Ubiquinol (reduced coenzyme Q10) as a metabolic resuscitator in post-cardiac arrest: A randomized, double-blind, placebo-controlled trial

被引:11
|
作者
Holmberg, Mathias J. [1 ,2 ,3 ,4 ]
Andersen, Lars W. [1 ,2 ,3 ,5 ,6 ]
Moskowitz, Ari [3 ,7 ]
Berg, Katherine M. [3 ,7 ]
Cocchi, Michael N. [3 ]
Chase, Maureen [3 ]
Liu, Xiaowen [3 ]
Kuhn, Duncan M. [8 ]
Grossestreuer, Anne, V [3 ]
Hoeyer-Nielsen, Anne Kirstine [3 ,9 ]
Kirkegaard, Hans [1 ,2 ]
Donnino, Michael W. [3 ,7 ]
机构
[1] Aarhus Univ, Res Ctr Emergency Med, Dept Clin Med, Aarhus, Denmark
[2] Aarhus Univ Hosp, Aarhus, Denmark
[3] Beth Israel Deaconess Med Ctr, Ctr Resuscitat Sci, Dept Emergency Med, One Deaconess Rd, Boston, MA 02215 USA
[4] Viborg Reg Hosp, Dept Cardiol, Viborg, Denmark
[5] Prehosp Emergency Med Serv, Aarhus, Central Denmark, Denmark
[6] Aarhus Univ Hosp, Dept Anesthesiol & Intens Care, Aarhus, Denmark
[7] Beth Israel Deaconess Med Ctr, Dept Internal Med, Div Pulm Crit Care & Sleep Med, Boston, MA 02215 USA
[8] Cambridge Hosp, Dept Med, Div Pulm Crit Care & Sleep Med, Cambridge Hlth Alliance, Cambridge, MA 02139 USA
[9] Aalborg Univ Hosp, Dept Nephrol, Aalborg, Denmark
基金
美国国家卫生研究院;
关键词
Heart arrest; Coenzyme Q10; Ubiquinol; Mitochondrial dysfunction; Oxygen consumption; Neuron specific enolase;
D O I
10.1016/j.resuscitation.2021.01.041
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Introduction: 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. Materials and methods: 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. Results: 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] hg/mL vs. 113 [IQR, 94-208] hg/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] hg/mL vs. 8.2 [IQR, 4.3-19.1] hg/mL, P = 0.61). Conclusions: 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.
引用
收藏
页码:388 / 395
页数:8
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