Significant deficiencies in coenzyme Q(10) have been documented in a wide variety of diseases in both animal and human studies. Known predominately for its functions as an antioxidant and membrane stabilizer, coenzyme Q(10) supplementation also has been demonstrated to effectively lower blood pressure, decrease total cholesterol and low-density lipoprotein cholesterol, increase levels of high-density lipoprotein cholesterol, and decrease symptoms of dyspnea, peripheral edema, enlarged liver, and insomnia. The majority of clinical work with coenzyme Q(10) in the past two decades has focused on its role in heart disease. While usually found in high concentrations in heart muscle cells, both serum and tissue levels of coenzyme Q(10) are often lower in people with congestive heart failure. The severity of coenzyme Q(10) deficiency is directly related to the severity of heart failure. Correcting deficits in coenzyme Q(10) in heart failure patients can mitigate or reverse myocardial dysfunction and necrosis. The addition of coenzyme Q(10) to conventional treatments in congestive heart failure patients has been shown to improve quality of life and decrease hospitalization rates. In an effort to improve outcomes in patients supplemented with coenzyme Q(10), various delivery mechanisms to improve the bioavailability of coenzyme Q(10) are currently under investigation.