Background

Whole body ischemia and reperfusion injury after cardiac arrest leads to the massive inflammation clinically manifested in the post-cardiac arrest syndrome. Previous studies on the inflammatory effect on circulatory failure after cardiac arrest have either investigated a selected patient group or a limited part of the inflammatory mechanisms. We examined the association between cardiac arrest characteristics and inflammatory biomarkers, and between inflammatory biomarkers and circulatory failure after cardiac arrest, in an unselected patient cohort.

Methods

This was a prospective study of 50 consecutive patients with out-of-hospital cardiac arrest. Circulation was invasively monitored from admission until day five, whereas inflammatory biomarkers, i.e. complement activation, cytokines and endothelial injury, were measured daily. We identified predictors for an increased inflammatory response, and associations between the inflammatory response and circulatory failure.

Results

We found a marked and broad inflammatory response in patients after cardiac arrest, which was associated with clinical outcome. Long time to return of spontaneous circulation and high lactate level at admission were associated with increased complement activation (TCC and C3bc), pro-inflammatory cytokines (IL-6, IL-8) and endothelial injury (syndecan-1) at admission. These biomarkers were in turn significantly associated with lower mean arterial blood pressure, lower cardiac output and lower systemic vascular resistance, and increased need of circulatory support in the initial phase. High levels of TCC and IL-6 at admission were significantly associated with increased 30-days mortality.

Conclusion

Inflammatory biomarkers, including complement activation, cytokines and endothelial injury, were associated with increased circulatory failure in the initial period after cardiac arrest.

中文翻译：

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炎症反应与院外心脏骤停后的循环衰竭有关：一项前瞻性队列研究

背景

心脏骤停后全身缺血再灌注损伤导致大量炎症，临床表现为心脏骤停后综合征。先前关于心脏骤停后对循环衰竭的炎症影响的研究要么研究了选定的患者组，要么研究了炎症机制的有限部分。我们在未选择的患者队列中检查了心脏骤停特征与炎症生物标志物之间的关联，以及心脏骤停后炎症生物标志物与循环衰竭之间的关联。

方法

这是一项针对 50 名院外心脏骤停患者的前瞻性研究。从入院到第 5 天，对循环进行有创监测，而每天测量炎症生物标志物，即补体激活、细胞因子和内皮损伤。我们确定了炎症反应增加的预测因子，以及炎症反应与循环衰竭之间的关联。

结果

我们发现心脏骤停后患者出现明显而广泛的炎症反应，这与临床结果相关。入院时恢复自主循环的时间长和高乳酸水平与入院时补体激活（TCC 和 C3bc）、促炎细胞因子（IL-6、IL-8）和内皮损伤（syndecan-1）增加有关。这些生物标志物又与较低的平均动脉血压、较低的心输出量和较低的全身血管阻力以及初始阶段对循环支持的需求增加显着相关。入院时高水平的 TCC 和 IL-6 与 30 天死亡率增加显着相关。

结论

炎症生物标志物，包括补体激活、细胞因子和内皮损伤，与心脏骤停后初始阶段的循环衰竭增加有关。