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Co-Enzyme Q10 in CHF

A few studies of Co-Q10 in CHF have shown no or minimal benefit.  These studies are published in cardiology journals, and in the introduction and discussion sections the authors will cite the few other studies that do not show benefit, and they typically do not cite the positive studies, which outnumber the "no benefit" studies five to one.  These "no benefit" studies typically involve patients who are doing well, such that the upside potential of CoQ supplementation is minimal.  The dose of Co-Q is less than what we use clinically, levels are typically not drawn, and the study patients are never co-treated with Carnitine, Ribose, or even antioxidants (remember, we can give you a ton of CoQ but is you have no Carnitine in your oxidatively stressed mitochondria you still cannot make ATP).  These studies are quoted by "health authorities" and "experts" as evidence that "vitamins don't work".  These "experts" have not done their reading, or maybe they do not have enough Co-Q10 in their brains.  You want all the information, the drug side and the nutritional side, and I trust that you do (or soon will) have enough CoQ in your brain, so in this section I will present some of the more interesting positive studies of CoQ10 supplementation in CHF.

Co-Enzyme Q10 Supplementation in CHF - 1991

Co-Enzyme Q10 Supplementation in pre-Transplantation CHF - 2005

Effect of Co-Enzyme Q10 Supplementation on Hemodynamics in Patients with CHF

Co-Enzyme Q10 Supplementation and Readmission Rate

Open Trial of Co-Q10 in CHF - Hemodynamics and Survival

Co-Enzyme Q10 Supplementation (1991) in CHF

180 patients with class IV CHF were randomized to receive, over 8 years, Co-Q10 100 mg/day plus usual therapy vs. usual therapy alone.  These were very sick patients.  All had required at least two hospital admissions with CHF over the preceding year, their ejection fraction was below 30% (mean EF was 20%), and all were doing poorly on conventional drug therapy.  The charts below present survival data:

Only 54% of the usual therapy patients survived one year, as expected, as the one-year survival of class IV CHF patients (in 1991) was around 50%.  Only one of the 90 usual therapy patients was alive at 5 years.  Of interest, the researchers noted that decompensation in the usual therapy group was heralded by a drop in blood CoQ10 levels (and doesn't this make sense?).  With supplementation, blood CoQ10 levels rose from 0.66 at baseline to 2.1 at 60 days (we want an on-treatment level of at least 2.0).  Heart rate was down by 9% at one year (cardiac output increased so the heart did not have to beat as many times a minute to supply adequate oxygen to the internal organs), and ejection fraction had increased by 76%, from 21% at baseline to an on-treatment value of 38%.  Eleven of the 90 Co-Q supplemented patients improved within two weeks, while the average response time was 40 days (remember, we need to be patient in nutritional medicine).  Some of the CoQ treated patients did not improve significantly.  Perhaps they were "too far gone" or maybe they had a problem not involving CoQ deficiency.  If you look only at the "CoQ responders", you see one, five, and eight year survival rates of 94, 50, and 36%.  Today we have drugs such as beta-blockers, ACEIs, Pentoxifylline, and Spironolactone, all of which have been shown to lower mortality in CHF (all discussed elsewhere on this site, which caters to individuals who want the best of both drug and nutritional therapies), but in 1991 the only agent that had been shown to lower mortality in CHF was CoQ10.  Isn't it a shame that the "experts" ignored this low cost agent in 1991.  Isn't it a shame that they continue to ignore it today?  Isn't it stupid for Medicare to pay 40K for a defibrillator/pacemaker while you have to pay out-of-pocket for CoQ (and in Toledo, Ohio you are not permitted to take CoQ in the hospital; my written order as a board certified cardiologist would not be honored and you would have to sneak it in).  The critics of nutritional medicine say that agents such as CoQ are no longer relevant, now that we have "modern day" drugs.  Let's see if this is true.

Co-Enzyme Q10 Supplementation in Pre-Transplantation CHF - 2005

In this study, 32 patients on the waiting list for cardiac transplantation were randomized to receive, over three months, Co-Q10 in a fat soluble form, 60 mg/day, or a placebo capsule.  We can assume that these patients were receiving as much "conventional" drug therapy as they could tolerate.  Specifically, 85% were receiving Digoxin, 79% a diuretic, 45% a ACEI, 65% a vasodilator, and 52% a beta-blocker.  This is not a large dose of CoQ10 (and the blood CoQ level rose from 0.18 to 0.83, below our target of ≥ 2.0), and three months is not really long enough for a nutritional medicine to exert its full effect, but none-the-less a significant therapeutic effect was exerted.  Ejection fraction did not rise, and maybe it couldn't in these individuals, 25 of whom had experienced one or more heart attacks, but symptoms and quality of life improved, as charted below: 

New York Work Functional Class ranges from Class I (symptoms only with strenuous exercise) to Class IV (symptoms at rest).  There was no significant change with placebo therapy while Functional Class improved with Co-Q treatment.   

How far the patients could walk in 6 minutes, a practical measure of functional status, deteriorated with three months of placebo therapy but improved on Co-Q10.

On Co-Q the patients experienced less fatigue; DOE (dyspnea, or shortness-of-breath with exertion) was less, and they had to arise from sleep less frequently to empty their bladders.

Functional status and quality of life in these too-far-gone patients clearly improved with CoQ10.  Other, non-placebo controlled trials have described patients going off the transplant list when Co-Q10 was added to their regimen.   

Effect of Co-Enzyme Q10 Supplementation on Hemodynamics in Patients with CHF

Twenty two patients with Class II-IV CHF underwent right heart catheterization and bicycle stress studies at baseline and following three moths supplementation with placebo or CoQ10, in a fat soluble preparation at a dose of 100 mg twice a day.  Blood Co-Q levels rose from 1.1 to 3.3, consistent with adequate supplementation.  Treatment results are presented in graphic form below:   The PCW (Pulmonary Capillary Wedge Pressure) is the blood pressure experienced by the lungs.  As heart pumping function falls, the wedge pressure will rise, and you will experience shortness of breath.  The patient with Class III CHF has to stop walking at one block because his wedge pressure has increased; if he kept walking his lungs would flood with blood.  Any therapy that decreases wedge pressure or that blunts the rise in wedge pressure that would otherwise occur with exercise would be expected to improve functional capacity.  The wedge pressure fell with CoQ supplementation.  The second graphic is difficult to interpret.  Basically it shows that the rise in wedge pressure that occurs with exercise is blunted with CoQ supplementation. 

Co-Enzyme Q10 Supplementation and Readmission Rate

Keeping you out of the hospital seems like a good idea to me (after all, in the hospital you will not be permitted to take Co-Q10).  Let's see what affect CoQ supplementation has on this parameter of medical benefit in a large group of patients..

641 patients with NYHA Functional Class III-IV CHF (symptoms within two blocks or two flights of stairs) were randomized to receive CoQ10 at a dose of 2 mg/kg/day, or a placebo capsule.  All standard medications were continued.  Hospital admission rate was monitored over the following 12 months:

Co-Q helps keep you out of the hospital; admission rate was 40% on placebo and 20% on CoQ10.  The nature of the hospital admissions was also affected in a favorable fashion, with less CHF (cardiac asthma), less pulmonary edema (severe CHF) and less new onset arrhythmia.

Open Trial of Co-Q10 in CHF - Hemodynamics and Survival

34 patients with NYHA Functional Class IV CHF (symptoms at rest) received Digitalis and Diuretics for 60 days.  CoQ10 100 mg/day was then added to their program and they were followed over two years.  

Heart chamber size (end diastolic volume) decreased, stroke volume (the amount of blood pumped forward with each heart beat) increased, as did ejection fraction (the percentage of blood that fills the heart that is pumped forward).  Cardiac index, a measure of pumping function, improved as well.  Survival in class IV CHF at this time was 50% at one year.  These patients, who received Co-Q10 along with then standard therapy, did much better.

                                                                                                                                                                James C. Roberts MD FACC
                                                                                                                                                                                                  1/01/07