Spiel Alexander O, Frossard Martin, Mayr Florian B, Kliegel Andreas, Janata Andreas, Uray Thomas, Wandaller Cosima, Sterz Fritz, Jilma Bernd
Departments of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria.
Crit Care Med. 2009 Mar;37(3):975-9. doi: 10.1097/CCM.0b013e3181962cb9.
Markers of platelet activation are increased in patients undergoing cardiopulmonary resuscitation. Hyperfunctional platelets may contribute to impairment of microcirculatory function and overall poor outcome despite restoration of spontaneous circulation (ROSC). Patients with myocardial infarction have hyperfunctional platelets, which predict the degree of myocardial necrosis. Thus, we hypothesized that platelets may be even more activated in patients whose myocardial infarction leads to cardiac arrest and compared them with patients whose cardiac arrest was due to a noncardiac origin.
Prospective observational study.
Emergency department of a tertiary care hospital.
One hundred four patients with witnessed cardiac arrest who achieved ROSC.
Blood sampling.
We assessed collagen adenosine diphosphate closure time with the platelet function analyzer-100, and measured plasma levels of von Willebrand factor: ristocetin cofactor activity levels by turbidometry. Independent physicians diagnosed the origin of cardiac arrest. The majority of cardiac arrests were caused by myocardial ischemia. Invariably, collagen adenosine diphosphate closure time values (55 seconds; 95% confidence interval: 52-58 seconds) were much shorter in these patients compared with patients with other causes of cardiac arrest (110 seconds; 95% confidence interval: 84-135 seconds, p < 0.001). von Willebrand factor: ristocetin cofactor activity plasma levels were more than three-fold above normal values in both groups.
Patients with myocardial ischemia-triggered cardiac arrest had the highest degree of platelet hyperfunction under high shear rates, which was not solely due to increased von Willebrand factor. Future trials are necessary to clarify whether rapid, more aggressive antiplatelet therapy improves outcome after cardiac arrest.
接受心肺复苏的患者血小板活化标志物会升高。尽管恢复了自主循环（ROSC），但功能亢进的血小板可能会导致微循环功能受损以及总体预后不良。心肌梗死患者存在功能亢进的血小板，这可预测心肌坏死程度。因此，我们推测心肌梗死导致心脏骤停的患者血小板可能被更强烈地激活，并将他们与心脏骤停由非心脏原因引起的患者进行比较。
前瞻性观察性研究。
一家三级护理医院的急诊科。
104例心脏骤停后实现自主循环恢复的患者。
采血。
我们使用血小板功能分析仪 - 100评估胶原二磷酸腺苷封闭时间，并通过比浊法测量血管性血友病因子：瑞斯托霉素辅因子活性水平的血浆浓度。独立医生诊断心脏骤停的病因。大多数心脏骤停是由心肌缺血引起的。这些患者的胶原二磷酸腺苷封闭时间值（55秒；95%置信区间：52 - 58秒）始终比其他原因导致心脏骤停的患者（110秒；95%置信区间：84 - 135秒，p < 0.001）短得多。两组患者的血管性血友病因子：瑞斯托霉素辅因子活性血浆水平均比正常值高出三倍以上。
心肌缺血引发心脏骤停的患者在高剪切率下血小板功能亢进程度最高，这并非仅仅由于血管性血友病因子增加所致。未来有必要进行试验以明确快速、更积极的抗血小板治疗是否能改善心脏骤停后的预后。
