Abstract
Though extracorporeal membrane oxygenation (ECMO) provides life-saving support, this intervention exposes patients to certain risks. Circulating free hemoglobin (fHb) resulting from mechanically induced hemolysis and insufficient haptoglobin/hemopexin may promote thrombosis within the ECMO circuit. Thrombi in the circuit can result in thromboembolic complications in these patients. Prevention of thrombus formation and propagation in the ECMO circuit may improve clinical outcome. fHb released during hemolysis has been shown to have multiple adverse effects, including thrombosis, but the mechanism by which fHb contributes to thrombosis in an ECMO circuit remains elusive. It is well established that (1) high shear stress generated in the circuit may cause hemolysis, and (2) plasma fibrinogen is adsorbed onto the inner tubing of the ECMO circuit over time. Plasma von Willebrand factor (pVWF) mediates platelet deposition at sites of vascular injury under high shear stress by sensing alterations in the hemodynamic environment. This biophysical property of pVWF that enables hemostasis may also contribute to the pathogenesis of ECMO-induced thrombosis. pVWF contains binding sites for both adsorbed fibrin(ogen) and fHb. High concentrations of fHb increase pVWF-mediated platelet adhesion and thrombus formation on a surface-adsorbed fibrin(ogen) under high shear stress. The molecular mechanism(s) by which fHb drives the conformation of pVWF into a prothrombotic state is currently unknown. Reduction of thrombotic risks during ECMO intervention warrants further investigations into the interaction between pVWF and fHb.
Highlights
Extracorporeal membrane oxygenation (ECMO) provides temporary multi-organ support for patients with congenital or acquired heart and/or lung disease or resuscitative support for patients with cardiopulmonary failure
Hemolysis associated with pathological hemodynamics within the ECMO circuit may contribute to systemic dysregulation of hemostasis [1,2,3]
In hemostasis, when the integrity of the vessel wall has been compromised, Plasma von Willebrand factor (pVWF) quickly binds to components exposed in the subendothelial matrix at high shear stress
Summary
Circulating free hemoglobin (fHb) resulting from mechanically induced hemolysis and insufficient haptoglobin/hemopexin may promote thrombosis within the ECMO circuit. FHb released during hemolysis has been shown to have multiple adverse effects, including thrombosis, but the mechanism by which fHb contributes to thrombosis in an ECMO circuit remains elusive. Plasma von Willebrand factor (pVWF) mediates platelet deposition at sites of vascular injury under high shear stress by sensing alterations in the hemodynamic environment. This biophysical property of pVWF that enables hemostasis may contribute to the pathogenesis of ECMO-induced thrombosis. PVWF contains binding sites for both adsorbed fibrin(ogen) and fHb. High concentrations of fHb increase pVWF-mediated platelet adhesion and thrombus formation on a surface-adsorbed fibrin(ogen) under high shear stress.
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