Holmberg Mathias J, Andersen Lars W, Moskowitz Ari, Berg Katherine M, Cocchi Michael N, Chase Maureen, Liu Xiaowen, Kuhn Duncan M, Grossestreuer Anne V, Hoeyer-Nielsen Anne Kirstine, Kirkegaard Hans, Donnino Michael W
Research Center for Emergency Medicine, Department of Clinical Medicine, Aarhus University and Aarhus University Hospital, Aarhus, Denmark; Center for Resuscitation Science, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA; Department of Cardiology, Viborg Regional Hospital, Viborg, Denmark.
Research Center for Emergency Medicine, Department of Clinical Medicine, Aarhus University and Aarhus University Hospital, Aarhus, Denmark; Center for Resuscitation Science, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA; Prehospital Emergency Medical Services, Central Denmark Region, Denmark; Department of Anesthesiology and Intensive Care, Aarhus University Hospital, Aarhus, Denmark.
Resuscitation. 2021 May;162:388-395. doi: 10.1016/j.resuscitation.2021.01.041. Epub 2021 Feb 9.
Ubiquinol (reduced coenzyme Q10) is essential for adequate aerobic metabolism. The objective of this trial was to determine whether ubiquinol administration in patients resuscitated from cardiac arrest could increase physiological coenzyme Q10 levels, improve oxygen consumption, and reduce neurological biomarkers of injury.
This was a randomized, double-blind, placebo-controlled trial in patients successfully resuscitated from cardiac arrest. Patients were randomized to receive enteral ubiquinol (300 mg) or placebo every 12 h for up to 7 days. The primary endpoint was total coenzyme Q10 plasma levels at 24 h after enrollment. Secondary endpoints included neuron specific enolase, S100B, lactate, cellular and global oxygen consumption, neurological status, and in-hospital mortality.
Forty-three patients were included in the modified intention-to-treat analysis. Median coenzyme Q10 levels were significantly higher in the ubiquinol group as compared to the placebo group at 24 h (441 [IQR, 215-510] ηg/mL vs. 113 [IQR, 94-208] ηg/mL, P < 0.001). Similar results were observed at 48 and 72 h. There were no differences between the two groups in any of the secondary endpoints. Median neuron specific enolase levels were not different between the two groups at 24 h (16.8 [IQR, 9.5-19.8] ηg/mL vs. 8.2 [IQR, 4.3-19.1] ηg/mL, P = 0.61).
Administration of enteral ubiquinol increased plasma coenzyme Q10 levels in post-cardiac arrest patients as compared to placebo. There were no differences in neurological biomarkers and oxygen consumption between the two groups.
泛醇(还原型辅酶Q10)对于充足的有氧代谢至关重要。本试验的目的是确定对心脏骤停复苏后的患者给予泛醇是否能提高生理辅酶Q10水平、改善氧消耗并降低损伤的神经生物标志物水平。
这是一项针对成功从心脏骤停中复苏的患者的随机、双盲、安慰剂对照试验。患者被随机分组,每12小时接受一次肠内泛醇(300毫克)或安慰剂,持续7天。主要终点是入组后24小时的辅酶Q10血浆总水平。次要终点包括神经元特异性烯醇化酶、S100B、乳酸、细胞和整体氧消耗、神经状态及院内死亡率。
43例患者纳入改良意向性分析。与安慰剂组相比,泛醇组在24小时时辅酶Q10水平中位数显著更高(441[四分位间距,215 - 510]纳克/毫升对113[四分位间距,94 - 208]纳克/毫升,P<0.001)。在48小时和72小时观察到类似结果。两组在任何次要终点方面均无差异。两组在24小时时神经元特异性烯醇化酶水平中位数无差异(16.8[四分位间距,9.5 - 19.8]纳克/毫升对8.2[四分位间距,4.3 - 19.1]纳克/毫升,P = 0.61)。
与安慰剂相比,对心脏骤停后患者给予肠内泛醇可提高血浆辅酶Q10水平。两组在神经生物标志物和氧消耗方面无差异。