Ville Jalkanen1, Jukka Vaahersalo2, Ville Pettilä3, Jouni Kurola4, Tero Varpula5, Marjaana Tiainen6, Heini Huhtala7, Ari Alaspää8, Seppo Hovilehto9, Outi Kiviniemi10, Anne Kuitunen11, Jyrki Tenhunen12. 1. Tampere University Hospital, Critical Care Medicine Research Group, PO Box 2000, 33521 Tampere, Finland. Electronic address: jyrki.tenhunen@surgsci.uu.se. 2. Helsinki University Central Hospital, Lohja Hospital, Emergency Department, Sairaalatie 8, 08200 Lohja, Finland. 3. Helsinki University Hospital, Department of Surgery, Division of Intensive Care Medicine, PO Box 340, 00029 Helsinki University Hospital, Finland. 4. Kuopio University Hospital, Centre for Prehospital Emergency Care, PO Box 100, 70029 Kuopio University Hospital, Finland. 5. Helsinki University Hospital, Jorvi Hospital, Department of Intensive Care, PO Box 800, 00029 Helsinki University Hospital, Finland. 6. Helsinki University Hospital, Department of Neurology, PO Box 340, 00029 Helsinki University Hospital, Finland. 7. University of Tampere, School of Health Sciences, 33014 University of Tampere, Finland. 8. Kanta-Häme Central Hospital, Department of Intensive Care, Ahvenistontie 20, 13530 Hämeenlinna, Finland. 9. South-Carelia Central Hospital, Department of Intensive Care, Valto Käkelänkatu 1, 53130 Lappeenranta, Finland. 10. Lapland Central Hospital, Department of Intensive Care, PL 8041, 96101 Rovaniemi, Finland. 11. Tampere University Hospital, Critical Care Medicine Research Group, PO Box 2000, 33521 Tampere, Finland. 12. Tampere University Hospital, Critical Care Medicine Research Group, PO Box 2000, 33521 Tampere, Finland; Uppsala University Hospital, Department of Surgical Sciences, 75185 Uppsala, Sweden.
Abstract
AIM: The whole body ischaemia-reperfusion after cardiac arrest (CA) induces a systemic inflammation-reperfusion response. The expression of urokinase plasminogen activator receptor (uPAR) is known to be induced after hypoxia and increased levels of soluble form suPAR have been measured after hypoxia and ischaemia. Our aim was to evaluate, whether ischaemia/reperfusion injury after out-of-hospital cardiac arrest (OHCA) increases suPAR concentrations in serum and to evaluate the prognostic value of suPAR regarding 90-day mortality and 12-month neurological outcome. METHODS: This is a pre-determined substudy of prospective FINNRESUSCI study. Total of 287 patients treated in the intensive care units after OHCA and with consent from the next-of-kin and serum samples between baseline and day 4 were included. Outcome and neurological outcome were evaluated according the Pittsburgh Cerebral Performance Categories (CPC). Kaplan-Meier survival curves, areas under receiver operational characteristics curves and positive likelihood ratios for mortality and poor neurological outcome were calculated. RESULTS: Non-survivors had higher levels of suPAR after OHCA. Kaplan-Meier survival curves indicated high 90-day mortality in the highest concentration quintiles. LR+ for 1-year CPC 3-5 was 1.8-2.7 for the whole patient cohort and in shockable rhythms 2.0-2.4. In therapeutic hypothermia prognostic value remained. CONCLUSIONS: We found that high SuPAR concentrations were associated with poor outcome in patients with OHCA admitted to critical care. However, suPAR alone had inadequate predictive value for poor outcome and did not associate with 12-month neurological outcome.
AIM: The whole body ischaemia-reperfusion after cardiac arrest (CA) induces a systemic inflammation-reperfusion response. The expression of urokinase plasminogen activator receptor (uPAR) is known to be induced after hypoxia and increased levels of soluble form suPAR have been measured after hypoxia and ischaemia. Our aim was to evaluate, whether ischaemia/reperfusion injury after out-of-hospital cardiac arrest (OHCA) increases suPAR concentrations in serum and to evaluate the prognostic value of suPAR regarding 90-day mortality and 12-month neurological outcome. METHODS: This is a pre-determined substudy of prospective FINNRESUSCI study. Total of 287 patients treated in the intensive care units after OHCA and with consent from the next-of-kin and serum samples between baseline and day 4 were included. Outcome and neurological outcome were evaluated according the Pittsburgh Cerebral Performance Categories (CPC). Kaplan-Meier survival curves, areas under receiver operational characteristics curves and positive likelihood ratios for mortality and poor neurological outcome were calculated. RESULTS: Non-survivors had higher levels of suPAR after OHCA. Kaplan-Meier survival curves indicated high 90-day mortality in the highest concentration quintiles. LR+ for 1-year CPC 3-5 was 1.8-2.7 for the whole patient cohort and in shockable rhythms 2.0-2.4. In therapeutic hypothermia prognostic value remained. CONCLUSIONS: We found that high SuPAR concentrations were associated with poor outcome in patients with OHCA admitted to critical care. However, suPAR alone had inadequate predictive value for poor outcome and did not associate with 12-month neurological outcome.
Authors: Heikki Kiiski; Ville Jalkanen; Marika Ala-Peijari; Mari Hämäläinen; Eeva Moilanen; Jukka Peltola; Jyrki Tenhunen Journal: Front Neurol Date: 2017-04-18 Impact factor: 4.003
Authors: Dimitrios Velissaris; Nicholas Zareifopoulos; Ioanna Koniari; Vasilios Karamouzos; Dimitris Bousis; Andreas Gerakaris; Christina Platanaki; Nicholas Kounis Journal: J Clin Med Res Date: 2021-03-19