Anticoagulation in the ICU: Contact Pathway Inhibition Future

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Bleeding and thrombotic complications are the main cause of morbidity and mortality in critically ill patients on the intensive care unit (ICU), receiving short-term percutaneous mechanical circulatory support (pMCS) by extracorporeal membrane oxygenation (ECMO), balloon pumps or microaxial flow pumps.

This is due to a bidirectional interplay of various factors influencing the hemostatic balance, including coagulopathy during critical illness, sepsis/inflammation, platelet consumption, hyperfibrinolysis, shear-induced acquired von Willebrand syndrome and direct contact pathway activation by the artificial surface of the pMCS device.

To prevent thrombotic complications and device-induced localized intravascular coagulopathy (LIC), anticoagulation is indicated.

Unfortunately, all currently available anticoagulants carry an increased bleeding risk, further jeopardizing patients’ outcomes.

Therefore, the search for safer anticoagulants continues: the holy grail for the treatment of patients on pMCS and by extension, all patients on anticoagulation is to prevent thrombosis without affecting hemostasis, thus lowering the bleeding risk.

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