Interleukin-6, tissue factor and von Willebrand factor in acute decompensated heart failure: relationship to treatment and prognosis

Interleukin-6, tissue factor and von Willebrand factor in acute decompensated heart failure: relationship to treatment and prognosis
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急性失代偿性心力衰竭中的白介素 6、组织因子和血管性血友病因子:与治疗和预后的关系

DOI:
10.1097/01.mbc.0000061301.28953.bc
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发表时间:
2003
影响因子:
1.1
通讯作者:
G. Lip
G. Lip
中科院分区:
医学4区
文献类型:
--
作者:
B. Chin;Dwayne S.G. Conway;Natalie A Y Chung;A. Blann;C. Gibbs;G. Lip

文献摘要

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动脉血栓形成和血栓栓塞症并发症在充血性心力衰竭(CHF)中增加,在急性失代偿性心力衰竭中尤其严重,预后不良。由于白介素6(IL-6)在实验模型中可诱导强大的促凝血剂组织因子(TF),我们推测,促炎性IL-6可能是导致心力衰竭血栓形成的机制之一,其机制是通过激活/受损细胞上TF的内皮表达[以血浆von Willebrand因子(VWF)为标志]。入选77例急性CHF患者(67%男性,纽约心脏协会III-IV级,87%),并与53例窦性心律慢性稳定型CHF患者(66%男性,纽约心脏协会III-IV级,2%)和37名健康对照组(68%男性)进行比较。与慢性充血性心力衰竭组和健康对照组比较,窦性心律急性充血性心力衰竭患者的IL-6(P&lt;0.0001)、Tf(P=0.041)和vWF(P&lt;0.0001)水平均升高。急性充血性心力衰竭患者基线Tf与IL-6之间存在相关性(r=0.64,P<0.0001)。治疗3个月后,随着心力衰竭症状的控制或缓解,40名患者的IL-6(P&lt;0.0001)和vWF(P&lt;0.0001)水平有所下降,但水平仍显著高于健康对照组。随访6个月死亡的患者IL-6(P=0.008)、Tf(P=0.037)和vWF(P=0.039)的基线水平也高于存活患者。IL-6升高可能通过增加Tf和vWF参与急性心力衰竭的血栓形成和血栓栓塞症并发症。急性充血性心力衰竭患者治疗后症状和血浆标志物的改善以及利用这些标志物预测预后可能在临床上有所帮助。
Arterial thrombotic and thromboembolic complications are increased in congestive heart failure (CHF), and are a particular problem in acute decompensated heart failure, which carries a poor prognosis. As interleukin-6 (IL-6) has been shown to induce the potent procoagulant tissue factor (TF) in experimental models, we hypothesized that the pro-inflammatory IL-6 may be one mechanism contributing to thrombosis in heart failure, mediated via endothelial expression of TF on activated/damaged cells [indicated by plasma von Willebrand factor (vWF)]. Seventy-seven patients (67% men, New York Heart Association class III–IV, 87%) with acute CHF were recruited, and were compared with 53 chronic stable CHF patients in sinus rhythm (66% men, New York Heart Association class III–IV, 2%) and 37 healthy controls (68% men). Acute CHF patients in sinus rhythm had elevated baseline levels of IL-6 (P < 0.0001), TF (P = 0.041) and vWF (P < 0.0001) (all measured by enzyme-linked immunosorbent assay) compared with both chronic CHF and healthy control groups. A correlation exists in acute CHF between baseline TF and IL-6 (Spearman r = 0.64, P < 0.0001). After 3 months treatment, with control or alleviation of heart failure symptoms in 40 patients, there was a fall in levels of IL-6 (P < 0.0001) and vWF (P < 0.0001), but levels still remained significantly higher than healthy controls. Patients who died at 6 months follow-up also had higher baseline levels of IL-6 (P = 0.008), TF (P = 0.037) and vWF (P = 0.039) when compared with those who remained alive. Elevated IL-6 may contribute to the thrombotic and thromboembolic complications in acute heart failure, in a process mediated via increased TF and vWF. Improvement of symptoms and plasma markers after treatment of acute CHF and prediction of prognosis by the markers may be useful in the clinical setting.