Authors

• Jure Samardžić — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-9346-6402
• Hrvoje Jurin — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-2599-553X
• Boško Skorić — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0001-5979-2346
• Miroslav Krpan — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-0639-953X
• Ivo Planinc — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0003-0561-6704
• Marijan Pašalić — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-3197-2190
• Nina Jakuš — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0001-7304-1127
• Maja Čikeš — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-4772-5549
• Davor Miličić — University of Zagreb School of Medicine, University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0001-9101-1570

Keywords

cardiorespiratory arrest, myocardial infarction, therapeutic hypothermia, platelet reactivity

DOI

Full Text

**Introduction**: Early targeted temperature management (TTM) below 36°C in patients who did not recover conscience after out of hospital arrest is crucial to reduce central nervous system damage. Myocardial infarction is often a cause of cardiac arrest and warrants dual antiplatelet therapy. Decrease in body temperature affects platelet reactivity and there are no special guidelines for antiplatelet management in this clinical setting. It is unclear how different TTM methods affects platelet reactivity. (1, 2) Herein, we compared platelet reactivity (PR) in two smaller cohort groups of patients with acute ST segment elevation myocardial infarction who underwent non-invasive and invasive TTM after cardiorespiratory arrest. **Methods**: We analyzed PR changes in patients during first three days using Multiplate function analyzer and arachidonic acid as platelet aggregation agonist. **Results**: Two and three and patients underwent invasive and noninvasive TTM, respectively. All but one had PR measurement on all three days. One patient in the invasive TTM group died on the second day and had no PR measure on day three. Patients in the noninvasive TTM group had higher PR levels (**Figure 1**). Figure 1. Platelet reactivity changes in AU*min - A) ASPItest (arachidonic acid as agonist) B) ADPtest (adenosin diphosphate as agonist). Blue lines - noninvasive temperature control; red lines - invasive temperature control. **Conclusion**: Data shows that there is a difference in PR in patients undergoing different methods of TTM after cardiac arrest and myocardial infarction. We hypothesize that this could be due to direct effect of invasive body temperature lowering on platelets which decrases their sensitivity on aspirin. Further investigations are needed to confirm our results, including measurements of ADP-dependant PR which is inhibited by P2Y12 antagonists.

Literature

1. Nolan JP, Morley PT, Vanden Hoek TL, Hickey RW, Kloeck WGJ, Billi J, et al. Therapeutic hypothermia after cardiac arrest: an advisory statement by the advanced life support task force of the International Liaison Committee on Resuscitation. Circulation. 2003;108:118–21. https://doi.org/10.1161/01.CIR.0000079019.02601.90
2. Llitjos JF, Sideris G, Voicu S, Bal Dit Sollier C, Deye N, Megarbane B, et al. Impaired biological response to aspirin in therapeutic hypothermia comatose patients resuscitated from out-of-hospital cardiac arrest. Resuscitation. 2016;105:16–21. https://doi.org/10.1016/j.resuscitation.2016.04.027