~ 102408 Low Plasma CoQ10 Predicts Mortality In Heart Failure Patients

The October 28, 2008 issue of the Journal of the American College of Cardiology featured a study conducted in New Zealand which found that coenzyme Q10 (CoQ10) levels are an independent predictor of survival in chronic heart failure patients. Coenzyme Q10 is a compound that occurs in all cells, which is needed for the production of energy. Studies have shown that depleted CoQ10 levels could worsen chronic heart failure.

The current study evaluated 236 heart failure patients with a median age of 77 years upon admission to Christchurch Hospital. Blood plasma samples were analyzed for coenzyme Q10, cholesterol and other factors. Participants were followed for a period of up to 5.75 years, during which 76 deaths occurred.

The median range of plasma CoQ10 among the study's participants was 0.68 micromoles per liter. At twelve months of follow-up, the 29 nonsurvivors were found to have lower plasma levels of CoQ10 compared with the 205 survivors. Over the entire follow-up period, 39 percent of the participants who had CoQ10 levels lower than 0.73 micromoles per liter died, compared with 22 percent of those whose levels were higher. Multivariable analysis determined that higher plasma CoQ10 levels, whether above the median level or greater than 0.73 micromoles per liter, were an independent predictor of survival.

Statin drugs are known to lower coenzyme Q10 levels, yet their use has been associated with a reduced risk of death in heart failure patients. Although participants with higher CoQ10 levels were less likely to be using statin drugs, statin therapy was not found to be independently associated with mortality. Nevertheless, the authors suggest that the failure of a recent trial of rosuvastatin in to elicit a reduction in major vascular events in heart failure patients could be due to a reduction in CoQ10 which offset the beneficial effects of the drug.

"No previous studies . . . have formally studied the relationship between CoQ10 and outcomes in chronic heart failure in a longitudinal observational study such as ours," the authors write. "Our findings in a clearly defined, prospectively studied group that CoQ10 depletion is associated with worse outcomes in CHF give further support to the rationale of the intervention studies that have already been initiated."

Related Health Concern: Congestive heart failure

CHF occurs when the heart cannot pump efficiently enough to supply the body with freshly oxygenated blood. It affects about 5 million people in the United States. Within 5 years, medical experts predict that about half of these patients will have died of their conditions (American Heart Association 2004). Hoping to prolong survival, patients with CHF are typically treated with an array of powerful medications that have been shown to increase survival, often at a high cost. The conventional drugs used to treat CHF have significant adverse effects and, in many cases, implantation of a lifesaving medical device, or even having a heart transplant, may be necessary.

Studies have shown that nutrients and supplements can strengthen the heart muscle, with fewer side effects than the powerful pharmaceuticals often used to treat the condition. CoQ10 is one of the most powerful.

The goal with nutrients and supplements is the same as with conventional medication: to slow the gradual enlargement and weakening of the heart. This process, which occurs in all forms of CHF, is called cardiac remodeling. During cardiac remodeling, the heart gradually changes shape, becoming larger and thinner. Cardiac remodeling is the driving force behind the reduced quality of life experienced by patients with CHF (Fedak PW et al 2005; Weisberg AD et al 2005).

By reinforcing the heart's function, it may be possible to slow cardiac remodeling. In this regard, CoQ10 has been studied since the middle 1960s. Present in high quantities throughout the heart muscle, CoQ10 has many beneficial effects, including energy production (Awata N et al 1980; Crane FL et al 1997; Nakamura Y et al 1982; Nayler WG 1980), an antioxidant effect (Frei B et al 1990), and stabilizing the heart membrane (Ondarroa M et al 1986).

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