Fabio Mangiacapra1, Mariano Pellicano2, Luigi Di Serafino2, Edoardo Bressi3, Aaron J Peace4, Giuseppe Di Gioia2, Carmine Morisco5, Jozef Bartunek2, William Wijns6, Bernard De Bruyne2, Emanuele Barbato7. 1. Cardiovascular Research Center Aalst, OLV Clinic, Aalst, Belgium; Unit of Cardiovascular Science, Department of Medicine, Campus Bio-Medico University, Rome, Italy. 2. Cardiovascular Research Center Aalst, OLV Clinic, Aalst, Belgium. 3. Unit of Cardiovascular Science, Department of Medicine, Campus Bio-Medico University, Rome, Italy. 4. Cardiovascular Research Center Aalst, OLV Clinic, Aalst, Belgium; Altnagelvin Hospital, WHSCT, Londonderry, Northern Ireland, United Kingdom. 5. Department of Advanced Biomedical Sciences, Federico II University, Naples, Italy. 6. Cardiovascular Research Center Aalst, OLV Clinic, Aalst, Belgium; The Lambe Institute for Translational Medicine and Curam, National University of Ireland, Galway, Ireland; Saolta University Healthcare Group, Galway, Ireland. 7. Cardiovascular Research Center Aalst, OLV Clinic, Aalst, Belgium; Department of Advanced Biomedical Sciences, Federico II University, Naples, Italy. Electronic address: emanuele.barbato@olvz-aalst.be.
Abstract
BACKGROUND AND AIMS: Increased platelet reactivity (PR) associated with variable degree of coronary microvascular impairment has been reported in patients on clopidogrel after elective percutaneous coronary intervention (PCI). Prasugrel provides more potent platelet inhibition than clopidogrel, though it is unknown whether it might also prevent PCI-related platelet activation. In stable patients undergoing elective PCI, we compared: (1) the effects of prasugrel vs. clopidogrel on peri-procedural variations of PR and (2) the correlation of platelet inhibition potency with PCI-induced coronary microvascular impairment. METHODS:Forty thienopyridine-naive patients were randomly assigned to a loading dose of either prasugrel 60 mg (n = 20) or clopidogrel 600 mg (n = 20) at least 12 h before PCI. At the time of PCI, we assessed adenosine diphosphate (ADP)-induced PR with the Multiplate Analyzer, and the pressure-derived index of microvascular resistance (IMR) in the treated coronary, both at baseline and post-procedure. RESULTS:ADP-induced PR was significantly lower in the prasugrel compared with clopidogrel group both at baseline (16.0 ± 8.7 vs. 33.9 ± 18.0 aggregation units [AU], p < 0.001) and post-procedure (16.2 ± 9.0 vs. 39.0 ± 18.6 AU, p < 0.001). A significant peri-procedural increase in PR was observed in the clopidogrel group (p = 0.008), but not in the prasugrel group (p = 0.822). A significant correlation was found between IMR and PR both at baseline (r = 0.458, p = 0.003) and post-PCI (r = 0.487, p = 0.001). CONCLUSIONS: A loading dose of prasugrel compared with clopidogrel is able to attenuate PCI-related increase in PR in patients with stable CAD undergoing PCI, which might contribute to the beneficial effect of this drug on peri-procedural coronary microvascular function.
RCT Entities:
BACKGROUND AND AIMS: Increased platelet reactivity (PR) associated with variable degree of coronary microvascular impairment has been reported in patients on clopidogrel after elective percutaneous coronary intervention (PCI). Prasugrel provides more potent platelet inhibition than clopidogrel, though it is unknown whether it might also prevent PCI-related platelet activation. In stable patients undergoing elective PCI, we compared: (1) the effects of prasugrel vs. clopidogrel on peri-procedural variations of PR and (2) the correlation of platelet inhibition potency with PCI-induced coronary microvascular impairment. METHODS: Forty thienopyridine-naive patients were randomly assigned to a loading dose of either prasugrel 60 mg (n = 20) or clopidogrel 600 mg (n = 20) at least 12 h before PCI. At the time of PCI, we assessed adenosine diphosphate (ADP)-induced PR with the Multiplate Analyzer, and the pressure-derived index of microvascular resistance (IMR) in the treated coronary, both at baseline and post-procedure. RESULTS:ADP-induced PR was significantly lower in the prasugrel compared with clopidogrel group both at baseline (16.0 ± 8.7 vs. 33.9 ± 18.0 aggregation units [AU], p < 0.001) and post-procedure (16.2 ± 9.0 vs. 39.0 ± 18.6 AU, p < 0.001). A significant peri-procedural increase in PR was observed in the clopidogrel group (p = 0.008), but not in the prasugrel group (p = 0.822). A significant correlation was found between IMR and PR both at baseline (r = 0.458, p = 0.003) and post-PCI (r = 0.487, p = 0.001). CONCLUSIONS: A loading dose of prasugrel compared with clopidogrel is able to attenuate PCI-related increase in PR in patients with stable CAD undergoing PCI, which might contribute to the beneficial effect of this drug on peri-procedural coronary microvascular function.
Authors: Nicholas P Iskandar; Akshay J Reddy; Allen Dang; Muhammad S Ghauri; Mildred Min; Mark Bachir; Alex Bachir; Himanshu Wagh; Nathaniel Tak; Hetal Brahmbhatt Journal: Cureus Date: 2022-08-25