Influence of mannan-binding lectin and MAp44 on outcome in comatose survivors of out-of-hospital cardiac arrest

AimThe lectin complement pathway, initiated by mannan-binding-lectin (MBL) plays a role in tissue destruction following ischemia/reperfusion, and MBL deficiency has been associated with favorable outcome in stroke patients. MAp44 is produced in the heart and may theoretically function as an endogenous inhibitor of MBL-mediated activities. The aim of this study was to investigate the possible association between MBL deficiency, MAp44 levels and outcome in comatose survivors of out-of-hospital cardiac arrest (OHCA).MethodsIn a single center post hoc analysis of the prospective multicenter randomized Target Temperature Management (TTM) trial, we measured MBL and MAp44 levels at baseline, 24, 48 and 72 h after OHCA in 169 consecutive patients randomly assigned to TTM at 33 °C or 36 °C for 24 h. Primary outcome was 30 days mortality and secondary outcome was favorable neurological outcome assessed by Cerebral Performance Category (CPC1-2) and modified Rankin Scale (mRS0-3) 180 days after OHCA.ResultsPatients with MBL deficiency (defined as plasma levels ≤100 ng ml−1 at baseline) (n = 22) carried a 30-day mortality of 41% compared to 32% in MBL sufficient patient (n = 147), p = 0.55. Baseline MAp44 levels were not associated with mortality, p = 0.25. There was no significant difference in neurological outcome between the two MBL groups assessed by CPC (p = 0.69) and mRS (p = 0.91). In multivariable models, baseline MBL (OR = 1.0, p = 0.70), (OR = 1.5, p = 0.30) and MAp44 levels (OR = 1.0, p = 0.99), (OR = 1.6, p = 0.21) were not associated with favorable neurological outcome assessed by CPC and mRS, respectively.ConclusionsIn comatose survivors after cardiac arrest, neither MBL deficiency nor levels of MBL and MAp44 were associated with mortality or neurological outcome.