Why the study?
Does clopidogrel or eptifibatide effectively inhibit platelet reactivity in comatose survivors of cardiac arrest undergoing PCI and hypothermia compared to normothermic ACS patients?
Does clopidogrel or eptifibatide effectively inhibit platelet reactivity in comatose survivors of cardiac arrest undergoing PCI and hypothermia compared to normothermic ACS patients?
In post-cardiac arrest patients undergoing hypothermia and PCI, clopidogrel loading provides inadequate platelet inhibition during the first 48 hours, suggesting eptifibatide may be needed as a bridge.
Answers are grounded in this paper and cite their sources.
Clopidogrel may fail to inhibit platelets adequately during post-arrest hypothermia; hypothesis-generating for eptifibatide bridging pending RCTs.
AIMS: To investigate the effects of clopidogrel and eptifibatide on platelet reactivity in patients resuscitated from cardiac arrest undergoing percutaneous coronary intervention (PCI) and hypothermia. METHODS AND RESULTS: VerifyNow® and Multiplate® aggregometry were used before, and 4, 12, 22 and 48 hours after 600 mg clopidogrel treatment in 28 post-cardiac arrest hypothermic patients and in 14 normothermic patients with acute coronary syndrome. Basal platelet reactivity after stimulation with iso-thrombin receptor-activating peptide (TRAP) and PAR4-activating peptide (BASE) was significantly lower in the post-cardiac arrest group and persisted up to 48 hours. The antiplatelet effect of clopidogrel measured by VerifyNow and expressed as % inhibition was significantly lower in the post-cardiac arrest group. It was close to zero with an increase to only around 10% after 48 hours. Post-cardiac arrest patients receiving eptifibatide showed profound platelet inhibition measured by both VerifyNow IIb/IIIa and Multiplate TRAP tests for at least 22 hours after administration. CONCLUSIONS: Post-resuscitation syndrome with ongoing hypothermia is associated with decreased platelet reactivity. Clopidogrel loading does not significantly affect platelet function during the first 48 hours. This is in contrast with eptifibatide which produces profound platelet inhibition, and may be used to bridge insufficient inhibition by clopidogrel.
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Steblovnik et al. (2015) studied this question.
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