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Ubiquinol (reduced Coenzyme Q10) as a Metabolic Resuscitator in Post-Cardiac Arrest: A Randomized, Double-Blind, Placebo-Controlled Trial

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

  • Mathias J Holmberg
  • Lars W Andersen
  • Ari Moskowitz, Harvard University
  • ,
  • Katherine M Berg, Beth Israel Deaconess Medical Center, Boston, MA, USA.
  • ,
  • Michael N Cocchi, Beth Israel Deaconess Medical Center, Boston, MA, USA.
  • ,
  • Maureen Chase, Beth Israel Deaconess Medical Center, Boston, MA, USA.
  • ,
  • Xiaowen Liu, Beth Israel Deaconess Medical Center, Boston, MA, USA.
  • ,
  • Duncan M Kuhn, Cambridge Hospital, Cambridge Health Alliance, Cambridge, MA, USA
  • ,
  • Anne V Grossestreuer, Beth Israel Deaconess Medical Center, Boston, MA, USA.
  • ,
  • Anne Kirstine Hoeyer-Nielsen, Aalborg University
  • ,
  • Hans Kirkegaard
  • Michael W Donnino, Harvard University

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 hours for up to 7 days. The primary endpoint was total coenzyme Q10 plasma levels at 24 hours 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 hours (441 [IQR, 215-510] ηg/mL vs. 113 [IQR, 94-208] ηg/mL, P < 0.001). Similar results were observed at 48 and 72 hours. 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 hours (16.8 [IQR, 9.5-19.8] ηg/mL vs. 8.2 [IQR, 4.3-19.1] ηg/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.

Original languageEnglish
Pages (from-to)388-395
Number of pages8
Publication statusPublished - May 2021

    Research areas

  • Coenzyme Q10, Heart arrest, Mitochondrial dysfunction, Neuron specific enolase, Oxygen consumption, Ubiquinol

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