Compared with vitamin E, there has been only very limited research on the potential cardiovascular benefits of CoQ1O. Singh et al. (1998) have reviewed the role of CoQ1O in CVD. CoQ1O deficiency has been observed in a wide variety of cardiovascular disorders, e.g. congestive heart failure, angina pectoris, coronary artery disease, cardiomyopathy, hypertension, mitral value prolapse (Singh et al., 1998). In the apoE gene knockout mice (an excellent model of human atherosclerosis) supplementation with both vitamin E and CoQ10 was found to inhibit atherosclerosis better than with vitamin E or CoQ10 alone (Thomas et al., 2001). It is not known, however, if CoQ10 supplementation in humans can decrease atherosclerosis.
Although ubiquinol may inhibit the formation of oxidized and atherogenic forms of LDL, it is likely that the primary mechanism whereby CoQ10 could prevent heart disease is through its ability to improve ATP synthesis in cells with a high ATP demand such as cardiac myocytes. As an antioxidant, ubiquinol could also inhibit the free radical damage to the myocardium that arises during ischemia-reperfusion injury. Heart failure (due to cardiomyopathy and congestive heart failure), as discussed above, is a major and increasing worldwide health problem. It is logical to suggest that dietary CoQ10 supplementation could increase ATP production and thereby improve myocardial contractility. A meta-analysis of eight randomized controlled studies looking at the effect of dietary CoQ10 supplementation on congestive heart failure indicates an improvement in stoke volume, ejection fraction, cardiac output, cardiac index, and end diastolic volume index (Soja and Mortensen, 1997). These results certainly support a role for dietary CoQ10 supplementation as an adjunctive treatment for congestive heart failure.
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