Ed, paired t-test for means, two-tailed paired Wilcoxon matched pairs signed test for medians and Fisher’s exact test for categorical variables. **P <0.01. ***P <0.001. aP <0.01 compared to the other analysed temperature. bP <0.001 compared to the other analysed temperature on the same sampling occasion. VASP, vasodilator-stimulated phosphorylated phosphoprotein; PRI, platelet reactivity index; AUC: area under the curve.Patients with dual platelet inhibition: platelet count, PT-INR and aPTT were all unchanged between T1 and T2. Fibrinogen increased from 3.2 ?0.9 (T1) to 4.9 tert-Butyl (2-bromothiazol-5-yl)carbamate ?1.3 (T2), (P =0.002) and CRP increased from 52 ?38 (T1) to 147 ?72 (T2) (P <0.001). VASP PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/4155310 decreased from 53 ?28 (T1) to 24 ?22 (T2), (P <0.001). Multiplate?analyses, with the analyses temperature set on the in vivo temperature, showed no changes in ADP-stimulated platelets. COL, TRAP and ASPI tests were all increased at T2 compared to T1 (Table 2 and Figure 2). In the Sonoclot-analyses ACT was unchanged but both CR and PF was increased at T2 compared to T1 (Table 2 and Figure 2). Patients with no platelet inhibition: platelet count, PT-INR, aPTT, and VASP did not change significantly. Multiplate?analyses were performed with the analyses temperature set on the patient's body temperature. ADPand TRAP tests were 4-(Benzyloxy)-4-oxobutanoic acid not changed significantly. COL and ASPI tests increased at T2 compared to T1 (Table 2 and Figure 2). In the Sonoclot?analyses ACT and CR were unchanged but PF was increased in T2 compared to T1 (Table 2 and Figure 2). Correlation aspirated gastric secretion – VASP: the median volume of gastric secretion aspirated in patients with dual platelet inhibition was 105 (10 to 200) ml during T1 and 65 (10 to 200) ml during T2 (not significant). The volume of gastric secretion aspirated during T1 correlated well with VASP (T1), r =0.81 (P <0.001) (Figure 3). This correlation was not detected at T2.Discussion In this prospective observational study on OHCA patients treated with MIH we have demonstrated an increase inKander et al. Critical Care 2014, 18:495 http://ccforum.com/content/18/5/Page 6 ofADP PI200 n.s 150 n.sCOLnPIPI ***nPI **AUCAUCT1 T2 T1 TT1 T2 T1 TTRAPPIASPInPI PI ******nPI **AUCAUCT1 T2 T1 TT1 T2 T1 TACTCRnPIn .sPIn .sPI ***nPIn .s60u/min100T1 T2 T1 TsecT1 T2 T1 TPFPIVASPnPI PI *** nPIn .s*****PRI ( )T1 T2 T1 TunitsT1 T2 T1 TFigure 2 Results from blood analyses for individual patients. Multiplate?and Sonoclot instruments set on the in-vivo temperature. PI, patients with dual platelet inhibition (n =14); nPI, patients with no platelet inhibition (n =9); T1, blood sampling 12 to 24 h after reaching 33 body temperature; T2, blood sampling 16 to 28 h after reaching normothermia. Multiple electrode aggregometry, Multiplate? ADP: PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/9544797 adenosine diphosphate-agonist; COL, collagen-agonist; TRAP, thrombin-agonist; ASPI, arachidonic-acid agonist. Sonoclot analyses: ACT, activated clotting time; CR, clotting rate; PF, platelet function. AUC, area under curve; **P <0.01; ***P <0.001.Multiplate?assays COL, TRAP, ASPI and Sonoclot assays CR and PF between the stable hypothermic and the stable normothermic state, indicating increased platelet aggregation and strengthened clot formation.This observational study did not include a normothermic control group, thus the cause for the increased platelet aggregability and viscoelastic clot formation between stable hypothermia (T1) and stable normothermiaKander et al. Critical Care 2014, 18:495 http://ccforum.com/content/18/5/Page 7 of.