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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DOI:
10.1097/00001721-200309000-00001
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发表时间:
2003-09-01
影响因子:
1.1
通讯作者:
Lip, GYH
Lip, GYH
中科院分区:
医学4区
文献类型:
--
作者:
Chin, BSP;Conway, DSG;Lip, GYH

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充血性心力衰竭(CHF)中动脉血栓形成和血栓栓塞并发症增加,并且是预后不良的急性失代偿性心力衰竭中的一个特殊问题。由于白细胞介素-6(IL-6)已显示在实验模型中诱导强效促凝血组织因子(TF),我们假设促炎性IL-6可能是导致心力衰竭血栓形成的一种机制,通过活化/受损细胞上TF的内皮表达介导[由血浆血管性血友病因子(vWF)表示]。招募了77例急性CHF患者(67%为男性,纽约心脏协会III-IV级,87%),并与53例窦性心律的慢性稳定性CHF患者(66%为男性,纽约心脏协会III-IV级,2%)和37例健康对照(68%为男性)进行比较。与慢性CHIF组和健康对照组相比,窦性心律的急性CHIF患者的IL-6(P< 0.0001)、TF(P= 0.041)和vWF(P < 0.0001)基线水平升高(均通过酶联免疫吸附测定法测量)。在急性CHF中,基线TF和IL-6之间存在相关性(斯皮尔曼r= 0.64,P < 0.0001)。治疗3个月后,40例患者的心力衰竭症状得到控制或缓解,IL-6(P < 0.0001)和vWF(P < 0.0001)水平下降,但仍明显高于健康对照组。随访6个月时死亡的患者与存活患者相比,IL-6(P = 0.008)、TF(P = 0.037)和vWF(P = 0.039)的基线水平也较高。升高的IL-6可能通过增加TF和vWF介导急性心力衰竭的血栓形成和血栓栓塞并发症。急性CHF治疗后症状和血浆标志物的改善以及通过标志物预测预后可能在临床环境中有用。(C)2003年利平科特威廉姆斯威尔金斯。
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 CH F 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 CHIF 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 CHIF 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. (C) 2003 Lippincott Williams Wilkins.