Microparticles and blood cells induce procoagulant activity via phosphatidylserine exposure in NSTEMI patients following stent implantation

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• 作者：Lixiu Wang^a ; Yayan Bi^a ; ^{biyayan@163.com" class="auth_mail" title="E-mail the corresponding author} ; Muhua Cao^b ; Ruishuang Ma^b ; Xiaoming Wu^b ; Yan Zhang^b ; Wenbo Ding^c ; Yan Liu^b ; Qian Yu^a ; Yingqian Zhang^c ; Hua Jiang^c ; Yingchun Sun^d ; Dongxia Tong^b ; Li Guo^b ; Zengxiang Dong^a ; Ye Tian^a ; Junjie Kou^c ; ^{junjiekou@163.com" class="auth_mail" title="E-mail the corresponding author} ; Jialan Shi^b ; ^e ; ^{jialan_shi73661@gmail.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：PS ; phosphatidylserine ; PCA ; procoagulant activity ; NSTEMI ; non-ST-elevated myocardial infarction ; MPs ; microparticles ; PCI ; percutaneous coronary intervention ; PMPs ; platelet-derived MPs ; EMPs ; endothelial-derived MPs ; MMPs ; monocyte-derived MPs ; LMPs ; leukocyte-derived MPs ; ErMPs ; erythrocyte-derived MPs ; CAD ; coronary artery disease ; TF ; tissue factor ; PLT ; platelet ; RBC ; red blood cell ; WBC ; white blood cell ; MDP ; MP-depleted plasma ; PRP ; platelet-rich plasma ; PFP ; platelet-free plasma ; PFP
• 刊名：International Journal of Cardiology
• 出版年：2016
• 出版时间：15 November 2016
• 年：2016
• 卷：223
• 期：Complete
• 页码：121-128
• 全文大小：1065 K

文摘

Relatively little is known about the role of phosphatidylserine (PS) in procoagulant activity (PCA) in patients with non-ST-elevated myocardial infarction (NSTEMI) after stent implantation. This study was designed to evaluate whether exposed PS on microparticles (MPs) and blood cells were involved in the hypercoagulable state in NSTEMI patients with stent implantation.

Methods

NSTEMI patients (n= 90) and healthy controls (n = 20) were included in our study. PS exposure on MPs and blood cells was analyzed with flow cytometer and confocal microscope. PCA was evaluated by clotting time, purified coagulation complex assays and fibrin production assays.

Results

Baseline levels of MPs and PS⁺ blood cells were significantly higher (P < 0.001) in the patients than in controls. After stent implantation, a remarkable increase was observed in both MPs and PS⁺ blood cells. Specifically, PS⁺ MPs, PS⁺ platelets and erythrocytes peaked at 18 h following stent implantation, while PS⁺ leukocytes peaked on day 2. In addition, circulating MPs (mostly derived from platelets, leukocytes, erythrocytes and endothelial cells) cooperating with PS⁺ blood cells, contributed to markedly shortened coagulation time and markedly increased FXa/thrombin/fibrin (all P < 0.01) generation in patient group. Moreover, blockade of exposed PS on MPs and cells with lactadherin inhibited PCA by approximately 70%.

Conclusions

Our results suggest that PS⁺ MPs and blood cells play a procoagulant role in NSTEMI patients following stent implantation. Blockade of PS could become a novel therapeutic modality for the prevention of thrombosis in these patients.