Related Experiment Video
Updated: Sep 20, 2026

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
Published on: August 14, 2017
Interleukin-6, tissue factor and von Willebrand factor in acute decompensated heart failure: relationship to
Bernard S P Chin1, Dwayne S G Conway, Natalie A Y Chung
1Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK.
Insights
Interleukin-6 (IL-6) elevation contributes to blood clots in acute heart failure by increasing tissue factor (TF) and von Willebrand factor (vWF). These markers may also predict patient prognosis.
Area of Science:
- Cardiology
- Hematology
- Immunology
Background:
- Arterial thrombotic and thromboembolic complications are increased in congestive heart failure (CHF).
- Acute decompensated heart failure carries a poor prognosis.
- Interleukin-6 (IL-6) induces tissue factor (TF), a procoagulant, in experimental models.
Purpose of the Study:
- To investigate the role of pro-inflammatory IL-6 in thrombosis in heart failure.
- To determine if IL-6 contributes to endothelial expression of TF, indicated by plasma von Willebrand factor (vWF).
Main Methods:
- Seventy-seven acute CHF patients, 53 chronic stable CHF patients, and 37 healthy controls were recruited.
- Plasma levels of IL-6, TF, and vWF were measured using enzyme-linked immunosorbent assay.
- Patient outcomes were assessed at 6-month follow-up.
Main Results:
- Acute CHF patients had elevated baseline IL-6, TF, and vWF compared to chronic CHF and healthy controls.
- A correlation was found between baseline TF and IL-6 in acute CHF patients.
- After 3 months of treatment, IL-6 and vWF levels decreased but remained higher than in controls.
- Higher baseline IL-6, TF, and vWF levels were associated with increased mortality at 6 months.
Conclusions:
- Elevated IL-6 may contribute to thrombotic complications in acute heart failure via increased TF and vWF.
- Plasma markers like IL-6, TF, and vWF may be useful for predicting prognosis in acute CHF.
- Improvement in symptoms and plasma markers after treatment suggests potential clinical utility.
Abstract:
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.
Related Concept Videos
Heart Failure VI: Adjunct Therapies
Heart Failure II: Pathophysiology
Acute Inflammation III: Local and Systemic Effects
Pathophysiology of Heart Failure
Heart Failure V: Medical Management
Venous Thrombosis III: Interprofessional Care