Why the study?
Does tirofiban inhibit platelet aggregation and preserve platelet function in an in vitro VAD circuit using human whole blood?
Does tirofiban inhibit platelet aggregation and preserve platelet function in an in vitro VAD circuit using human whole blood?
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In an in vitro VAD circuit, tirofiban preserved platelet count and inhibited pathologic platelet aggregation, suggesting potential utility for clinical VAD use.
A recent development in antithrombotic research allows the inhibition of platelet aggregation via protection of the glycoprotein IIb/IIIa receptor on the platelet membrane. We hypothesized that a GP IIb/IIIa receptor inhibitor would inhibit thromboxane-induced platelet aggregation during circulation in our in vitro ventricular assist device (VAD) circuit and preserve long-term platelet function. Twenty-one in vitro nonpulsatile centrifugal VAD circuits were simulated for 4 days using 450 ml of fresh human whole blood with or without glycoprotein IIb/IIIa receptor inhibitor (tirofiban). Platelet aggregation and degranulation were measured in whole blood induced by ristocetin, collagen, ADP, and thromboxane A2 (TXA2). The tirofiban-treated group preserved the platelet count and tended to exert these beneficial effects by inhibiting pathologic platelet aggregation induced by TXA2, collagen, and ADP as well as degranulation. Tirofiban may be useful in preserving platelet number and function during clinical VAD use.
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Yomo et al. (2000) studied this question.
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