (adjusted hazard ratio [HRadj]: 1.46; 95% CI: 1.12 to 1.89; p = 0.005). CONCLUSIONS: HAPR, measured at the time point of the PCI, is associated with a higher risk for death or ST during the first year after PCI. Present data are in support of the addition of HAPR to a panel of prognostic biomarkers in PCI-treated patients.
BACKGROUND:Aspirin administration, as part of a dual antiplatelet treatment regimen, is essential for patients undergoing percutaneous coronary intervention (PCI). Although the correlation between high on-clopidogrel treatment platelet reactivity (HCPR) and clinical outcome is well established, data for high on-aspirin treatment platelet reactivity (HAPR) are conflicting. OBJECTIVES: The aim of the ISAR-ASPI (Intracoronary Stenting and Antithrombotic Regimen-ASpirin and Platelet Inhibition) registry was to assess the value of HAPR as a possible prognostic biomarker in PCI-treated patients with regard to clinical outcome. METHODS: From February 2007 to May 2013, we identified 7,090 consecutive PCI-treated patients with measured on-aspirin treatment platelet aggregation values directly before PCI. Platelet function was assessed with a Multiplate analyzer. The primary endpoint was death or stent thrombosis (ST) at 1 year. RESULTS: The upper quintile of patients (n = 1,414), according to Multiplate measurements, was defined as the HAPR cohort. Compared with non-HAPR patients (n = 5,676), HAPR patients showed a significantly higher risk of death or ST at 1 year (6.2% vs. 3.7%, respectively; odds ratio [OR]: 1.78; 95% confidence interval [CI]: 1.39 to 2.27; p < 0.0001). HAPR was found to be an independent predictor of the primary outcome (adjusted hazard ratio [HRadj]: 1.46; 95% CI: 1.12 to 1.89; p = 0.005). CONCLUSIONS: HAPR, measured at the time point of the PCI, is associated with a higher risk for death or ST during the first year after PCI. Present data are in support of the addition of HAPR to a panel of prognostic biomarkers in PCI-treated patients.
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