LAS VEGAS—Co-enzyme Q10 supplementation can improve heart function and survival in patients with congestive heart failure, provided it is given early on in the course of disease, said Stephen Sinatra, MD, at the American College of Nutrition’s annual meeting.

“You see the best effects among patients treated within a year” of presentation of heart disease, said Dr. Sinatra, a cardiologist and psychotherapist, who is director of the New England Heart Center, Manchester, CT. “CoQ10 improves myocyte function, but you have to have some myocytes there.”

He believes that two recent, widely-publicized negative studies on CoQ10 in congestive heart-failure were flawed, in large measure because they enrolled patients with far-advanced disease. Since this enzyme improves the metabolic functioning of normal myocardium, the more damaged myocardium a patient has, the less likely he or she is to respond to CoQ10 supplementation.

Endogenous CoQ10 is also known as ubiquinone, owing to its presence in many tissues throughout the body. But it has its highest concentration in the myocardium. In all tissues, it promotes cellular ATP (adenosine triphosphate) production. The synthetic analog of CoQ10 used in many supplement products is called idebenone.

“Myocardial tissue requires ATP to contract and, importantly, to relax. One of the earliest indicators of heart muscle dysfunction is diastolic dysfunction—dysfunction in the relaxation phase, which requires a huge amount of ATP.” About one third of cases of congestive heart failure are “pure diastolic dysfunction,” said Dr. Sinatra.

Many studies, he noted, show CoQ10 deficiency correlates with impaired myocardial function. The rationale for supplementation is that by enhancing ATP production in myocytes, one can reverse the diastolic dysfunction. “We believe we’re correcting a deficient state,” said Dr. Sinatra, whose interest in comprehensive nutrition and lifestyle-based cardiovascular care has led him to develop his own line of supplement products, including a CoQ10 gel cap.

The first studies of CoQ10 in humans took place in Japan in the late 1960s. To date, there have been 18 randomized controlled trials of CoQ10 in heart failure, comprising about 1,400 patients. Dr. Sinatra contends nearly all have found some beneficial effects.

Among the positive data are a 1993 study showing long-term CoQ10 supplementation plus conventional therapy decreased rates of hospitalization and the incidence of pulmonary edema and other complications in patients with chronic congestive heart failure (Morisco C et al. Clin Investig 1993;71(8 Suppl):S134–6).

A more recent study showed CoQ10 further decreased blood pressure in hypertensive coronary artery disease patients on conventional antihypertensives (Singh RB et al. J Hum Hypertens 1999 Mar;13(3):203–8)

There are also three studies indicating that treatment with CoQ10 before heart surgery can improve surgical outcomes (Chello M et al. J Cardiovasc Surg (Torino) 1996 Jun;37(3):229–35; Chello M et al. Ann Thorac Surg 1994 Nov;58(5):1427–32; Chen YF et al. J Thorac Cardiovasc Surg 1994 Jan;107(1):242–7).

Despite the positive research, the American cardiology community has barely registered CoQ10 on its radar screen. The American Heart Association holds that positive trials to date have involved too few patients and not enough long-term follow-up to make a solid case for routine use of the supplement.

The general skepticism was further bolstered by two very recent studies finding that CoQ10 had no positive effect on ventricular function in patients with congestive heart failure (Khatta M et al. Ann Intern Med 2000;132(8):636–40; Watson PS et al. J Am Coll Cardiol 1999;33:1549–52).

Dr. Sinatra says those studies are poorly designed in that they failed to use effective dosages of the supplement and focused on patients with disease beyond realistic hope for improvement. He contends that one needs to achieve blood levels of CoQ10 that are in the ballpark of 3.5 mcg/ml, which is 4 to 7 times the physiologic norm, in order to see improvement in patients with CHF (Sinatra S. Heart Disease 2000;2:16–20).

Both of the negative studies used doses of CoQ10 that were too low to have much myocardial impact, and did not adjust dosages to achieve therapeutic blood levels. Further, they focused on patients with advanced heart disease of long duration; one would expect that in these cases, myocyte loss was so significant, the patients’ hearts would be essentially beyond repair, said Dr. Sinatra.

He and others believe CoQ10 supplementation should start as early as possible in treatment, ideally within 1–2 years of a heart failure diagnosis, in dosages ranging from 100–600 mg/day, depending on individual bioavailability, which can be measured by evaluating serum levels.

In an interview, Dr. Sinatra said, “There is no downside to this drug. It’s in foods we eat all the time (pork heart, beef heart, liver, and salmon). Any physician who is treating things like arrhythmias and heart failure should consider starting patients on low doses of CoQ10 and titrating up.” Ideally, it should be used in the context of a heart-healthy low carbohydrate, plant-rich Mediterranean style diet.

The National Cancer Institute confirms Dr. Sinatra’s contention about the supplement’s safety, stating, “No serious toxicity associated with the use of coenzyme Q10 has been reported,” although various minor side effects were noted with some dosages in some studies (National Cancer Institute. Coenzyme Q10, PDQ® [Online]. Available online at http://cancernet.nci.nih.gov/cam/Q10.htm).

Dr. Sinatra has not seen any problems in giving CoQ10 in conjunction with conventional pharmacologic therapies, and he holds that supplementation is essential for anyone receiving a statin drug, since these agents block the metabolism of endogenous CoQ10.

Several studies presented at the ACN conference back up this assertion. A study by Emile Bliznakov, MD, indicated that, “inhibition of mevalonate pathway [by statin drugs] restricts the biosynthesis of other consequential, non-sterol products of this loop, including CoQ10.” Dr. Bliznakov held that “some of the side effects resulting from statin treatment, such as myopathies and rhabdomyolysis, also suggest a more generalized mitochondrial injury and CoQ10 involvement.”

In another study presented at the meeting, Peter H. Langsjoen, MD, noted, “The availability of commercial blood CoQ10 assays and a better understanding of requisite blood CoQ10 level to attain adequate tissue CoQ10 levels will help to take out much of the empiricism which characterizes current CoQ10 dosages and formulations.”

Consumer interest in CoQ10 is on the rise, and has spurred sales of CoQ10 for a range of conditions, including various cancers, AIDS, and weight loss. Despite this trend, and the positive preliminary evidence suggesting benefit, there are no large-scale studies underway in the US that could definitively answer the question of whether CoQ10 supplementation should be a standard part of treatment for heart disease.

Dr. Sinatra has written a number of books on subjects related to CoQ10, nutrition and cardiovascular health; the most recent is Heart Sense for Women. To learn more about his nutritional approach and his experience with CoQ10, visit: www.sinatramd.com or www.drsinatra.com.

THE REDUX: Coenzyme Q10 supplementation, at dose ranges between 100–600 mg/day can improve myocardial function in congestive heart failure, provided it is begun early in the course of disease—ideally within a year of diagnosis. This enzyme, which can be depleted by statin drugs, increases cellular ATP production. Its effect will be proportional to the amout of healthy myocardium present. It is unlikely to work in advanced disease.