Key result
ADP-to-TRAP aggregation ratio quantifies P2Y12 inhibition independently of platelet count, unlike conventional ADP.
Why the study?
Does the ratio of ADP- to TRAP-induced platelet aggregation quantify P2Y12-dependent platelet inhibition independently of platelet count compared to conventional ADP-induced aggregation in patients after recent coronary stent-implantation?
Observational (n=359)
No
Does the ratio of ADP- to TRAP-induced platelet aggregation quantify P2Y12-dependent platelet inhibition independently of platelet count compared to conventional ADP-induced aggregation in patients after recent coronary stent-implantation?
Effect estimate: r = -0.003
p-value: p=0.960
The ratio of ADP- to TRAP-induced platelet aggregation quantifies P2Y12-dependent platelet inhibition independently of platelet count, providing a potentially more valid measure of platelet reactivity after coronary stenting.
May offer platelet count-independent P2Y12 assessment post-stenting; leaves open whether it improves risk stratification or outcomes.
OBJECTIVE: This study aimed to assess the association of clinical factors with P2Y12-dependent platelet inhibition as monitored by the ratio of ADP- to TRAP-induced platelet aggregation and conventional ADP-induced aggregation, respectively. BACKGROUND: Controversial findings to identify and overcome high platelet reactivity (HPR) after coronary stent-implantation and to improve clinical outcome by tailored anti-platelet therapy exist. Monitoring anti-platelet therapy ex vivo underlies several confounding parameters causing that ex vivo platelet aggregation might not reflect in vivo platelet inhibition. METHODS: In a single centre observational study, multiple electrode aggregometry was performed in whole blood of patients after recent coronary stent-implantation. Relative ADP-induced aggregation (r-ADP-agg) was defined as the ratio of ADP- to TRAP- induced aggregation reflecting the individual degree of P2Y12-mediated platelet reactivity. RESULTS: Platelet aggregation was assessed in 359 patients. Means (± SD) of TRAP-, ADP-induced aggregation and r-ADP-agg were 794 ± 239 AU*min, 297 ± 153 AU*min and 37 ± 14%, respectively. While ADP- and TRAP-induced platelet aggregation correlated significantly with platelet count (ADP: r = 0.302; p<0.001; TRAP: r = 0.509 p<0.001), r-ADP-agg values did not (r = -0.003; p = 0.960). These findings were unaltered in multivariate analyses adjusting for a range of factors potentially influencing platelet aggregation. The presence of an acute coronary syndrome and body weight were found to correlate with both ADP-induced platelet aggregation and r-ADP-agg. CONCLUSION: The ratio of ADP- to TRAP-induced platelet aggregation quantifies P2Y12-dependent platelet inhibition independently of the platelet count in contrast to conventional ADP-induced aggregation. Furthermore, r-ADP-agg was associated with the presence of an acute coronary syndrome and body weight as well as ADP-induced aggregation. Thus, the r-ADP-agg is a more valid reflecting platelet aggregation and potentially prognosis after coronary stent-implantation in P2Y12-mediated HPR than conventional ADP-induced platelet aggregation.
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Olivier et al. (2016) conducted an observational in Patients after recent coronary stent-implantation (n=359). Ratio of ADP- to TRAP-induced platelet aggregation (r-ADP-agg) vs. Conventional ADP-induced aggregation was evaluated on Correlation with platelet count (r = -0.003, p=0.960). The ratio of ADP- to TRAP-induced platelet aggregation quantifies P2Y12-dependent platelet inhibition independently of platelet count (r=-0.003), unlike conventional ADP-induced aggregation (r=0.302).
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