The widely prescribed HMG CoA-reductase inhibitors block the endogenous biosynthesis both
of cholesterol and of coenzyme Qlo, and the decrease in both substances is related to the dose as
well as the potency of those drugs. The depletion of the essential co-factor required for energy
production, coenzyme Q 10, appears to be well tolerated in younger and healthier patients,
particularly in the short term, but the data reveal detrimental cardiac effects in humans with preexisting
cardiac dysfunction and in several animal models, particularly in older animals. CoQlo
is known to be deficient in congestive heart failure (CHF), with the degree of deficiency in blood
and cardiac tissue correlating with the severity of the CHF (Kitamura 1984, Folkers 1985).
Normal whole blood levels of CoQlo are about 1 .O+/-0.2 :g/ml with deficiency in the range of
0.6+/-0.2:g/ml. It is also known that CoQ10 levels steadily fall after the age of 40 (Kalen 1989,
Soderberg 1990). The best recent data documenting impairment in myocardial hction
secondary to age-related CoQlo deficiency in older patients undergoing coronary artery bypass
graft surgery is by an Australian group of cardiovascular surgeons who obtained atrial muscle
from patients at the time of open heart surgery and evaluated it for a post-ischemic contractile
recovery. Older patients had significantly lower myocardial tissue levels of CoQ 10. Incubation
of the atrial myocardium with CoQlo completely abolished the difference between the contractile
recovery of the senescent atrial tissue (greater than the age of 70) as compared to the atrial tissue
from patients under the age of 60 (Rosenfeldt 1999). Later those researchers performed a
randomized, double-blind, placebo controlled trial of preoperative supplemental CoQ 10 therapy
and found improved outcomes in coronary artery bypass surgery. The results of that trial were
presented at the 2001 American Heart Association Scientific Sessions in Anaheim (Pepe 2001).
Certainly, patients undergoing bypass surgery may be more susceptible to statin-induced
lowering of coenzyme Qlo cardiac tissue levels, and elderly patients who are on statin therapy
would greatly benefit from supplemental CoQ 10