Impaired biological response to aspirin in therapeutic hypothermia comatose patients resuscitated from out-of-hospital cardiac arrest.

Abstract

Acute coronary syndrome is one of the main causes of out-of-hospital cardiac arrest (OHCA). OHCA patients are particularly exposed to high platelet reactivity (HPR) under aspirin (ASA) treatment. The aim was to evaluate HPR-ASA in therapeutic hypothermia comatose patients resuscitated from OHCA. Twenty-two consecutive patients with OHCA of cardiac origin were prospectively included after therapeutic hypothermia and randomized to receive ASA 100mg per day, either intravenously (n=13) or orally via a gastric tube (n=9). ADP inhibitors (prasugrel or, if contra-indicated, clopidogrel) were administered in the event of angioplasty. HPR-ASA was assessed by light transmission aggregometry (LTA) with arachidonic acid (AA) and by the PFA-100(®) system with collagen/epinephrine. Clinical, biological and angiographic characteristics were similar in both groups. Using LTA-AA, maximum aggregation intensity was significantly lower in the intravenous group compared to the oral group (15% vs. 29%, respectively; p=0.04). Overall, 10 patients (45%) had HPR-ASA (38% intravenously vs 56% orally; p=0.7). Similarly, closure time was significantly increased in the IV group (277s vs. 155s, respectively; p=0.04). This study suggests that impaired response to both intravenous and oral aspirin is frequent in comatose patients resuscitated from OHCA.