Millions of Americans suffer from heart failure.
In fact, it is the number
one reason for hospitalization in older Americans. When people
have heart failure, their heart muscle does not function properly and
the heart becomes unable to pump enough blood to supply oxygen to the
organs of the body. It stems from many causes, including high
blood pressure, viral disease, alcohol abuse, valvular disease, and
ischemia secondary to heart attacks. Symptoms of heart failure
include shortness of breath, inability to sleep horizontally, fatigue,
and swelling of the feet and ankles. Multiple randomized,
controlled trials have found clinical benefits of CoQ10 in the
treatment of heart failure. Namely,
fewer hospitalizations, reduced dyspnea, and reduced edema.
In her book Miracle Cures, Jean Carper tells the story of a
woman in severe heart failure who was not improving with conventional medical
therapy. Her doctor suggested taking 30 mg of CoQ10 each day. By accident, she began taking 300 mg each day and subsequently experienced
considerable improvement. Similar anecdotal evidence is reported by Dr.
Stephen Sinatra in his discussion of two case studies of refractory heart failure
successfully managed with high dose CoQ10 (7).
In 1985, Langsjoen et al. studied the response of 19 patients with severe
cardiomyopathy (New York Heart Association class III and IV) to therapy in a
blind and cross-over trial with CoQ10 (8). CoQ10 (100 mg per day) and a
matching placebo were administered orally to two groups of patients with heart
failure. Blood levels of CoQ10 were determined after a 4 week
stabilization period and again after 12 weeks of treatment with either CoQ10 or
placebo. Ejection fraction (a measure of left ventricular function) and
stroke volume were measured before and after treatment. It was found that
both blood levels and cardiac function increased after treatment with
CoQ10. Similarly, 18 out of 19 patients reported clinical improvement, as
evidenced by increased activity tolerance. No side effects were noted.
Problems with this study:
1. Small sample size. 2. Some patients had normal CoQ10
blood levels prior to treatment (they had no deficiency even though they had
severe heart failure clinically).
A 1990 study, also by Langsjoen et al. studied the long-term efficacy of
coenzyme Q10 for idiopathic dilated cardiomyopathy. This study
involved patients with cardiomyopathy in NYHA class II, III, and IV.
Again, patients were given 100 mg of CoQ10 daily while their conventional
medical therapy was maintained. The mean CoQ10 blood level more than
doubled after 3 months of treatment. The mean ejection fraction was 41% at
entry and rose to 59%. Thus, they concluded that CoQ10 was safe and
effective.
Major insufficiencies with this study
include lack of controls, lack of blinded randomization, and use of inaccurate
methods to assess ventricular function.
In 1997, Soja and Mortensen completed a meta-analysis of clinical trials of
CoQ10 as a treatment for congestive heart failure (10). They selected
eight double-blind, placebo controlled studies and investigated stroke volume,
cardiac output, ejection fraction, cardiac index, end diastolic volume index,
systolic time intervals, and total work capacity. Statistically
significant improvement after treatment with CoQ10 were demonstrated for all of
the parameters except the systolic time interval and total work capacity.
However, homogeneity could only be established for cardiac output and stroke
volume.
Problems with this study:
1. Small sample sizes of trials included in the meta-analysis (14, 12, 20,
79, 25, 20, 6, and 180). 2. Lack of homogeneity (this means that the
primary studies cannot be regarded as test samples from the same population,
and, according to some researcher, cannot therefore be included in the
meta-analysis). 3. Lack of control for other medications (for
example: diuretics, which can affect stroke volume, and inotropes, which
can affect cardiac output).
In 2004, a study by Berman et al.
researched the effects of coenzyme q10 in patients with end-stage heart failure
who were awaiting cardiac transplantation (16). This was a randomized,
placebo-controlled study of 32 patients. After three months, changes in
ANF levels, TNF levels, echocardiograms, 6-min walk tests and Living
questionnaires were analyzed. The study participants showed significant
improvement with symptoms of CHF, daily functioning and quality of life.
There was no significant change in ANF levels, TNF levels, and echocardiogram
results after three months.
Problems with this study: 1. Small sample size (32 patients started the study
only 27 completed the study)
A 1999 investigation by Watson et al. concluded that coenzyme Q10 had no
effect on left ventricular function in patients with congestive heart failure
(11). Thirty patients with cardiomyopathy and chronic left ventricular
dysfunction (ejection fraction less than 35%) were randomized to a double-blind
cross-over trial of 100 mg oral CoQ10 daily versus placebo, each for 3
months. Right heart catheterization was performed to measure right heart
pressures and cardiac output at baseline and after treatment.
Echocardiographic left ventricular volumes and blood levels of CoQ10 also were
measured at entry and after treatment. In addition, quality of life was
assessed with a questionnaire. They found no significant difference in
left ventricular ejection fraction, cardiac volumes, or quality of life after
treatment with coenzyme Q10 or placebo, although plasma levels of CoQ10
increased greater than twofold.
Problems with this study include a
small sample size.
A recent study was published in April 2000 by Khatta et al. in
the Annals of Internal Medicine (12). The study was a randomized,
double-blind, controlled trial to determine the effect of coenzyme Q10 (200 mg
daily) or placebo on peak oxygen consumption, exercise duration, and ejection
fraction. Fifty-five patients with NYHA class III and IV cardiomyopathy
began the trial with ejection fractions less than 40%, and peak oxygen
consumption less than 17.0 mL/kg per minute (or less than 50% of
predicted). Left ventricular ejection fraction (measured by radionuclide
ventriculography) and peak oxygen consumption and exercise duration (measured by
an evaluation using the Naughton protocol) were measured. The
investigators found that although the mean serum concentration of CoQ10
increased more than twofold, ejection fraction, peak oxygen consumption, and
exercise duration remained unchanged in both the coenzyme Q10 and placebo
group. They concluded that coenzyme Q10 does not affect ejection fraction,
peak oxygen consumption, or exercise duration in patients with congestive heart
failure receiving standard medical therapy.
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