Coagulopathy after successful cardiopulmonary resuscitation following cardiac arrest - Implication of the protein C anticoagulant pathway
Coagulopathy after successful cardiopulmonary resuscitation following cardiac arrest - Implication of the protein C anticoagulant pathway
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DOI：
10.1016/j.jacc.2005.03.046
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发表时间：
2005-07-05
影响因子：
24
通讯作者：
Dhainaut, JF
中科院分区：
文献类型：
--
作者：
Adrie, C;Monchi, M;Dhainaut, JF
目的 我们调查了院外心脏骤停 (OHCA) 患者的凝血异常，特别关注蛋白 C 抗凝途径。 背景 成功复苏的心脏骤停后会出现全身炎症反应和凝血激活，这两者都可能导致器官衰竭和神经功能障碍。 方法 对 OHCA 成功复苏后入院的所有患者进行凝血参数测量。 结果 入院时，67 名患者出现全身炎症反应，白细胞介素 6 和凝血活性增加（凝血酶-抗凝血酶复合物），抗凝作用降低（抗凝血酶、蛋白 C 和蛋白 S），激活纤溶（纤溶酶-抗纤溶酶复合物），并且在某些情况下抑制纤溶（纤溶酶原激活物抑制剂-1 增加，在第 1 天达到峰值）。这些异常在两天内死亡的患者中更为严重（67 例中的 50 例，75%），并且在死于早期难治性休克的患者中最为严重。与健康志愿者相比，蛋白质 C 和 S 水平较低，并将 OHCA 幸存者与非幸存者区分开来。此外，一部分患者入院时血浆活化蛋白 C 出现短暂升高，随后达到检测不到的水平。这与可溶性血栓调节蛋白随时间的增加一起表明，继发性内皮损伤和蛋白 C 抗凝途径功能障碍与严重脓毒症中观察到的情况相似。 结论 心脏骤停成功复苏后发现主要凝血异常。这些异常与血栓调节蛋白-内皮蛋白 C 受体途径的继发性下调一致。 (J Am Coll Cardiol 2005；46:21-8) (c) 2005 年，美国心脏病学会基金会。
OBJECTIVES We investigated coagulation abnormalities in out-of-hospital cardiac arrest (OHCA) patients, with special attention to the protein C anticoagulant pathway.BACKGROUND Successfully resuscitated cardiac arrest is followed by a systemic inflammatory response and by activation of coagulation, both of which may contribute to organ failure and neurological dysfunction.METHODS Coagulation parameters were measured in all patients admitted after successfully resuscitated OHCA.RESULTS At admission, 67 patients had a systemic inflammatory response with increased interleukin-6 and coagulation activity (thrombin-antithrombin complex), reduced anticoagulation (antithrombin, protein C, and protein S), activated fibrinolysis (plasmin-antiplasmin complex), and, in some cases, inhibited fibrinolysis (increased plasminogen activator inhibitor-1 with a peak on day 1). These abnormalities were more severe in patients who died within two days (50 of 67, 75%) and were most severe in patients dying from early refractory shock. Protein C and S levels were low compared to healthy volunteers and discriminated OHCA survivors from nonsurvivors. Furthermore, a subgroup of patients had a transient increase in plasma-activated protein C at admission followed by undetectable levels. This, along with an increase in soluble thrombomodulin over time, suggests secondary endothelial injury and dysfunction of the protein C anticoagulant pathway similar to that observed in severe sepsis.CONCLUSIONS Major coagulation abnormalities were found after successful resuscitation of cardiac arrest. These abnormalities are consistent with secondary down-regulation of the thrombomodulin-endothelial protein C receptor pathway. (J Am Coll Cardiol 2005;46:21-8) (c) 2005 by the American College of Cardiology Foundation.