Coenzyme Q10
I. Actions
II. Clinical Study
III. Prospective and Research Implications
GLOSSARY
heart failure failure of the heart to pump sufficient blood from the chambers into the aorta; and inadequate supply of blood reaches organs and tissues.
pulmonary edema fluid in the air sacs and alveoli; the lungs become congested and severe shortness of breath occurs.
- I. ACTIONS
The enzyme Q10 (ubiquinone), a quinine, was discovered in 1957, and since that time there has been considerable controversy regarding its use in heart failure and other forms of heart disease. This enzyme serves as a mitocho-ndrial enzyme supplement and appears to improve defective myocyte energetics in patients with heart failure. Coenzyme Q10 plays an intermediary role in the electron transport chain during the oxidation of reduced nicota-mide adenine dinucleotide (NADH) or succinate, with the conversion of oxygen to water within the mitochondria (see Fig. 1). This enzyme is involved in electron proton transfer during oxidative phosphorylation. Also, coenzyme Q10 possesses antioxidant, free radical scavenging, and membrane stabilizing properties. - II. CLINICAL STUDY
Several small clinical studies of coenzyme Q10 that have not been randomized indicate an improvement in physical activity. A nonrandomized, nonblinded, four-week study of 1715 patients reported improvement in symptoms and quality of life. A longer study using 100 mg daily for over 6 years reported improvement in ejection fraction. A small study suggested degeneration in symptoms and hemo-dynamic features on discontinuation of the enzyme. A randomized study without placebo control in 806 patients showed improvement in functional class and heart failure symptoms over a 6-month follow up. - III. PROSPECTIVE AND RESEARCH IMPLICATIONS
A small study indicated that statin therapy reduces plasma levels of coenzyme Q10, which may have adverse effects on heart failure states. Further studies are needed to determine whether ubiquinone reductions are limiting the maximum favorable effects of statin therapy on the microcirculation. The use of enzyme Q10 carries only one disadvantage — neglect of approved heart failure remedies. Further studies are clearly indicated because the enzyme appears to cause no harm and appears to alter parameters that are deranged in heart failure that are not corrected by the excellent cardioactive agents available for the management of heart failure. These agents include ACE inhibitors, diuretics, beta-blockers, digoxin, spironolactone, and eplerenone. Intensive research is required to obtain new cardioactive agents to manage heart failure (see the chapter Heart Failure).