Coenzyme Q-10 and Pulmonary Arterial Hypertension
The purpose of this study is to evaluate the effects of Coenzyme Q-10, an antioxidant, in the treatment of pulmonary hypertension.
|Study Design:||Allocation: Non-Randomized
Endpoint Classification: Safety/Efficacy Study
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Treatment
|Official Title:||Coenzyme Q-10 in the Treatment of Pulmonary Arterial Hypertension|
- Evidence of clinically definite ischemic stroke (focal neurological deficits persisting for more than 24 hours) confirmed by non-investigational CT or MRI [ Time Frame: Within 30 (plus or minus 3 days) after surgery ] [ Designated as safety issue: Yes ]Measures of superoxide dismutase (SOD) activity, exhaled nitric oxide (NO), and its circulating products, and circulating progenitor cells in relation to clinical outcomes.
|Study Start Date:||January 2010|
|Estimated Study Completion Date:||August 2014|
|Estimated Primary Completion Date:||August 2014 (Final data collection date for primary outcome measure)|
Experimental: Coenzyme Q and Pulmonary Hypertension
Pulmonary Hypertension subjects and Normal Healthy Controls
Other: Nutritional Supplement Coenzyme Q-10
Other Name: Coenzyme Q: Nutritional Supplement
Abnormalities in the blood vessels in the lung are the hallmark of pulmonary hypertension. Links between increased free radical production, mitochondrial dysfunction and pulmonary hypertension have been studied but are poorly understood. The mitochondria of cells is the location where cellular energy is created and free radicals are atoms or groups of atoms with an odd (unpaired) number of electrons and can be formed when oxygen interacts with certain molecules. Once formed these reactive radicals can start a chain reaction, like dominoes. Their chief danger comes from the damage they can do when they react with important cellular components. Cells may function poorly or die if this occurs. The body produces free radicals in the normal course of energy production and in pulmonary hypertension, free radical production is found to be increased. To prevent free radical damage the body has a defense system of antioxidants. Coenzyme Q-10 is an antioxidant and it helps to protect cells from damage caused by the body's own free radicals. By providing oral supplementation of coenzyme Q-10, free radical levels will be decreased and cellular functioning in the pulmonary blood vessels may improve and even return to near normal functioning.
The purpose of this study is to evaluate the effects of coenzyme Q-10, an antioxidant, in the treatment of pulmonary hypertension. We will assess coenzyme Q-10 supplementation in the treatment of pulmonary hypertension by clinical measurements and blood levels of certain cellular components. We would like to assess the effects of coenzyme Q-10 on the pulmonary vessels by measuring the lung diffusing capacity (a breathing test) and exhaled Nitric Oxide (NO) (a substance in the body that relaxes or dilates blood vessels). We will also measure endothelial progenitor cells (cells from the bone marrow) from a blood sample; these cells are markers of measure of blood vessel formation and repair. We will also measure the activity of superoxide dismutase (a protein in cells that executes the breakdown of a free radical into oxygen and hydrogen peroxide) in the blood. In addition, we will measure levels of coenzyme Q-10 in the blood. Other markers of disease response to therapy will be done including physical exam, BNP level (a blood marker that correlates with heart function), 6-minute walk and echocardiography (ultrasound of the heart). A total of 60ml (5 tablespoons) of blood will be drawn at each visit.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01148836
|United States, Ohio|
|Cleveland, Ohio, United States, 44195|
|Principal Investigator:||Jackie Sharp, CNP||The Cleveland Clinic|