Background and aim. Comatose survivors of out-of-hospital cardiac arrest (OHCA) undergoing percutaneous coronary intervention (PCI) and target temperature management are at increased risk of stent thrombosis (ST) which may be partially explained by delayed onset of platelet inhibition even after novel P2Y12 agents. We hypothesized that periprocedural intravenous cangrelor will induce immediate and profound platelet inhibition and thereby bridge the “P2Y12 inhibition gap”.
Methods. Between July 2019 and November 2021, 30 consecutive comatose patients after OHCA undergoing PCI and mild therapeutic hypothermia were randomized to cangrelor and control groups. All patients received standard doses of unfractioned heparin, acetylsalicylic acid and crushed/dissolved tablets of ticagrelor via enteral tube. The cangrelor group received an intravenous bolus of cangrelor followed by 4-hour infusion. Platelet aggregation was measured by VerifyNow® and Multiplate® ADP at baseline and 1, 3, 5 and 8 hours after passage of PCI guidewire.
Results. There was no significant difference in patient characteristics. Platelet reactivity according to VerifyNow® was decreased in cangrelor group at one (30 vs 221 PRU; p < 0,001) and three hours (24 vs 180 PRU; p < 0,001) with no change at five and eight hours. This effect was mirrored in decreased high on-treatment platelet reactivity (HPR) in cangrelor group at one (0 % vs 67%; p < 0,001) and three hours (0 % vs 47 %; p = 0,007). Multiplate® ADP was also significantly decreased at one (14 vs 48 U; p < 0,001) and three hours (11 vs 42 U; p = 0,001). No difference in bleeding rates was observed.
Conclusions. In comatose survivors of OHCA undergoing PCI and mild therapeutic hypothermia, cangrelor safely induced immediate and profound platelet inhibition thereby bridging the “P2Y12 inhibition gap” after ticagrelor. There was no rebound in platelet reactivity after discontinuation of cangrelor infusion indicating lack of drug-drug interaction.
|
