한빛사논문
- 조회200
Osung Kwon 1,2, Jong-Hwa Ahn 3, Jin-Sin Koh 4, Yongwhi Park 3, Seok Jae Hwang 4, Udaya S. Tantry 5, Paul A. Gurbel 5, Jin-Yong Hwang 4*, Young-Hoon Jeong 6,7*
1Division of Cardiology, Department of Internal Medicine, Eunpyeong St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
2Cardiovascular Research Institute for Intractable Disease, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
3Department of Internal Medicine, Gyeongsang National University School of Medicine and Cardiovascular Center, Gyeongsang National University Changwon Hospital, Changwon, Republic of Korea.
4Department of Internal Medicine, Gyeongsang National University School of Medicine and Gyeongsang National University Hospital, 79, Gangnam-ro, Jinju 52727, Republic of Korea.
5Sinai Center for Thrombosis Research and Drug Development, Sinai Hospital of Baltimore, Baltimore, MD, USA.
6CAU Thrombosis and Biomarker Center, Chung-Ang University Gwangmyeong Hospital, 110, Deokan-ro, Gwangmyeong 14353, Republic of Korea.
7Department of Internal Medicine, Chung-Ang University College of Medicine, 84, Heukseok-ro, Seoul 06974, Republic of Korea.
*Corresponding authors : Jin-Yong Hwang, Young-Hoon Jeong
Abstract
Background and aims: Platelet-fibrin clot strength (PFCS) is linked to major adverse cardiovascular event (MACE) risk. However, the association between PFCS and platelet reactivity and their prognostic implication remains uncertain in patients undergoing percutaneous coronary intervention (PCI).
Methods: In PCI-treated patients (n = 2512) from registry data from January 2010 to November 2018 in South Korea, PFCS using thromboelastography and platelet reactivity using VerifyNow were measured. High PFCS (PFCSHigh) was defined as thromboelastography maximal amplitude ≥ 68 mm, and high platelet reactivity (HPR) was defined as >208 P2Y12 reaction units. Patients were stratified into four groups according to maximal amplitude and P2Y12 reaction unit levels: (i) normal platelet reactivity (NPR)-PFCSNormal (31.8%), (ii) HPR-PFCSNormal (29.0%), (iii) NPR-PFCSHigh (18.1%), and (iv) HPR-PFCSHigh (21.1%). Major adverse cardiovascular event (all-cause death, myocardial infarction, or stroke) and major bleeding were followed up to 4 years.
Results: High platelet reactivity and PFCSHigh showed an additive effect for clinical outcomes (log-rank test, P < .001). Individuals with NPR-PFCSNormal, NPR-PFCSHigh, HPR-PFCSNormal, and HPR-PFCSHigh demonstrated MACE incidences of 7.5%, 12.6%, 13.4%, and 19.3%, respectively. The HPR-PFCSHigh group showed significantly higher risks of MACE compared with the NPR-PFCSNormal group [adjusted hazard ratio (HRadj) 1.89; 95% confidence interval (CI) 1.23-2.91; P = .004] and the HPR-PFCSNormal group (HRadj 1.60; 95% CI 1.12-2.27; P = .009). Similar results were observed for all-cause death. Compared with HPR-PFCSNormal phenotype, NPR-PFCSNormal phenotype was associated with a higher risk of major bleeding (HRadj 3.12; 95% CI 1.30-7.69; P = .010).
Conclusions: In PCI patients, PFCS and platelet reactivity demonstrated important relationships in predicting clinical prognosis. Their combined assessment may enhance post-PCI risk stratification for personalized antithrombotic therapy.
논문정보
- Research article
- 2024년 05월 (BRIC 등록일 2024-05-29)
- 국내(교신)+국외 연구진
- 의약학 > 응용의학
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