Haemostatic and inflammatory biomarkers in advanced chronic heart failure: role of oral anticoagulants and successful heart transplantation
Haemostatic and inflammatory biomarkers in advanced chronic heart failure: role of oral anticoagulants and successful heart transplantation
复制标题
DOI：
10.1111/j.1365-2141.2004.04977.x
复制
发表时间：
2004-07-01
影响因子：
6.5
通讯作者：
Gregorini, L
中科院分区：
文献类型：
--
作者：
Cugno, M;Mari, D;Gregorini, L
晚期慢性心力衰竭(CHF)与异常止血和炎症有关，但目前尚不清楚这些异常是如何相关的，无论是口服抗凝剂(OAT)改变它们，还是在成功的心脏移植后持续存在。我们对25例CHF患者(纽约心脏协会IV级，其中10例接受了心脏移植)和25例年龄和性别匹配的健康对照组的血浆凝血酶原片段1+2(F1+2)、凝血酶-抗凝血酶(TAT)复合体、组织纤溶酶原激活物(t-PA)、纤溶酶原激活物抑制物(PAI-1)、D-二聚体、因子VII(FVII)、纤维蛋白原(Fg)、血管性血友病因子(VWF)、肿瘤坏死因子(TNF)、可溶性肿瘤坏死因子受体II(STNFRII)、白细胞介素6(IL-6)、可溶性细胞间黏附分子-1(sICAM-1)、可溶性血管细胞黏附分子-1(sVCAM-1)、内皮-选择素(E-选择素)和血栓调节蛋白。充血性心力衰竭患者血浆TAT、D-二聚体、t-PA、纤维蛋白原、vWF、肿瘤坏死因子、IL-6、sTNFRII、sVCAM-1(P=0.0001)、sICAM-1(P=0.003)和血栓调节蛋白(P=0.007)水平均高于对照组。凝血、纤溶、内皮功能障碍与炎症指标呈显著正相关(r=0.414~0.595)，燕麦组较低。心脏移植组血浆纤维蛋白原(P=0.001.0 5)、血管紧张素转换酶(VWF)、D-二聚体(P=0.0 5)和IL-6(P=0.0 5)均低于对照组，但仍显著高于对照组(P=0.0 1~0.0001)。晚期CHF与凝血激活、内皮功能障碍和促炎细胞因子水平升高有关。这些异常中的大多数相互平行，在接受燕麦片治疗的患者中趋于正常化，尽管患者接受了成功的心脏移植，但尽管没有CHF的临床迹象，这些异常仍然存在。
Advanced chronic heart failure (CHF) is associated with abnormal haemostasis and inflammation, but it is not known how these abnormalities are related, whether they are modified by oral anticoagulants (OAT), or if they persist after successful heart transplantation. We studied 25 patients with CHF (New York Heart Association class IV, 10 of whom underwent heart transplantation) and 25 age- and sex-matched healthy controls by measuring their plasma levels of prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin (TAT) complexes, tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), D-dimer, factor VII (FVII), fibrinogen, von Willebrand factor (VWF), tumour necrosis factor (TNF), soluble TNF receptor II (sTNFRII), interleukin 6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), endothelial-selectin (E-selectin) and thrombomodulin. CHF patients had higher plasma levels of TAT, D-dimer, t-PA, fibrinogen, VWF, TNF, IL-6, sTNFRII, sVCAM-1 (P = 0.0001), sICAM-1 (P = 0.003) and thrombomodulin (P = 0.007) than controls. There were significant correlations (r = 0.414-0.595) between coagulation, fibrinolysis, endothelial dysfunction and inflammation parameters, which were lower in those patients treated with OATs. Heart transplantation led to reductions in fibrinogen (P = 0.001), VWF (P = 0.05), D-dimer (P = 0.05) and IL-6 levels (P = 0.05), but all the parameters remained significantly higher (P = 0.01-0.0001) than in the controls. Advanced CHF is associated with coagulation activation, endothelial dysfunction and increased proinflammatory cytokine levels. Most of these abnormalities parallel each other, tend to normalize in patients treated with OATs and, although reduced, persist in patients undergoing successful heart transplantation, despite the absence of clinical signs of CHF.