Key result
Cangrelor yields lower platelet inhibition in STEMI, while switching to oral P2Y12 increases non-STEMI HRPR.
Why the study?
Does the pharmacodynamic effect of cangrelor differ between patients with and without STEMI undergoing PCI?
Observational (n=126)
Does the pharmacodynamic effect of cangrelor differ between patients with and without STEMI undergoing PCI?
Cangrelor provides lower platelet inhibition in STEMI patients compared to non-STEMI patients during PCI, highlighting potential differences in pharmacodynamic response based on clinical presentation.
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Warrants caution with cangrelor in STEMI and switching in non-STEMI; leaves open optimal periprocedural P2Y12 strategies pending RCTs.
BACKGROUND: Cangrelor is approved for oral P2Y12 inhibitor naïve patients undergoing percutaneous coronary intervention (PCI). Pharmacodynamic (PD) investigations in different clinical settings, using various assays have shown contrasting data in terms of entity of platelet inhibition and rates of high residual platelet reactivity (HRPR). We assessed the PD effects in patients with or without ST elevation myocardial infarction (STEMI) receiving cangrelor during PCI. METHODS: The PharmacOdynaMic effects of cangrelor in PatiEnts wIth acute or chronIc coronary syndrome undergoing percutaneous coronary intervention (POMPEII) registry (NCT04790032) is an investigator-initiated, prospective study assessing PD at 4 time-points with 3 assays. RESULTS: From March 2021 to June 2024, 126 patients naïve from oral P2Y12 inhibitors underwent PCI with cangrelor (32 with STEMI and 94 without [NSTE-ACS=30, CCS=64]). All STEMI patients switched from cangrelor to ticagrelor, while most patients without STEMI switched to clopidogrel. Inhibition of platelet aggregation (IPA%) during cangrelor infusion was lower in patients with STEMI compared with those without STEMI (LTA 20-μM-ADP 51.5±16.2% vs 59.7±16.2%; p=0.017). Conversely, after switching from cangrelor to an oral P2Y12 inhibitor, IPA was greater in patients with STEMI compared to those without STEMI. Rates of HRPR were consistent with lower platelet inhibition in STEMI during cangrelor and greater after its discontinuation compared with patients without STEMI. Within STEMI patients, cangrelor-induced IPA was lower compared with ticagrelor-induced IPA (p=0.036). CONCLUSIONS: Cangrelor-induced platelet inhibition was lower in patients with STEMI compared to those without STEMI, and was lower than that induced by ticagrelor among STEMI patients. The switch from cangrelor to an oral P2Y12 inhibitor exposed patients without STEMI to greater HRPR compared to those with STEMI.
Gargiulo et al. (2026) conducted an observational in Patients undergoing percutaneous coronary intervention (PCI) (n=126). ST elevation myocardial infarction (STEMI) vs. Patients without STEMI was evaluated on Inhibition of platelet aggregation (IPA%) during cangrelor infusion (p=0.017). During cangrelor infusion for PCI, inhibition of platelet aggregation was significantly lower in patients with STEMI compared to those without STEMI (51.5% vs 59.7%; p=0.017).
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