Coenzyme Q10 in Post-Cardiac Arrest Cerebral Resuscitation
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|ClinicalTrials.gov Identifier: NCT01319110|
Recruitment Status : Completed
First Posted : March 21, 2011
Results First Posted : April 28, 2017
Last Update Posted : July 31, 2017
Specific Aim #1: To determine if levels of CoQ10 are low post-cardiac arrest (CA). We will perform a prospective trial with the primary endpoint of describing the prevalence of low serum CoQ10 levels.
Specific Aim #2: To determine if CoQ10 levels in post-CA patients can be increased with the administration of exogenous CoQ10.. We will perform a randomized control trial (RCT) of post-CA patients with the secondary endpoint of comparing CoQ10 levels among those randomized to CoQ10 supplementation vs placebo.
|Condition or disease||Intervention/treatment||Phase|
|Cardiac Arrest Sudden Cardiac Arrest||Drug: Coenzyme Q10 Dietary Supplement: Placebo||Phase 2|
Cardiac arrest (CA) occurs in nearly 350,000 patients in the U.S. each year with an estimated mortality of 60% in those surviving the initial arrest. Moreover, the overall prognosis for survivors is often limited by neurologic injury. Two randomized control trials (RCTs) have demonstrated that therapeutic hypothermia (TH) after CA improves survival and reduces neurologic morbidity. As a result of these studies, TH has become the standard of care in post-CA patients. The mechanism of action for TH is hypothesized to be a reduction in cerebral oxygen consumption that occurs following an ischemia-reperfusion injury. Another similar potential target following ischemia-reperfusion injury is mitochondrial function in the injured brain cells and attenuation of potentially damaging oxygen-free radicals. Specifically, optimizing mitochondrial function and reducing oxygen free radicals may enhance cellular function and mitigate cellular injury thereby leading to improved neurologic outcomes. Coenzyme Q10 (CoQ10) is an essential mitochondrial co-factor and free radical scavenger that has been found to have neuroprotective effects in various neurodegenerative disorders such as Parkinson's disease and Huntington's disease. Whether CoQ10 can provide neuroprotection in acute ischemia-reperfusion injury remains less clear, but has been recognized by the American Heart Association as a potentially promising neuroprotective agent. We hypothesize that the administration of exogenous CoQ10 will raise serum concentrations of CoQ10 and as such may mitigate the adverse effects of the post-CA ischemia-reperfusion injury on the brain by optimizing mitochondrial function and reducing oxygen-free radicals. We support this hypothesis by the following:
- Ischemia-reperfusion injury disrupts normal mitochondrial function and increases O2 free radicals.
- CoQ10 has been found to attenuate the effects of ischemia-reperfusion injury through optimizing mitochondrial function and mitigation of cellular apoptosis.
- CoQ10 has neuroprotective effects in other neurodegenerative disorders.
- Our group has unpublished preliminary data showing low CoQ10 levels in a majority of patients with septic shock, and that lower CoQ10 levels are significantly associated with multiple markers of the inflammatory cascade.
- A pilot human trial in post-CA patients demonstrated a reduction in mortality and trend toward reduction in neurologic morbidity.
To test our hypothesis, we propose the following pilot study as proof of concept in preparation for a larger multicenter trial powered toward neurologic outcome and mortality. This pilot study will allow for a more informed power analysis for a larger trial, provide proof of concept for enrollment and administration of therapy, examine the time-frame for drug absorption into serum, and evaluate for tolerability.
|Study Type :||Interventional (Clinical Trial)|
|Actual Enrollment :||10 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)|
|Official Title:||Coenzyme Q10 in Post-Cardiac Arrest Cerebral Resuscitation|
|Actual Study Start Date :||February 2011|
|Actual Primary Completion Date :||December 31, 2011|
|Actual Study Completion Date :||December 31, 2011|
Patients will receive CoenzymeQ10 200mg three times per day for 7 days, until return to baseline neurologic status, or until death/discharge (whichever comes first). CoQ10 will be given through pre-existing NG or OG tube, and mixed with 20 ml of chocolate Ensure so as to blind investigators and staff.
Drug: Coenzyme Q10
Patients will receive CoQ10 200mg three times per day for 7 days, until return to baseline neurologic status, or until death/discharge (whichever comes first). CoQ10 will be given through pre-existing NG or OG tube, and mixed with 20 ml of chocolate Ensure so as to blind investigators and staff.
Other Name: Ubiquinone
Placebo Comparator: Placebo
Patients will receive 20 ml chocolate Ensure (as a placebo) three times per day for 7 days, until return to baseline neurologic status, or until death/discharge (whichever comes first). Placebo will be given through pre-existing NG or OG tube.
Dietary Supplement: Placebo
Patients will be given Chocolate Ensure via NG/ OG 3x daily as a placebo.
- Prevalence of Low Serum CoQ10 Levels in Cardiac Arrest Patients [ Time Frame: Baseline ]The primary outcome will be describing the prevalence of low serum CoQ10 levels compared to standard laboratory control values.
- Comparison of Serum CoQ10 Levels Randomized to Supplementation vs. Placebo [ Time Frame: 1 year ]The secondary outcome will be to compare serum CoQ10 levels among those post-arrest patients randomized to CoQ10 supplementation vs placebo.
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01319110
|United States, Massachusetts|
|Beth Israel Deaconess Medical Center|
|Boston, Massachusetts, United States, 02215|
|Principal Investigator:||Michael N Cocchi, MD||Beth Israel Deaconess Medical Center|