Aim: Activation of the complement system is known to be a potent inducer of systemic inflammation, which is an important component of post-cardiac arrest syndrome. Mannan-binding-lectin associated protein of 19 kDa (MAp19) is suggested to be a regulatory component of the lectin pathway of complement activation. The aims of this study were to describe serial levels of MAp19 protein in comatose survivors of out-of-hospital cardiac arrest (OHCA), to evaluate the effect of two different regimes of targeted temperature management and to investigate the possible association between levels of MAp19 and mortality. Methods: In this post-hoc study, we analysed data from two large randomized controlled studies: ‘Targeted temperature management at 33 degrees C versus 36 degrees C after cardiac arrest’ (TTM) and ‘Targeted temperature management for 48 versus 24 h and neurological outcome after out-of-hospital cardiac arrest’ (TTH). We measured serial levels of MAp19 in 240 patients within 72 h after OHCA and in 82 healthy controls. The effect of targeted temperature management on MAp19 levels was analysed according to temperature allocation in main trials. Results: MAp19 levels were significantly lower in OHCA patients within 48 h after OHCA ( p-values <0.001) compared with healthy controls. A target temperature at 33°C compared with 36°C for 24 h was associated with significantly lower levels of MAp19 (–57 ng/mL (95% confidence interval (CI): –97 to −16 mg/mL), p=0.006). Target temperature at 33°C for 48 h compared with 24 h was not associated with a difference in MAp19 levels (–31 ng/mL (95% CI: –120 to 60 mg/mL), p=0.57). Low MAp19 levels at admission were associated with higher 30-day mortality (12% vs. 38%, plog-rank =0.0008), also in adjusted analysis (two-fold higher, hazard ratio =0.48 (95% CI: 0.31 to 0.75), p=0.001). Analysis of MAp19 levels at 24–72 h showed they were not associated with 30-day mortality. Conclusion: Survivors after OHCA have lower levels of MAp19 protein compared with healthy controls. A targeted temperature management at 33°C compared with 36°C was associated with significantly lower MAp19 levels, whereas target temperature at 33°C for 48 h compared with 24 h did not influence MAp19 protein levels. Low MAp19 levels at admission were independently associated with increased mortality.
The lectin pathway (LP) of the complement system may initiate inflammatory reactions when body tissue is altered. We aimed to investigate levels of the LP proteins in out-of-hospital cardiac arrest patients, and to compare these with healthy individuals. Furthermore, we aimed to clarify whether duration of targeted temperature management influenced LP protein levels, and we further examined whether LP proteins were associated with 30-day mortality. We included 82 patients resuscitated from out-of-hospital cardiac arrest. The patients were randomly assigned to 24 or 48 hours of targeted temperature management at 33±1 °C. Blood samples were obtained 22, 46 and 70 hours after target temperature was reached. Levels of the LP proteins (mannan-binding lectin (MBL), M-ficolin, H-ficolin, collectin liver 1 (CL-L1), MBL-associated serine protease 1 (MASP-1), MASP-2, MASP-3 and MBL-associated protein of 44 kDa (MAp44)) were measured using time-resolved immunofluorometric assays. Data from 82 gender matched healthy individuals were used for comparison. Levels of CL-L1, MASP-1, MASP-2 and MAp44 were significantly higher, whereas M-ficolin levels were significantly lower in cardiac arrest patients compared with healthy individuals. MASP-2, MASP-3 and M-ficolin levels changed significantly when comparing 24 and 48 hours of targeted temperature management. The LP protein levels were not different between 30-day survivors and non-survivors after cardiac arrest. The differences in LP protein levels between patients and healthy individuals may indicate that cardiac arrest patients have an activated LP. Overall, the LP protein levels were not influenced by duration of targeted temperature management, and the levels were not associated with 30-day mortality. This article is protected by copyright. All rights reserved.
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