Key result
LVAD support markedly elevates coagulation markers and depletes protein C in postcardiotomy heart failure.
Why the study?
The study evaluated the hemostatic alterations in adult patients supported by LVADs for postcardiotomy heart failure.
Does left ventricular assist device support cause hemostatic alterations in adult patients with postcardiotomy heart failure?
Case Report (n=2)
Does left ventricular assist device support cause hemostatic alterations in adult patients with postcardiotomy heart failure?
LVAD support strongly activates both coagulation and fibrinolytic systems and consumes protein C, potentially predisposing patients to thromboembolic complications even in the absence of overt clinical signs.
Answers are grounded in this paper and cite their sources.
May indicate heightened thromboembolic risk during LVAD support; hypothesis-generating and leaves open need for prospective validation in postcardiotomy HF.
The hemostatic alterations in two adult patients who were supported by left ventricular assist devices (LVADs) because of postcardiotomy heart failure were evaluated. In both patients, fibrinopeptide A and thrombin-antithrombin III complex increased markedly during the first several days, and thereafter decreased moderately but remained above normal over the entire procedure. Furthermore, fibrinopeptide B beta 15-42 and alpha 2 plasmin inhibitor-plasmin complex were also markedly increased over the entire course of LVAD treatment. These data show that the LVAD system strongly activates both the coagulation and the fibrinolytic system, even when thromboembolic or bleeding complications are not clinically evident. Furthermore, the decrease in physiological coagulation inhibitors, especially protein C, indicates that these factors are activated and consumed during LVAD treatment. Because protein C is important in regulating the coagulation cascade during LVAD treatment, exhaustion of this system might result in thromboembolic complications during LVAD treatment.
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Tanaka et al. (1991) conducted a case report in Postcardiotomy heart failure (n=2). Left ventricular assist device (LVAD) was evaluated on Hemostatic alterations (fibrinopeptide A, thrombin-antithrombin III complex, fibrinopeptide B beta 15-42, alpha 2 plasmin inhibitor-plasmin complex, and protein C). LVAD support in 2 postcardiotomy heart failure patients markedly increased coagulation and fibrinolytic markers while decreasing protein C over the entire procedure.
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