Key result
New P2Y12 inhibitors linked to ~61% lower stent thrombosis but double the bleeding post-ACS.
Why the study?
The impact of new P2Y12 inhibitors on platelet reactivity and clinical outcomes after ACS was not well characterized in a large single center registry.
Does the introduction of new P2Y12 inhibitors (prasugrel, ticagrelor) improve platelet reactivity and clinical outcomes in patients with Acute Coronary Syndrome?
Cohort (n=1,999)
No
Does the introduction of new P2Y12 inhibitors (prasugrel, ticagrelor) improve platelet reactivity and clinical outcomes in patients with Acute Coronary Syndrome?
Odds Ratio: 2.1 (95% CI 1.4–3.2)
Absolute Event Rate: 10% vs 5%
p-value: p=<0.01
The real-world introduction of newer P2Y12 inhibitors for ACS reduced high platelet reactivity and stent thrombosis but significantly increased bleeding risk compared to older regimens.
New P2Y12 inhibitors were linked to more bleeding despite fewer stent thromboses; leaves open optimal platelet reactivity targets after ACS.
We retrospectively studied the impact of the introduction of new P2Y12 inhibitors (prasugrel, ticagrelor) on platelet reactivity and clinical outcomes after Acute Coronary Syndrome (ACS) from a large single center registry. Consecutive patients admitted for ACS since 2007 and discharged on dual antiplatelet therapy were enrolled. Biological response was assessed one month after discharge by PRI VASP and ADP-induced aggregation (%ADP). Patients were classified according to PRI VASP as very low on-treatment platelet reactivity (VLTPR) (PRI VASP ≤ 10%), low on-treatment platelet reactivity (LTPR) (PRI VASP ≤ 20%) and high on-treatment platelet reactivity HTPR (PRI VASP > 50%). Ischemic and bleeding complications were reported. 1999 patients were analyzed, 605 before (July 2007–February 2010) and 1394 after introduction of new P2Y12 blockers (February 2010–August 2013). After introduction, we reported a significant lower PRI VASP values (38% ± 0.53 vs. 42% ± 0.81 p = 0.001), %ADP aggregation (52% ± 0.4 vs. 54% ± 0.6 p = 0.03) and HTPR incidence (22% versus 34% OR [95% CI]:0.65 [0.53–0.80]; p < 0.001). Conversely, incidence of VLTPR and LTPR were significantly higher after the introduction of new P2Y12 inhibitors: 6% versus 3% (OR [95% CI]: 2.0 [1.2–3.3]; p < 0.01) and 19% versus 8% (OR [95% CI]: 2.8 [2.0–3.9]; p < 0.001) respectively. Clinical follow-up confirmed biological findings with higher incidence of bleeding 10% versus 5% (OR [95% CI]: 2.1 [1.4–3.2]; p < 0.01) and lower incidence of stent thrombosis 1.3% versus 3.3% (OR [95% CI]: 0.39 [0.20–0.73]; p < 0.01) with new P2Y12 blockers. The introduction of new P2Y12 inhibitors modified both platelet reactivity and clinical outcome of ACS patients, with higher rate of hyper responders and bleedings, and lower rate of non responders and thrombotic events.
No takes yet. Share an insight, caveat, or question.
Deharo et al. (2014) conducted a cohort in Acute Coronary Syndrome (ACS) (n=1,999). New P2Y12 inhibitors (prasugrel, ticagrelor) vs. Before introduction of new P2Y12 blockers was evaluated on bleeding (OR 2.1, 95% CI 1.4-3.2, p=<0.01). New P2Y12 inhibitors after ACS were associated with lower stent thrombosis (1.3% vs 3.3%; OR 0.39) but higher bleeding (10% vs 5%; OR 2.1, 95% CI 1.4-3.2) compared to older agents.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: