Key result
Tirofiban cessation is linked to ~60% lower ADP-induced platelet aggregation immediately versus 24 hours later.
Why the study?
Platelet function testing in patients receiving combined antiplatelet therapy including glycoprotein IIb/IIIa inhibitors requires special laboratory methods due to potential influence on test results.
Does concurrent tirofiban administration influence ADP-induced platelet function testing in patients receiving aspirin and clopidogrel after primary coronary intervention?
Observational (n=37)
Randomly assigned time for second sample
Does concurrent tirofiban administration influence ADP-induced platelet function testing in patients receiving aspirin and clopidogrel after primary coronary intervention?
Absolute Event Rate: 17.43% vs 43.92%
p-value: p=≤0.0001
ADP-induced residual platelet reactivity is significantly influenced by concurrent tirofiban, indicating that ADP-receptor-specific efficiency measurements are valid only after total elimination of GPIIb/IIIa inhibitors.
Background Following percutaneous coronary intervention, combined antiplatelet therapy is necessary. Platelet function testing (PFT) has prognostic value and may be applied in the risk assessment of acute coronary syndrome. In case of combined antiplatelet therapy, PFT may require special laboratory methods, as different antiplatelet agents may influence test results. Materials and methods Platelet functions were measured in stent thrombosis-segment elevation myocardial infarction patients receiving aspirin, clopidogrel, and tirofiban. The first sampling was obtained immediately after the termination of administration of tirofiban. The second sample was drawn at a randomly assigned time between 1 and 6 h. The third sampling was done after a minimum of 24 h of tirofiban cessation. Adenosine diphosphate (ADP)- and thrombin receptor-activating peptide (TRAP)-induced aggregations were measured. Results Thirty-seven patients were included. Both TRAP- and ADP-induced aggregation values were significantly lower immediately after tirofiban termination, than after 24 h [TRAP: 26.41 ± 25.00 units (U) vs. 109.86 ± 23.69 U, p < 0.0001; ADP: 17.43 ± 10.10 U vs. 43.92 ± 23.35 U, p ≤ 0.0001]. Elimination half-life of tirofiban and clopidogrel were 1.34 ± 0.49 and 1.269 ± 0.78, respectively. Conclusion ADP-induced residual platelet reactivity is significantly influenced by the presence of concurrent glycoprotein IIb/IIIa inhibitor. In patients receiving combined antiplatelet treatment, ADP-receptor-specific efficiency measurements are valid only after total elimination of GPIIb/IIIa inhibitors.
No takes yet. Share an insight, caveat, or question.
Kupó et al. (2016) conducted an observational in ST-segment elevation myocardial infarction (n=37). Tirofiban cessation vs. 24 hours post-cessation was evaluated on ADP-induced aggregation values (U) (p=≤0.0001). In patients receiving combined antiplatelet treatment, ADP-induced platelet aggregation was significantly lower immediately after tirofiban termination compared to 24 hours later (17.43 vs 43.92 U, p≤0.0001).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: