Some studies conclude that mild hypothermia causes platelet dysfunction leading to an increased bleeding risk, whereas others state that platelet aggregation is enhanced during mild hypothermia. Therefore, the aim of this study was to clarify whether standard or prolonged duration of targeted temperature management affected platelet aggregation. We randomised 82 comatose patients resuscitated after out-of-hospital cardiac arrest to either 24 hours (standard group) or 48 hours (prolonged group) of targeted temperature management at 33±1°C. Blood samples were collected 22 hours, 46 hours and 70 hours after reaching target temperature. Platelet aggregation was assessed by impedance aggregometry employing a Multiplate®Analyser, using the COLtest®, TRAPtest®, ADPtest® and ASPItest® as agonists, and with the results reported as area under the curve (AUC, AU*min). The platelet aggregation was below the normal range in all blood samples. No differences were observed between the standard group and the prolonged group in either of the blood samples (all p ≥ 0.11), except for a 24% decreased aggregation (95% confidence interval (CI) (10%;37%), p = 0.002) when using the COLtest® in the 46-hour sample. Comparing the 22-hour sample with the 46-hour sample in the prolonged group separately, we found no differences when employing the COLtest®, the ASPItest® or the ADPtest® in patients without the use of adenosine diphosphate receptor inhibitors (all p values ≥0.21), but aggregation induced by the TRAPtest® decreased by 14% (95% CI -8%;-20%), p < 0.001). We concluded that the platelet aggregation post cardiac arrest was below the normal range independent of the core temperature. Moreover, no substantial difference was found in platelet aggregation between standard and prolonged targeted temperature management.
Keywords: Aggregation; haemostasis; heart arrest; multiplate; platelets; targeted temperature management.