However, shocked STEMI patients without cardiac arrest who receive a comparable IV injection of heparin [21] display lower circulating syndecan-1 level compared to STEMI OHCA patients (median 129 ng/ml vs. 206 ng/ml), indicating that other factors than heparin i.e., exogenous adrenaline administration, defibrillations, time from OHCA to ROSC, pH and lactate (shock) (these were all correlated with syndecan-1 in the present study) contribute to the glycocalyx damage [8, 39]. This evidence concerns the gene SDC1 and cardiac arrest.