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Impact of low‐dose prasugrel on platelet reactivity and cardiac dysfunction in acute coronary syndrome patients requiring primary drug‐eluting stent implantation: A randomized comparative study
Author(s) -
Kitano Daisuke,
Takayama Tadateru,
Fukamachi Daisuke,
Migita Suguru,
Morikawa Tomoyuki,
Tamaki Takehiro,
Kojima Keisuke,
Mineki Takashi,
Murata Nobuhiro,
Akutsu Naotaka,
Sudo Mitsumasa,
Hiro Takafumi,
Hirayama Atsushi,
Okumura Yasuo
Publication year - 2020
Publication title -
catheterization and cardiovascular interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.988
H-Index - 116
eISSN - 1522-726X
pISSN - 1522-1946
DOI - 10.1002/ccd.28277
Subject(s) - prasugrel , medicine , clopidogrel , acute coronary syndrome , percutaneous coronary intervention , cardiology , conventional pci , loading dose , p2y12 , myocardial infarction
Objective The aim of this study was to compare how prasugrel and clopidogrel affect platelet aggregation reactivity, cardiac enzyme release, cardiac remodeling, and the formation of in‐stent thrombi after primary percutaneous coronary intervention (PCI). Background The advantages of using prasugrel over clopidogrel in cardiac injury following acute coronary syndrome (ACS) remain unclear. Methods A total of 78 ACS patients were randomly allocated into clopidogrel (300 mg loading/75 mg maintenance) or prasugrel (20 mg loading/3.75 mg maintenance) treatment groups, followed by undergoing primary PCI. Platelet reactivity and cardiac enzymes were measured before and after primary PCI. Moreover, cardiac function was measured by ultrasound echocardiography and coronary angioscopic observation was after primary PCI up to 8 months later. Results Antiplatelet reactivity in the prasugrel treatment group reached optimal levels (P2Y 12 reaction units [PRU] less than 262) immediately after the administration and was maintained even at 8 months, independently of the CYP2C19 genotype. Prasugrel treatment significantly suppressed creatine kinase elevation compared to clopidogrel treatment (median value 404 IU/L to 726 IU/L vs. 189 IU/L to 1,736 IU/L, p = 0.018 for maximum values) and reduced left ventricular mass (217.2–168.8 g in prasugrel, p = 0.045; 196.9–176.4 g in clopidogrel, p = 0.061). There were no significant differences in the incidence of in‐stent attached thrombi between the two groups. Conclusions Compared to clopidogrel, prasugrel produced a stable platelet aggregation inhibitory effect in patients with ACS regardless of CYP2C19 genotype, reduced cardiac enzyme release, and prevented cardiac remodeling after ACS.