Raffaele Piccolo1, Gennaro Galasso2, Giuseppe De Luca3, Guido Parodi4, David Antoniucci4, Giovanni Esposito1, Bruno Trimarco1, Federico Piscione5. 1. Department of Advanced Biomedical Sciences, Federico II University, Via S. Pansini 5, 80131 Naples, Italy. 2. Department of Advanced Biomedical Sciences, Federico II University, Via S. Pansini 5, 80131 Naples, Italy. Electronic address: gengalas@unina.it. 3. Division of Cardiology, Ospedale "Maggiore della Carità", Eastern Piedmont University, Novara, Italy. 4. Department of Cardiology, Careggi Hospital, Florence, Italy. 5. Department of Medicine and Surgery, University of Salerno, Salerno, Italy.
Abstract
OBJECTIVE: High on-treatment platelet reactivity (HPR) is a well-known risk factor for adverse events in patients undergoing percutaneous coronary intervention (PCI). However, whether reducing platelet reactivity can lead to a lower incidence of ischemic events after PCI is still controversial. Therefore, we sought to investigate this issue by a meta-regression analysis of randomized trials. METHODS: We collected randomized trials reporting HPR rates in patients receiving different antiplatelet therapies. ΔHPR was defined as the difference between HPR rates achieved in control vs. experimental arms, and the relationship between ΔHPR and clinical outcomes was evaluated. RESULTS: Thirty trials totalling 6683 patients with a mean follow-up of 3-month were included. Reducing platelet reactivity was associated to a decreased risk of major adverse cardiac events (MACE), with a linear relationship between ΔHPR and MACE (change in tau(2) = -2.50; p = 0.023). Particularly, achieving a 10% difference in HPR rates resulted in a parallel risk reduction in MACE of about 11% (Exp((b)) = 0.98; 95% CI, 0.97-0.99). Changes in HPR predict the risk of ischemic events in patients with acute coronary syndrome (change in tau(2) = -2.52; Exp((b)) = 0.98; 95% CI, 0.97-0.99; p = 0.03), but not in patients with poor response to clopidogrel (change in tau(2) = -1.44; Exp((b)) = 0.98; 95% CI, 0.96-1.01; p = 0.19) or stable coronary artery disease (change in tau(2) = -0.14; Exp((b)) = 0.99; 95% CI, 0.94-1.05; p = 0.89). CONCLUSION: Reducing HPR occurrence decreases the risk of ischemic events in patients with acute coronary syndrome undergoing PCI, whereas a strategy of reducing platelet reactivity does not improve clinical outcomes in patients with poor response to clopidogrel or stable coronary artery disease.
OBJECTIVE: High on-treatment platelet reactivity (HPR) is a well-known risk factor for adverse events in patients undergoing percutaneous coronary intervention (PCI). However, whether reducing platelet reactivity can lead to a lower incidence of ischemic events after PCI is still controversial. Therefore, we sought to investigate this issue by a meta-regression analysis of randomized trials. METHODS: We collected randomized trials reporting HPR rates in patients receiving different antiplatelet therapies. ΔHPR was defined as the difference between HPR rates achieved in control vs. experimental arms, and the relationship between ΔHPR and clinical outcomes was evaluated. RESULTS: Thirty trials totalling 6683 patients with a mean follow-up of 3-month were included. Reducing platelet reactivity was associated to a decreased risk of major adverse cardiac events (MACE), with a linear relationship between ΔHPR and MACE (change in tau(2) = -2.50; p = 0.023). Particularly, achieving a 10% difference in HPR rates resulted in a parallel risk reduction in MACE of about 11% (Exp((b)) = 0.98; 95% CI, 0.97-0.99). Changes in HPR predict the risk of ischemic events in patients with acute coronary syndrome (change in tau(2) = -2.52; Exp((b)) = 0.98; 95% CI, 0.97-0.99; p = 0.03), but not in patients with poor response to clopidogrel (change in tau(2) = -1.44; Exp((b)) = 0.98; 95% CI, 0.96-1.01; p = 0.19) or stable coronary artery disease (change in tau(2) = -0.14; Exp((b)) = 0.99; 95% CI, 0.94-1.05; p = 0.89). CONCLUSION: Reducing HPR occurrence decreases the risk of ischemic events in patients with acute coronary syndrome undergoing PCI, whereas a strategy of reducing platelet reactivity does not improve clinical outcomes in patients with poor response to clopidogrel or stable coronary artery disease.
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