Recent studies indicate that lipoprotein(a) is a genetically determined risk factor of premature coronary artery disease (CAD). Serum levels of lipoprotein(a) have been shown to correlate well with the presence, severity and lesion score on a coronary angiography, as well as with the occurrence and recurrence of myocardial infarction and cardiac death.

It is possible that higher levels of lipoprotein(a) may initiate and promote an thrombogenic and thrombogenic state in the body which may be responsible for a higher prevalence of premature coronary artery disease (CAD) and increased mortality. Niacin, neomycin, Colestipol, N-acetylcysteine and Danazol are effective but have limitations in reducing lipoprotein(a) concentrations. The results of a recent clinical trial were published in the International Journal of Cardiology 1999 Jan;68(1):23-9 and was headlined:

Serum concentration of lipoprotein(a) decreases on treatment with hydrosoluble coenzyme Q10 in patients with coronary artery disease: discovery of a new role.

The stated OBJECTIVE of this clinical trial was to examine the effect of coenzyme Q10 supplementation on serum lipoprotein(a) in patients with acute coronary disease. The study was a randomized double blind placebo controlled trial.

SUBJECTS AND METHODS: Subjects with clinical diagnosis of acute myocardial infarction, unstable angina, angina pectoris (based on WHO criteria) with moderately raised lipoprotein(a) were randomized to either coenzyme Q10 as Q-Gel (60 mg twice daily) (coenzyme Q10 group, n=25) or placebo (placebo group, n=22) for a period of 28 days.

RESULTS: Serum lipoprotein(a) showed significant reduction in the coenzyme Q10 group compared with the placebo group (31.0% vs 8.2% P<0.001) with a net reduction of 22.6% attributed to coenzyme Q10. HDL cholesterol showed a significant increase in the intervention group without affecting total cholesterol, LDL cholesterol, and blood glucose showed a significant reduction in the coenzyme Q10 group. Coenzyme Q10 supplementation was also associated with significant reductions in thiobarbituric acid reactive substances, malon/dialdehyde and diene conjugates, indicating an overall decrease in oxidative stress.

CONCLUSION: Supplementation with hydrosoluble coenzyme Q10 (Q-Gel®) decreases lipoprotein(a) concentration in patients with acute coronary disease.

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For more information on what CoQ10 is and how it works, "click" on the "What is CoQ10?" button. For more information on Q-Gel® CoQ10 specifically, "click" on the "Q-Gel® CoQ10" button. Both buttons are located on upper left hand side of the screen (you may have to "scroll up" to see them).

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