Key result
Mild therapeutic hypothermia significantly attenuated and delayed the antiplatelet effect of ticagrelor in patients with myocardial infarction after cardiac arrest, with higher platelet reactivity at 4 hours compared to uncomplicated cases (75.8 vs 25.8 U, p=0.002).
Why the study?
The study was designed to assess the antiplatelet effect of ticagrelor in patients with MI after OHCA treated with PCI and mild therapeutic hypothermia compared to MI patients without OHCA treated with PCI.
Does mild therapeutic hypothermia attenuate the early antiplatelet effect of a ticagrelor loading dose in patients with MI complicated by out-of-hospital cardiac arrest?
Observational (n=41)
No
Does mild therapeutic hypothermia attenuate the early antiplatelet effect of a ticagrelor loading dose in patients with MI complicated by out-of-hospital cardiac arrest?
In comatose survivors of cardiac arrest with acute MI undergoing mild therapeutic hypothermia, the antiplatelet effect of a ticagrelor loading dose is significantly attenuated and delayed compared to uncomplicated MI patients.
Answers are grounded in this paper and cite their sources.
Suggests mild therapeutic hypothermia may delay ticagrelor onset in cardiac.
BACKGROUND: The aim of the study was to assess the antiplatelet effect of ticagrelor in patients with myocardial infarction (MI) after out-of-hospital cardiac arrest (OHCA) treated with percutaneous coronary intervention (PCI) and mild therapeutic hypothermia (MTH) vs. MI patients without OHCA treated with PCI. METHODS: The study was designed and performed as a phase IV, single-center, investigator-initiated, prospective, observational study assessing the early pharmacodynamic effect (within first 24 h) of a ticagrelor loading dose (180 mg) in both groups of patients (MTH group vs. MI group). For assessment of ticagrelor pharmacodynamics Multiple Electrode Aggregometry (MEA) was applied. RESULTS: Compared with the MTH group, platelet inhibition was persistently stronger in the MI group over the entire observation period (up to 24 h), with the highest differesnce at 4 hours after loading with ticagrelor (25.8 ± 26.4 vs. 75.8 ± 40.9 U, p = 0.002). As a consequence, there was a higher prevalence of high platelet reactivity in the MTH group, with the most explicit difference at 6 hours after the loading dose of ticagrelor (78% vs. 7%, p < 0.001). CONCLUSIONS: In comparison with patients treated with primary PCI for uncomplicated MI, the antiplatelet effect of ticagrelor in patients with MI complicated with OHCA, undergoing MTH and primary PCI, is attenuated and delayed.
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A 2022 study conducted an observational in Acute myocardial infarction with out-of-hospital cardiac arrest (n=41). Mild therapeutic hypothermia vs. No mild therapeutic hypothermia (uncomplicated myocardial infarction) was evaluated on Platelet reactivity at 4 hours after ticagrelor loading dose (ADP-induced platelet aggregation units) (p=0.002). Mild therapeutic hypothermia significantly attenuated and delayed the antiplatelet effect of ticagrelor in patients with myocardial infarction after cardiac arrest, with higher platelet reactivity at 4 hours compared to uncomplicated cases (75.8 vs 25.8 U, p=0.002).
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