P2Y 12 Inhibition in Patients Requiring Oral Anticoagulation After Percutaneous Coronary Intervention: The SWAP-AC-2 Study.

Autor: Ortega-Paz L; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA. Electronic address: https://twitter.com/Ortega_Paz., Bor W; St. Antonius Hospital, Nieuwegein, the Netherlands., Franchi F; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., van den Broek WWA; St. Antonius Hospital, Nieuwegein, the Netherlands., Rollini F; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Giordano S; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Galli M; Maria Cecilia Hospital, GVM Care & Research, Cotignola, Italy., Been L; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Ghanem G; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Shalhoub A; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Garabedian H; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Al Saleh T; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Uzunoglu E; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Zhou X; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Rivas A; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Pineda AM; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Suryadevara S; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Soffer D; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Mahowald MK; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Choi CY; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Zenni MM; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA., Phoenix F; Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, United Kingdom., Ajjan RA; Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, United Kingdom., Ten Berg JM; St. Antonius Hospital, Nieuwegein, the Netherlands., Angiolillo DJ; Division of Cardiology, University of Florida College of Medicine-Jacksonville, Jacksonville, Florida, USA. Electronic address: dominick.angiolillo@jax.ufl.edu.
Jazyk: angličtina
Zdroj: JACC. Cardiovascular interventions [JACC Cardiovasc Interv] 2024 Jun 10; Vol. 17 (11), pp. 1356-1370. Date of Electronic Publication: 2024 Apr 07.
DOI: 10.1016/j.jcin.2024.03.027
Abstrakt: Background: Among patients treated with a novel oral anticoagulant (NOAC) undergoing percutaneous coronary intervention (PCI), combination therapy with clopidogrel (ie, known as dual antithrombotic therapy [DAT]) is the treatment of choice. However, there are concerns for individuals with impaired response to clopidogrel.
Objectives: The authors sought to assess the pharmacodynamic (PD) effects of clopidogrel vs low-dose ticagrelor in patients with impaired clopidogrel response assessed by the ABCD-GENE score.
Methods: This was a prospective, randomized PD study of NOAC-treated patients undergoing PCI. Patients with an ABCD-GENE score ≥10 (n = 39), defined as having impaired clopidogrel response, were randomized to low-dose ticagrelor (n = 20; 60 mg twice a day) or clopidogrel (n = 19; 75 mg once a day). Patients with an ABCD-GENE score <10 (n = 42) were treated with clopidogrel (75 mg once a day; control cohort). PD assessments at baseline and 30 days post-randomization (trough and peak) were performed to assess P2Y 12 signaling (VerifyNow P2Y 12 reaction units [PRU], light transmittance aggregometry, and vasodilator-stimulated phosphoprotein); makers of thrombosis not specific to P2Y 12 signaling were also assessed. The primary endpoint was PRU (trough levels) at 30 days.
Results: At 30 days, PRU levels were reduced with ticagrelor-based DAT compared with clopidogrel-based DAT at trough (23.0 [Q1-Q3: 3.0-46.0] vs 154.5 [Q1-Q3: 77.5-183.0]; P < 0.001) and peak (6.0 [Q1-Q3: 4.0-14.0] vs 129.0 [Q1-Q3: 66.0-171.0]; P < 0.001). Trough PRU levels in the control arm (104.0 [Q1-Q3: 35.0-167.0]) were higher than ticagrelor-based DAT (P = 0.005) and numerically lower than clopidogrel-based DAT (P = 0.234). Results were consistent by light transmittance aggregometry and vasodilator-stimulated phosphoprotein. Markers measuring other pathways leading to thrombus formation were largely unaffected.
Conclusions: In NOAC-treated patients undergoing PCI with an ABCD-GENE score ≥10, ticagrelor-based DAT using a 60-mg, twice-a-day regimen reduced platelet P2Y 12 reactivity compared with clopidogrel-based DAT. (Tailoring P2Y12 Inhibiting Therapy in Patients Requiring Oral Anticoagulation After PCI [SWAP-AC-2]; NCT04483583).
Competing Interests: Funding Support and Author Disclosures The study was funded by institutional grants from the University of Florida. Dr Franchi has received consulting fees or honoraria from AstraZeneca; and institutional grants from PLx Pharma and the Scott R. MacKenzie Foundation. Dr Galli has received consulting fees or honoraria from Terumo, outside the present work. Dr Ajjan has received institutional research grants and honoraria/educational support/consultancy from Abbott Diabetes Care, AstraZeneca, Bayer, Boehringer Ingelheim, Eli Lilly, GlaxoSmithKline, Menarini Pharmaceuticals, Novo Nordisk, and Roche. Dr Angiolillo has received consulting fees or honoraria from Abbott, Amgen, AstraZeneca, Bayer, Biosensors, Boehringer Ingelheim, Bristol Myers Squibb, Chiesi, CSL Behring, Daiichi-Sankyo, Eli Lilly, Faraday, Haemonetics, Janssen, Merck, Novartis, PhaseBio, PLx Pharma, Pfizer, and Sanofi; and has received institutional research grants from Amgen, AstraZeneca, Bayer, Biosensors, CeloNova, CSL Behring, Daiichi-Sankyo, Eisai, Eli Lilly, Faraday, Gilead, Idorsia, Janssen, Matsutani Chemical Industry Co., Merck, Novartis, and the Scott R. MacKenzie Foundation. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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