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Hematological problems during the use of cardiac assist devices: clinical experiences in Japan
1Department of Thoracic Surgery, Mie University School of Medicine, Japan.
Insights
Left ventricular assist device (LVAD) use can activate blood coagulation and fibrinolysis. The anticoagulant nafamostat mesilate (FUT-175) effectively minimized these hematological changes in LVAD patients.
Area of Science:
- Cardiology
- Hematology
- Biochemistry
Background:
- Left ventricular assist devices (LVADs) are crucial for managing cardiogenic shock.
- Understanding hematological changes during LVAD support is vital for patient outcomes.
Observation:
- Three patients with postcardiotomy cardiogenic shock received LVADs for 6-9 days.
- Two patients received no anticoagulants; one received nafamostat mesilate (FUT-175).
- Blood samples were analyzed for markers of coagulation and fibrinolysis.
Findings:
- Without anticoagulants, LVAD use led to significant activation of coagulation (increased fibrinopeptide A and thrombin-antithrombin III complex) and fibrinolysis (increased FDP-D-dimer and alpha 2 plasmin inhibitor-plasmin complex).
- Activation of coagulation and fibrinolysis markers correlated with decreased levels of Factor XII and prekallikrein, suggesting contact activation due to blood-device interaction.
- Nafamostat mesilate (FUT-175) effectively suppressed both coagulation and fibrinolysis, maintaining minimal levels of activation markers and preventing contact factor consumption.
Implications:
- LVAD therapy can induce significant prothrombotic and profibrinolytic states.
- Nafamostat mesilate (FUT-175) demonstrates potential as an effective anticoagulant for patients requiring LVAD support.
- Further research into FUT-175 may optimize anticoagulation strategies in mechanical circulatory support.
Abstract:
Hematological changes occurring during use of left ventricular assist devices (LVADs) were evaluated in 3 patients suffering from postcardiotomy cardiogenic shock. LVAD treatment ranged from 6 to 9 days. During the procedure, no anticoagulants were used in the first two cases, while in the third case, a protease-inhibiting agent, nafamostat mesilate (FUT-175), was used. In the first two cases without any anticoagulants, fibrinopeptide A (FPA) and thrombin-antithrombin III complex (TAT) increased markedly over the course of LVAD treatment, suggesting the excessive activation of the coagulatory system. The fibrinolytic system also became activated during LVAD treatment as was indicated by a marked increase in FDP-D-dimer and alpha 2 plasmin inhibitor-plasmin complex (PIC). Continual decreases observed in Factor XII and prekallikrein indicate that the coagulofibrinolytic activation occurring during LVAD treatment is presumably the result of contact activation of these factors due to interaction of blood with the internal surface of the LVAD. In the third case with FUT-175, both coagulation and fibrinolysis were successfully maintained at minimum levels as was demonstrated by the extremely low levels of these molecular markers. There was also no significant consumption of any contact factors. FUT-175 looks promising as an anticoagulant during the use of cardiac assist devices.