Key result
Inhibition of TAFI and alpha2-antiplasmin in normal human plasma significantly decreased the time of onset of fibrinolysis (by 70% and 85%) and increased the rate of lysis (by 70% and 557%) (P<0.05).
p-value: p=< 0.05
Thrombelastography can effectively quantify the distinct antifibrinolytic contributions of TAFI and alpha2-antiplasmin in human plasma, demonstrating that alpha2-antiplasmin inhibition produces a more profound fibrinolytic response.
Supports targeted antifibrinolytic research; leaves open translation to clinical thrombosis outcomes.
Two major proteins that inhibit fibrinolysis include thrombin activatable fibrinolysis inhibitor (TAFI) and alpha2-antiplasmin. Our goal was to quantify the contribution of TAFI and alpha2-antiplasmin to antifibrinolytic defenses with thrombelastography. Plasma activated with tissue factor/kaolin was subjected to fibrinolysis with tissue-type plasminogen activator (100 U/ml). Prior to activation, TAFI activity was inhibited with either potato carboxypeptidase inhibitor (25 microg/ml) or an anti-TAFI antibody, and alpha2-antiplasmin activity was inhibited with an anti-alpha2-antiplasmin antibody. Data were collected for 30 min, with the time of onset and rate of fibrinolysis determined. Compared with uninhibited samples, TAFI inhibition significantly (P < 0.05) decreased the time of onset of fibrinolysis by 70% and increased the rate of lysis by 70%. There was no difference between potato carboxypeptidase inhibitor and anti-TAFI antibody inhibition. Inhibition of alpha2-antiplasmin resulted in a significantly (P < 0.05) decreased time of onset (85%) and increased the rate of lysis (557%) compared with uninhibited samples. Inhibition of alpha2-antiplasmin activity resulted in a significantly (P < 0.05) greater fibrinolytic response than TAFI inhibition. In conclusion, utilization of standard inhibitors and thrombelastography permitted quantification of the effects of TAFI and alpha2-antiplasmin on fibrinolysis in plasma. Future investigation of diseases involving hypofibrinolysis (e.g. left ventricular assist devices) could be conducted using this assay system.
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Nielsen et al. (2006) studied normal human plasma. TAFI inhibition and alpha2-antiplasmin inhibition vs. uninhibited samples was evaluated on time of onset and rate of fibrinolysis (p=< 0.05). Inhibition of TAFI and alpha2-antiplasmin in normal human plasma significantly decreased the time of onset of fibrinolysis (by 70% and 85%) and increased the rate of lysis (by 70% and 557%) (P<0.05).
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