TY - JOUR
T1 - Relationship between platelet aggregation and stroke risk after percutaneous coronary intervention
T2 - a PENDULUM analysis
AU - Matsumaru, Yuji
AU - Kitazono, Takanari
AU - Kadota, Kazushige
AU - Nakao, Koichi
AU - Nakagawa, Yoshihisa
AU - Shite, Junya
AU - Yokoi, Hiroyoshi
AU - Kozuma, Ken
AU - Tanabe, Kengo
AU - Akasaka, Takashi
AU - Shinke, Toshiro
AU - Ueno, Takafumi
AU - Hirayama, Atsushi
AU - Uemura, Shiro
AU - Kuroda, Takeshi
AU - Takita, Atsushi
AU - Harada, Atsushi
AU - Iijima, Raisuke
AU - Murakami, Yoshitaka
AU - Saito, Shigeru
AU - Nakamura, Masato
N1 - Funding Information:
Y. Matsumaru has received remuneration from Daiichi Sakyo Co., Ltd., and Otsuka Pharmaceutical Co., Ltd. T. Kitazono has received remuneration and scholarship funds or donations from Daiichi Sakyo Co., Ltd. K. Kadota has received remuneration from Daiichi Sankyo Co., Ltd., and Sanofi K.K. K. Nakao has received remuneration from Daiichi Sankyo Co., Ltd. Y. Nakagawa has received remuneration from Bristol Myers Squibb K.K., Kowa Pharmaceutical Co., Ltd., Daiichi Sankyo Co., Ltd., Bayer Yakuhin Ltd., Sanofi K.K., Boston Scientific Corporation, and Abbott Medical Japan LLC., and research funding from Daiichi Sankyo Co., Ltd., Bayer Yakuhin Ltd., Sanofi K.K., Boston Scientific Corporation, and Abbott Medical Japan LLC. J. Shite has received remuneration from Daiichi Sankyo Co., Ltd., Nipro Corporation, Abbott Japan LLC, and Terumo Corporation. H. Yokoi has received remuneration and scholarship funds or donations from Daiichi Sankyo Co., Ltd. K. Kozuma has received remuneration and research funding from Daiichi Sankyo Co., Ltd. K. Tanabe has received remuneration from Daiichi Sankyo Co., Ltd., Sanofi K.K., AstraZeneca K.K., Abbott Medical Japan LLC., Boston Scientific Corporation, and Terumo Corporation. T. Akasaka has received remuneration from Abbot Medical Japan LLC., and Otsuka Pharmaceutical Co., Ltd., research funding from Daiichi Sankyo Co., Ltd., scholarship funds or donations from Abbot Medical Japan LLC., Nipro Corporation, and Terumo Corporation, and has a personal relationship with Terumo Corporation. T. Shinke has received remuneration and research funding from Daiichi Sankyo Co., Ltd., Bayer Yakuhin Ltd., Bristol Myers Squibb K.K., and Nippon Boehringer Ingelheim Co., Ltd. T. Ueno received consultancy fees from Japan Medical Device Technology Co., Ltd., and Nipro Corporation. A. Hirayama has received remuneration from Daiichi Sankyo Co., Ltd., Bayer Yakuhin Ltd., and Takeda Pharmaceutical Co., Ltd. S. Uemura has received remuneration from Daiichi Sankyo Co., Ltd., Nippon Boehringer Ingelheim Co., Ltd., Amgen Astellas BioPharma Co., Ltd., Abbot Medical Japan LLC., Sanofi K.K., Terumo Corporation, and Bayer Yakuhin Ltd.; and research funding from Daiichi Sankyo Co., Ltd.; and scholarship funds or donations from Daiichi Sankyo Co., Ltd., Astellas Pharma Inc., Otsuka Pharmaceutical Co., Ltd., Goodman Co., Ltd., Shionogi Inc., Sumitomo Dainippon Pharma Co., Ltd., Boston Scientific Japan K.K., Kaken Pharmaceutical Co., Ltd., Takeda Pharmaceutical Co., Ltd., Taisho Pharmaceutical Co., Ltd., Mitsubishi Tanabe Pharmaceutical Co., Ltd., Japan Lifeline Co., Ltd., MSD K.K., Nipro Corporation, Actelion Pharmaceuticals Japan Ltd., Pfizer Japan Inc., Abbot Medical Japan LLC., Sanofi K.K., Terumo Corporation, and Bayer Yakuhin Ltd. T. Kuroda, A. Takita, and A. Harada, are employees of Daiichi Sankyo Co., Ltd. Y. Murakami has received remuneration from SRD Co., Ltd. S. Saito has received consultancy fees from Japan Lifeline Inc., and Terumo Corporation; and remuneration from Daiichi Sankyo Co., Ltd, Abbott Medical Japan LLC., Boston Scientific Corporation, and Medtronic Japan Co., Ltd. M. Nakamura has received remuneration from Daiichi Sankyo Co., Ltd., Sanofi K.K., Terumo Corporation, and Bristol Myers Squibb K.K, and research funding from Daiichi Sankyo Co., Ltd., Sanofi K.K., and Bayer Yakuhin K.K. R. Iijima has no conflicts of interest to declare.
Funding Information:
We thank Sally-Anne Mitchell, PhD, of Edanz ( www.edanz.com ) for providing medical writing support, which was funded by Daiichi Sankyo Co., Ltd.
Publisher Copyright:
© 2021, The Author(s).
PY - 2022/6
Y1 - 2022/6
N2 - In patients undergoing percutaneous coronary intervention (PCI) with a stent, high on-treatment platelet reactivity may be associated with an increased risk of stroke. This post hoc analysis of the PENDULUM registry compared the risk of post-PCI stroke according to on-treatment P2Y12 reaction unit (PRU) values. Patients aged ≥ 20 years who underwent PCI were stratified by baseline PRU (at 12 and 48 h post-PCI) as either high (HPR, > 208), optimal (OPR, > 85 to ≤ 208), or low on-treatment platelet reactivity (LPR, ≤ 85). The incidences of non-fatal ischemic and non-ischemic stroke through to 12 months post-PCI were recorded. Almost all enrolled patients (6102/6267 [97.4%]) had a risk factor for ischemic stroke, and most were receiving dual antiplatelet therapy. Of the 5906 patients with PRU data (HPR, n = 2227; OPR, n = 3002; LPR, n = 677), 47 had a non-fatal stroke post-PCI (cumulative incidence: 0.68%, ischemic; 0.18%, non-ischemic stroke). Patients with a non-fatal ischemic stroke event had statistically significantly higher post-PCI PRU values versus those without an event (P = 0.037). The incidence of non-fatal non-ischemic stroke was not related to PRU value. When the patients were stratified by PRU ≤ 153 versus > 153 at 12–48 h post-PCI, a significant difference was observed in the cumulative incidence of non-fatal stroke at 12 months (P = 0.044). We found that patients with ischemic stroke tended to have higher PRU values at 12–48 h after PCI versus those without ischemic stroke. Clinical trial registration: UMIN000020332.
AB - In patients undergoing percutaneous coronary intervention (PCI) with a stent, high on-treatment platelet reactivity may be associated with an increased risk of stroke. This post hoc analysis of the PENDULUM registry compared the risk of post-PCI stroke according to on-treatment P2Y12 reaction unit (PRU) values. Patients aged ≥ 20 years who underwent PCI were stratified by baseline PRU (at 12 and 48 h post-PCI) as either high (HPR, > 208), optimal (OPR, > 85 to ≤ 208), or low on-treatment platelet reactivity (LPR, ≤ 85). The incidences of non-fatal ischemic and non-ischemic stroke through to 12 months post-PCI were recorded. Almost all enrolled patients (6102/6267 [97.4%]) had a risk factor for ischemic stroke, and most were receiving dual antiplatelet therapy. Of the 5906 patients with PRU data (HPR, n = 2227; OPR, n = 3002; LPR, n = 677), 47 had a non-fatal stroke post-PCI (cumulative incidence: 0.68%, ischemic; 0.18%, non-ischemic stroke). Patients with a non-fatal ischemic stroke event had statistically significantly higher post-PCI PRU values versus those without an event (P = 0.037). The incidence of non-fatal non-ischemic stroke was not related to PRU value. When the patients were stratified by PRU ≤ 153 versus > 153 at 12–48 h post-PCI, a significant difference was observed in the cumulative incidence of non-fatal stroke at 12 months (P = 0.044). We found that patients with ischemic stroke tended to have higher PRU values at 12–48 h after PCI versus those without ischemic stroke. Clinical trial registration: UMIN000020332.
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U2 - 10.1007/s00380-021-02003-w
DO - 10.1007/s00380-021-02003-w
M3 - Article
C2 - 34973085
AN - SCOPUS:85122043207
SN - 0910-8327
VL - 37
SP - 942
EP - 953
JO - Heart and Vessels
JF - Heart and Vessels
IS - 6
ER -