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).

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.