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

<bold>Aim: </bold>The 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).<bold>Methods: </bold>In 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 24h. 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.<bold>Results: </bold>Patients with MBL deficiency (defined as plasma levels ≤100 ngml(-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.<bold>Conclusions: </bold>In comatose survivors after cardiac arrest, neither MBL deficiency nor levels of MBL and MAp44 were associated with mortality or neurological outcome. [ABSTRACT FROM AUTHOR]