ubiquinone and Heart-Arrest

Topics: Amyotrophic Lateral Sclerosis; Child; Clinical Trials as Topic; Coenzymes; Friedreich Ataxia; Heart Arrest; Humans; Huntington Disease; Mitochondrial Diseases; Nervous System Diseases; Parkinson Disease; Ubiquinone

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.

Topics: Biomarkers; Double-Blind Method; Heart Arrest; Humans; Ubiquinone

Therapeutic hypothermia can improve survival after cardiopulmonary resuscitation (CPR). Coenzyme Q10 (CoQ10) has shown a protective effect in neurodegenerative disorders. We investigated whether combining mild hypothermia with CoQ10 after out-of-hospital cardiac arrest provides additional benefit.. Forty-nine patients were randomly assigned to either hypothermia plus CoQ10 or hypothermia plus placebo after CPR. Hypothermia with a core temperature of 35 degrees C was instituted for 24 hours. Liquid CoQ10 250 mg followed by 150 mg TID for 5 days or placebo was administered through nasogastric tube. Age, sex, premorbidity, cause of arrest, conditions of CPR, and degree of hypoxia were similar in both groups; no side effects of CoQ10 were identified. Three-month survival in the CoQ10 group was 68% (17 of 25) and 29% (7 of 24) in the placebo group (P=0.0413). Nine CoQ10 patients versus 5 placebo patients survived with a Glasgow Outcome Scale of 4 or 5. Mean serum S100 protein 24 hours after CPR was significantly lower in the CoQ10 group (0.47 versus 3.5 ng/mL).. Combining CoQ10 with mild hypothermia immediately after CPR appears to improve survival and may improve neurological outcome in survivors.

Topics: Adult; Aged; Biomarkers; Brain Damage, Chronic; Combined Modality Therapy; Electroencephalography; Evoked Potentials, Somatosensory; Female; Glasgow Outcome Scale; Heart Arrest; Humans; Hypothermia, Induced; Life Tables; Male; Middle Aged; Neuropsychological Tests; S100 Proteins; Single-Blind Method; Survival Analysis; Treatment Outcome; Ubiquinone

Topics: Double-Blind Method; Heart Arrest; Humans; Resuscitation; Ubiquinone

Survival after cardiac arrest (CA) is limited by the profound neurologic insult from ischemia-reperfusion injury. Therapeutic options are limited. Previous data suggest a benefit of coenzyme Q(10) (CoQ(10)) in post-arrest patients. We hypothesized that plasma CoQ(10) levels would be low after CA and associated with poorer outcomes.. Prospective observational study of post-arrest patients presenting to a tertiary care center. CoQ(10) levels were drawn 24h after return of spontaneous circulation (ROSC) and compared to healthy controls. Levels of inflammatory cytokines and biomarkers were analyzed. Primary endpoints were survival to discharge and neurologic status at time of discharge.. 23 CA subjects and 16 healthy controls were enrolled. CoQ(10) levels in CA patients (0.28 μmol L(-1), inter-quartile range (IQR): 0.22-0.39) were significantly lower than in controls (0.75 μmol L(-1), IQR: 0.61-1.08, p<0.0001). The mean CoQ(10) level in CA patients who died was significantly lower than in those who survived (0.27 vs 0.47 μmol L(-1), p = 0.007). There was a significant difference in median CoQ(10) level between patients with a good vs poor neurological outcome (0.49 μmol L(-1), IQR: 0.30-0.67 vs 0.27 μmol L(-1), IQR: 0.21-0.30, p = 0.02). CoQ(10) was a statistically significant predictor of poor neurologic outcome (adjusted p = 0.02) and in-hospital mortality (adjusted p = 0.026).. CoQ(10) levels are low in human subjects with ROSC after cardiac arrest as compared to healthy controls. CoQ(10) levels were lower in those who died, as well as in those with a poor neurologic outcome.

Topics: Aged; Biomarkers; Cytokines; Female; Heart Arrest; Hospital Mortality; Humans; Male; Middle Aged; Outcome Assessment, Health Care; Patient Discharge; Prospective Studies; Survival Analysis; Ubiquinone

Topics: Cytokines; Female; Heart Arrest; Humans; Male; Ubiquinone

The distribution patterns of amyloid precursor protein (APP) fragments were studied immunocytochemically in the rat brain before, after 10 min ischemia and following treatment by idebenone. Six months after brain ischemia intense staining for APP appeared in extra- and intracellular space. These findings indicate that APP is involved in the degeneration process of brain neuronal and glial cells following ischemia-reperfusion injury and anti-oxidative therapy did not prevent and/or stop this phenomenon.

Topics: Alzheimer Disease; Amyloid beta-Protein Precursor; Amyloidosis; Animals; Antioxidants; Benzoquinones; Cell Death; Drug Evaluation, Preclinical; Extracellular Space; Female; Free Radicals; Heart Arrest; Hypoxia-Ischemia, Brain; Intracellular Fluid; Neuroglia; Neurons; Neuroprotective Agents; Oxidative Stress; Rats; Rats, Wistar; Reperfusion Injury; Risk Factors; Ubiquinone