Level of systemic inflammation and endothelial injury is associated with cardiovascular dysfunction and vasopressor support in post cardiac arrest patients
Resuscitation Sep 28, 2017
Bro-Jeppesen JB, et al. - An investigation was performed regarding the associations between systemic inflammation, endothelial damage and hemodynamic parameters including vasopressor support in patients with out-of-hospital cardiac arrest (OHCA). In comatose survivors after OHCA, an increase in need of vasopressor support was observed with increased systemic inflammation and endothelial injury. Systemic inflammation, in particular interleukin (IL)-6, seemed to have a consistent association with vasopressor support, however, endothelial injury could also play a role in post-cardiac arrest syndrome (PCAS) associated cardiovascular dysfunction after OHCA.
Methods
- Authors undertook this post-hoc study and analyzed data from 163 comatose patients included at a single center in the Target Temperature Management (TTM) trial, randomly assigned to TTM at 33 °C or 36 °C for 24 hours.
- At randomization and 24, 48 and 72 hours after OHCA, they measured inflammatory biomarkers (interleukin (IL)-6, IL-10, procalcitonin and Tumor Necrosis Factor-α (TNF-α)) and endothelial biomarkers (thrombomodulin, sE-selectin, syndecan-1 and VE-cadherin).
- They reported corresponding hemodynamic status, heart rate (HR), mean arterial pressure (MAP) and Cumulative Vasopressor Index (CVI).
Results
- At randomization, there appeared a negative correlation of level of IL-6 with MAP (r = -0.19,p=0.03) and a positive correlation of level of IL-6 with HR (r = 0.29,p=0.0002).
- A consistent correlation was observed between serial IL-6 levels and CVI at 24 h: (r = 0.19,p=0.02) 48 h: (r = 0.31,p=0.0001) and 72 h: (r = 0.39,p<0.0001).
- Findings suggested a correlation of thrombomodulin (r = 0.23,p=0.004) and syndecan-1 (r = 0.27,p=0.001) with CVI at 48 h.
- All inflammatory markers excerpt IL-10 and all endothelial markers seemed correlated with CVI at 72 h.
- Multivariable regression models adjusting for potential confounders established an association of IL-6 (β=0.2 (95%CI:0.06-0.3),p=0.004) and TTM-group (TTM36: β=-0.5 (95%CI:-0.9- -0.1),p=0.01) with CVI at 48 h.
- At 72h after OHCA, IL-6 (β=0.3 (95%CI:0.03-0.6),p<0.0001), TNF-α (β=-0.4 (95%CI:-0.5- -0.2),p<0.0001) and TTM-group (TTM36: β=-0.4 (95%CI:-0.8- -0.1),p=0.008) seemed associated with CVI.
- An overall two-fold increase in levels of IL-6 (β = 0.2 (95%CI:0.1-0.3),p<0.0001)) and IL-10 (β = -0.2 (95%CI:-0.3- -0.06),p=0.005)) within 72 h after OHCA seemed markedly associated with CVI.
- In this study, TTM-group seemed modifying the interaction between CVI and IL-6 (pinteraction=0.008), but not with IL-10 (pinteraction=0.23).
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