Galectin-3 as a marker to characterize post-cardiac arrest syndrome in initially survived out-of-hospital cardiac arrest: a prospective two-center study.

BACKGROUND

Survivors after out-of-hospital cardiac arrest (OHCA) experience post-cardiac arrest syndrome (PCAS), which encompasses cerebral edema, hemodynamic instability and systemic inflammation and causes high in-hospital mortality rates. Galectin (GAL) 3 is a predictor of mortality and unfavorable neurological outcome following OHCA. This study aims to investigate the relationship between GAL3 levels and key features of PCAS including in-hospital mortality, cerebral edema, post-cardiac arrest shock and systemic inflammation in OHCA patients.

METHODS

This prospective, two-center study included 71 adults after non-traumatic OHCA. Blood samples were taken on hospital admission (day 0) and day 2 after return of spontaneous circulation (ROSC). Serum GAL3 concentrations were quantified by enzyme-linked immunosorbent assay and compared with serum levels of 39 patients with coronary artery disease (CAD).

RESULTS

Serum GAL3 levels were highest on day 0 and declined on day 2 after ROSC to levels comparable to CAD controls. GAL3 levels were higher in non-survivors at both time- points. Admission GAL3 concentrations positively correlated with lactate on admission, a marker for no-flow/low-flow time and were elevated in patients with cerebral edema on cerebral computed tomography. Furthermore, admission GAL3 was higher in patients with inadequate lactate clearance and GAL3 levels on day 2 were significantly elevated in OHCA patients who required prolonged vasopressor/inotropic medication, both indicators of persistent hypoperfusion and shock. Moreover, a positive correlation was observed between GAL3 and interleukin-6 on admission.

CONCLUSION

Serum GAL3 levels are associated with in-hospital mortality and distinct features of PCAS including cerebral edema, persistent shock and systemic inflammation following OHCA.