Elliott M Groves1, Deepak L Bhatt1, Philippe Gabriel Steg1, Efthymios N Deliargyris1, Gregg W Stone1, C Michael Gibson1, Christian W Hamm1, Kenneth W Mahaffey1, Harvey D White1, Dominick J Angiolillo1, Jayne Prats1, Robert A Harrington1, Matthew J Price2. 1. From the Division of Cardiology, Scripps Clinic, La Jolla, CA (E.M.G., M.J.P.); Brigham and Women's Hospital Heart & Vascular Center and Harvard Medical School, Boston, MA (D.L.B.); FACT (French Alliance for Cardiovascular clinical Trials), DHU FIRE, INSERM Unité 1148, Université Paris-Diderot, and Hôpital Bichat, Assistance-Publique-Hôpitaux de Paris, France (P.G.S.); NHLI, Imperial College, Royal Brompton Hospital, London, United Kingdom (P.G.S.); Science and Strategy Consulting Group, Basking Ridge, NJ (E.N.D.); Columbia University Medical Center and the Cardiovascular Research Foundation, New York City, NY (G.W.S.); Division of Cardiology, Beth Israel Deaconess Medical Center, Boston, MA (C.M.G.); Kerckhoff Heart and Thorax Center, Bad Nauheim, Germany (C.W.H.); Division of Cardiology (K.W.M.), Department of Medicine, Division of Cardiology (R.A.H.), Stanford University Medical School, CA; Green Lane Cardiovascular Service, Auckland, New Zealand (H.D.W.); Division of Cardiology, University of Florida, Jacksonville (D.A.); and Elysis, Llc, Carlisle, MA (J.P.). 2. From the Division of Cardiology, Scripps Clinic, La Jolla, CA (E.M.G., M.J.P.); Brigham and Women's Hospital Heart & Vascular Center and Harvard Medical School, Boston, MA (D.L.B.); FACT (French Alliance for Cardiovascular clinical Trials), DHU FIRE, INSERM Unité 1148, Université Paris-Diderot, and Hôpital Bichat, Assistance-Publique-Hôpitaux de Paris, France (P.G.S.); NHLI, Imperial College, Royal Brompton Hospital, London, United Kingdom (P.G.S.); Science and Strategy Consulting Group, Basking Ridge, NJ (E.N.D.); Columbia University Medical Center and the Cardiovascular Research Foundation, New York City, NY (G.W.S.); Division of Cardiology, Beth Israel Deaconess Medical Center, Boston, MA (C.M.G.); Kerckhoff Heart and Thorax Center, Bad Nauheim, Germany (C.W.H.); Division of Cardiology (K.W.M.), Department of Medicine, Division of Cardiology (R.A.H.), Stanford University Medical School, CA; Green Lane Cardiovascular Service, Auckland, New Zealand (H.D.W.); Division of Cardiology, University of Florida, Jacksonville (D.A.); and Elysis, Llc, Carlisle, MA (J.P.). price.matthew@scrippshealth.org.
Abstract
BACKGROUND: The influence of cangrelor on the incidence and outcomes of post-percutaneous coronary intervention (PCI) thrombocytopenia is not defined. We aimed to explore the incidence, predictors, and clinical impact of thrombocytopenia after PCI in cangrelor-treated patients. METHODS AND RESULTS: This was a pooled, patient-level analysis of the CHAMPION trials (Cangrelor Versus Standard Therapy to Achieve Optimal Management of Platelet Inhibition), which compared cangrelor with clopidogrel for prevention of thrombotic complications during and after PCI. Acquired thrombocytopenia was defined as either a drop in platelet count to <100 000 after PCI or a drop of >50% between baseline and a follow-up. The main efficacy outcome was major adverse cardiac events. The primary safety outcome was noncoronary artery bypass grafting-related Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries-defined severe bleeding at 48 hours. Patients (23 783) were enrolled, and 3009 (12.7%) received aGPI (glycoprotein IIb/IIIa inhibitor). Acquired thrombocytopenia occurred in 200 patients (0.8%). The adjusted rate of major adverse cardiovascular events at 48 hours was significantly higher in patients who developed thrombocytopenia compared with those who did not (odds ratio, 3.00; 95% confidence interval, 1.89-4.69; P<0.001), as was major bleeding (odds ratio, 14.71; 95% confidence interval, 5.96-36.30; P<0.001). GPI use was the strongest independent predictor of acquired thrombocytopenia (odds ratio, 2.93; 95% confidence interval, 2.15-3.97; P<0.0001). There was no difference in the rate of acquired thrombocytopenia in patients randomized to cangrelor or clopidogrel. CONCLUSIONS:Acquired thrombocytopenia after PCI is strongly associated with substantial early morbidity and mortality, as well as major bleeding. GPI use is a significant predictor of thrombocytopenia. Cangrelor is not associated with acquired thrombocytopenia, and its clinical efficacy and safety is consistent irrespective of thrombocytopenia occurrence. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifiers: NCT00305162, NCT00385138, and NCT01156571.
RCT Entities:
BACKGROUND: The influence of cangrelor on the incidence and outcomes of post-percutaneous coronary intervention (PCI) thrombocytopenia is not defined. We aimed to explore the incidence, predictors, and clinical impact of thrombocytopenia after PCI in cangrelor-treated patients. METHODS AND RESULTS: This was a pooled, patient-level analysis of the CHAMPION trials (Cangrelor Versus Standard Therapy to Achieve Optimal Management of Platelet Inhibition), which compared cangrelor with clopidogrel for prevention of thrombotic complications during and after PCI. Acquired thrombocytopenia was defined as either a drop in platelet count to <100 000 after PCI or a drop of >50% between baseline and a follow-up. The main efficacy outcome was major adverse cardiac events. The primary safety outcome was noncoronary artery bypass grafting-related Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries-defined severe bleeding at 48 hours. Patients (23 783) were enrolled, and 3009 (12.7%) received a GPI (glycoprotein IIb/IIIa inhibitor). Acquired thrombocytopenia occurred in 200 patients (0.8%). The adjusted rate of major adverse cardiovascular events at 48 hours was significantly higher in patients who developed thrombocytopenia compared with those who did not (odds ratio, 3.00; 95% confidence interval, 1.89-4.69; P<0.001), as was major bleeding (odds ratio, 14.71; 95% confidence interval, 5.96-36.30; P<0.001). GPI use was the strongest independent predictor of acquired thrombocytopenia (odds ratio, 2.93; 95% confidence interval, 2.15-3.97; P<0.0001). There was no difference in the rate of acquired thrombocytopenia in patients randomized to cangrelor or clopidogrel. CONCLUSIONS: Acquired thrombocytopenia after PCI is strongly associated with substantial early morbidity and mortality, as well as major bleeding. GPI use is a significant predictor of thrombocytopenia. Cangrelor is not associated with acquired thrombocytopenia, and its clinical efficacy and safety is consistent irrespective of thrombocytopenia occurrence. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifiers: NCT00305162, NCT00385138, and NCT01156571.
Authors: Davide Capodanno; Deepak L Bhatt; C Michael Gibson; Stefan James; Takeshi Kimura; Roxana Mehran; Sunil V Rao; Philippe Gabriel Steg; Philip Urban; Marco Valgimigli; Stephan Windecker; Dominick J Angiolillo Journal: Nat Rev Cardiol Date: 2021-08-23 Impact factor: 32.419