建設中

Intravascular cells and circulating microparticles induce procoagulant activity via phosphatidylserine exposure in heart failure

心不全患者と健常人で比較すると

内皮細胞由来のPSでは違いがなかったが

血液細胞由来のPSでは心不全患者のほうが多くて、血液凝固し易かった

　推論すると

＋αのリスクでAfがあると、心房内で血栓形成しやすい状態になっていると考えられる

こう考えるほうがアブレ－ションの臨床成績とコンパチブルである

Relatively little information is known about the definitive role of phosphatidylserine (PS) in the hypercoagulability of heart failure (HF). Our objectives were to assess the levels of PS exposure on microparticles (MPs) and blood cells (BCs) in each group of HF patients and to evaluate their procoagulant activity (PCA). HF patients in each NYHA functional class II-IV (II n = 30, III n = 30, IV n = 30) and healthy controls (n = 25) were enrolled in the present study. PS exposure on MPs, BCs was analyzed with flow cytometry. MPs were classified based on their cellular origin: platelets (CD41a⁺), neutrophils (CD66b⁺), endothelial cells (CD31⁺CD41a^-), erythrocytes (CD235a⁺), monocytes (CD14⁺), T lymphocytes (CD3⁺), and B lymphocytes (CD19⁺). PCA was evaluated by clotting time, extrinsic/intrinsic FXa and prothrombinase production assays, as well as fibrin formation assays. Inhibition assays of PCA of PS⁺ BCs and MPs were performed by lactadherin. There was no significant difference in MP cellular origin between healthy and HF subjects. However, the total number of PS⁺ MPs was significantly increased in HF patients compared with healthy controls. In addition, circulating PS⁺ BCs cooperated with PS⁺ MPs to markedly shorten coagulation time and dramatically increase FXa/thrombin generation and fibrin formation in each HF group. Moreover, blockade of exposed PS on BCs and MPs with lactadherin inhibited PCA by approximately 80%. Our results lead us to believe that exposing PS on the injured BCs and MPs played a pivotal role in the hypercoagulability state in HF patients.

Phosphatidylserine on microparticles and associated cells contributes to the hypercoagulable state in diabetic kidney disease