This may question the hypothesis that acute and temporary changes in blood coagulation and platelet function during the early post-cardiac arrest phase are the main reasons for the incidence of stent thrombosis. NSTEMI after OHCA were included into the analysis (30 male and 8 female patients; ages 42 to 91?years; Table?1). Of these primary OHCA survivors, about a third died despite maximum intensive care treatment (intrahospital mortality 36.8?%). 24 patients could be discharged from hospital. Using the Utstein reporting guidelines for the cerebral performance category (CPC) for neurologic outcome , 17 Rabbit polyclonal to 2 hydroxyacyl CoAlyase1 patients (44.7?%) were classified as CPC 1 or CPC 2. Table?1 Patient demographics coronary artery disease, cerebral performance category, dialysis for acute or chronic kidney failure, left ventricular function, return of spontaneous circulation, ST-elevation myocardial infraction, temperature There were no cases of stent thrombosis, recurrent MI, or unscheduled re-angiography within the hospital stay. Most deaths were attributed Fluvastatin to fatal hypoxic brain damage, while other patients died despite maximum intensive care treatment in a catecholamine refractory cardiogenic shock. Of note, in none of the 27 patients, hypothermia had to be discontinued ahead of schedule. On admission, all but three patients had elevated white blood cell counts. C-reactive protein levels were within the normal range or mildly elevated in most patients on admission, but started to increase within 24?h (Table?2). Table?2 Serum chemistry, blood count and blood gas analysis on admission and at the time point of platelet function measurements base excess, c-reactive protein, red blood count, thrombocytes, high-sensitivity troponin T, white blood count a Hs-TnT measured at day 3 after admission Platelet aggregation Platelet function was measured by impedance aggregometry 25.6??13.6?h after OHCA. 37 out of 38 (97.4?%) patients had a sufficient platelet inhibition within 24?h after admission. In the hypothermia group, impedance aggregometry showed a good efficacy of ticagrelor in all patients (Fig.?1a). In the non-hypothermic group, one patient with significant gastroesophageal reflux had insufficient platelet inhibition by ticagrelor 24?h after admission. Platelet function was measured after re-application of a loading dose of ticagrelor (180?mg) and showed sufficient inhibition in this patient at 48?h. Other than that Fluvastatin there were no hints that gastroesophageal reflux significantly affects platelet inhibition by ticagrelor (Fig.?1b). There was no significant correlation between the impedance measured by platelet aggregometry and neither the core body temperature on admission nor the body temperature at the time point of loading with ticagrelor (Fig.?2a?+?b). Furthermore, there neither was an association between impedance and hs-CRP as a marker for inflammation nor between impedance and pH as a surrogate parameter for acidosis (Fig.?2c?+?d). Open in a separate window Fig.?1 Efficacy of crushed ticagrelor in MI patients after OHCA in pre-specified subgroups. a Results of the impedance aggregometry 24?h after admission in n?=?27 hypothermic patients at 33.0?C body temperature and n?=?11 normothermic patients. b Results of the impedance aggregometry 24?h after admission in n?=?15 patients with >50?mL gastroesophageal reflux within the first 6?h after admission and n?=?20 patients with <50?mL reflux Open in a separate window Fig.?2 Effects of body temperature, acidosis and inflammation on platelet inhibition by ticagrelor. Correlation between the impedance measured by platelet aggregometry and the body temperature a on admission, b at the time point of loading with ticagrelor, c pH and d hs-CRP, respectively To assess how the temperature of the instruments and blood samples affect the aggregometry results, we compared the platelet aggregation at Fluvastatin 33 and at 37?C in a separate cohort of cardio-circulatory stable patients on dual platelet inhibition (Fig.?3a?+?b). There was a strong correlation between Fluvastatin the paired samples at 33 and 37?C for clopidogrel (n?=?66; R?=?0.875; p?0.001) and ticagrelor (n?=?19; R?=?0.847; p?0.001), respectively. The mean impedance was significantly higher in the cooled samples than in the samples at body temperature for clopidogrel.