CoQ10 An Independent Predictor of CHF Mortality

Molyneux, S and others of the Clinical Biochemistry Unit of New Zealand reported recently on the relationship between plasma coenzyme Q10 (CoQ10) and survival in patients with Congestive Heart Failure ( CHF ). This work derives from the known effect of Co-enzyme Q10 on heart function.

This ubiquitous substance is vital to mitochondrial function and Adenosine Triphosphate ( ATP ) energy production. One of the known consequences of CoQ10 deficiency is congestive heart failure, reflecting a failing heart due to lack of sufficient bioavailability of CoQ10.

The heart consumes at least 25% of the total ATP energy produced by the body and usually is the first organ to fail in cases of CoQ10 deficiency. Molyneux and team stated at the beginning of their paper that patients with CHF have low plasma concentrations of CoQ10, an essential cofactor for mitochondrial electron transport and myocardial energy supply. Additionally, they found that low plasma total cholesterol ( TC ) concentrations - such as might result from statin use - have been associated with higher mortality in heart failure.

They then proceeded to test the hypothesis that plasma CoQ10 is a predictor of total mortality in CHF. In my judgment this is one bit of research where you already know the outcome but you do it anyway. No mention was made of statin drug use but in most countries the majority of patients admitted with CHF are on statin drugs. Statins, as reductase inhibitors, block the vital mevalonate pathway, inevitably reducing CoQ10 bioavailability while at the same time reducing cholesterol synthesis and are now well known to be provokers of CHF.

Plasma samples from 236 patients admitted to the hospital with CHF were measured for CoQ10 and LDL cholesterol. The median age at admission was 77 years. The results showed the median CoQ10 concentration was 0.69 with a range of 0.18 to 1.75. They found the optimal CoQ10 concentration for prediction of mortality was 0.73 µmol/l.  CoQ10 levels above this level were associated with survival. Their conclusion was that "CoQ10 deficiency might be detrimental to the long-term prognosis of CHF" and admitted there is a rationale for "controlled intervention studies with CoQ10."

We have known of the relationship of CHF to CoQ10 for nearly a decade now.  Peter Langsjoen reported years ago on the benefit of CoQ10 supplementation in CHF. All doctors have an obligation to familiarize themselves with the current literature. If this was done in this case my question then becomes why was a CoQ10 supplementation study not structured that perhaps would have saved a few lives?

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

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