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Congestive Heart Failure
According to a report from the American Heart Association, an estimated
81,100,000 American adults, equaling more than one in three, have one or more types of
cardiovascular disease (CVD), the leading cause of morbidity and mortality in the United
States. Within the classification of CVD, 5,800,000 experience heart failure, ranking it to
be the third most common cause.1 During heart failure, the heart is unable to pump
enough blood to meet the body’s needs for blood and oxygen. In a healthy heart, 50% of
the blood in the ventricle is pumped in one beat. However, in a failing heart, only 40% or
less of the blood in the ventricle is pumped in one beat. The high prevalence of heart
failure makes it a major public health concern in the United States.
The Registered Dietitian (RD) plays a critical role in the multidisciplinary team which can include a physician, pharmacist, psychologist, nurse, and social worker - who
work together to positively impact the patient’s outcomes. When the RD is conducting
an assessment on a heart failure patient, more than half are malnourished. The hallmark
signs and symptoms are shortness of breath, fatigue, and fluid retention. Patients may
also experience anorexia, nausea, abdominal pain and feeling of fullness, constipation,
malabsorption, cardiac cachexia, hypomagenesmia and hyponatremia.
Important interventions for this condition are education and counseling. The
patient should receive nutrition education to promote behavioral change and the benefits
of medical nutrition therapy should be explained. It is important that the total diet be
addressed due to the underlying risk factors associated with the condition, such as
dyslipidemia or hypertension. The DASH diet (dietary approaches to stop hypertension)
is an appropriate diet for a heart failure patient that emphasizes lower sodium foods and
higher intakes of potassium. The diet should be low in saturated fat, trans fat and
cholesterol while high in whole grains, fruits and vegetables. Tobacco use and alcohol
should also be avoided. Patients are recommended to consume small, frequent meals to
reduce abdominal distention. For patients with severe heart failure, the energy needs are
increased by 30% to 50% due to increased energy expenditure by the heart and lungs.
The recommended intake is 31-35 kcal/kg of body weight, and 1.12 g protein/kg.
Sodium restriction is approximately 2 grams per day but it depends on the individual and
should be the least restrictive diet that will still achieve the desired results. Fluids also
need to be limited, 2 liters per day. Some patients that are severely decompensated may
have to reduce even more to 1000-1500 mL a day. It is important to ensure that the
patient consumes adequate levels of B6, B12 and folate in the diet, and they may also
need to be supplemented with magnesium and thiamin. The RD should also encourage
the patient to increase physical activity, manage stress, get adequate rest, lose or maintain
appropriate weight, and develop a network of support. Nutrition education is very
important in this condition. Educating the patients on salt alternatives and label reading
is necessary for managing the condition.2
With over half of heart failure patients being malnourished, deficiency in
micronutrients has been shown to be a contributing factor to the progression of heart
failure. These patients may become deficient in these micronutrients not only because of
reduced intake, but also because of increased wasting secondary to cachexia and diuretic
therapy.3 Nutraceuticals, normal components of foods that are delivered for therapeutic
purposes in concentrations higher than what is found in a normal diet, in these patients
may attribute to their capability to modulate altered metabolic pathways found in heart
failure.4 One micronutrient, coenzyme Q10 (CoQ10), ubiquinone, is an antioxidant that
is found in high concentrations within the heart. The main function of this enzyme is the
generation of adenosine triphosphate (ATP) in the electron transport chain in the
mitochondria.5 Myocardial deficiency of CoQ10 has been demonstrated in patients with
heart failure through endomyocardial biopsy samples. Also, patients that were placed in
the functional Class IV (based on the New York Heart Association’s classification
guidelines), reported significantly lower levels of CoQ10 than patients identified as
functional Class I. Therefore, higher levels of deficiency have been associated with
higher levels of adverse symptoms.6 Due to the degree of morbidity and mortality that
results from heart failure, research has been underway to study the therapeutic effects that
CoQ10 supplementation may have on patients suffering from heart failure.7
Since heart failure patients are shown to have lower levels of CoQ10, Molyneuz
et al. collected plasma samples from 236 patients that were severely symptomatic with
heart failure upon admittance to the hospital to determine the predictability of mortality
in chronic heart failure from these concentrations. These patients were an average of 77
years of age and were followed for an average of 2.69 years, at a minimum of 3 monthly
intervals to record their medications, adverse events, readmissions to the hospital, and
death. At the end of the study, there was a total of 76 deaths. The results of the study
found an independent association between lower concentrations of CoQ10 and an
increased risk of mortality in heart failure. There was a significant predictive power of
CoQ10, indicating that it may be plausible that a deficiency of CoQ10 might be an
important mechanism for the complications associated with heart failure.8
Other studies have researched the effects of supplementing CoQ10 in these heart
failure patients and several have presented results to support the administration of
CoQ10. Peter and Alena Langsjoen researched if supplemental ubiquinol could achieve
improved plasma CoQ10 levels in patients with end-stage class IV heart failure. Their
research consisted of seven patients who had worsening heart failure on maximal medical
therapy. Their conventional therapy, including digitalis, diuretics, potassium, angiotensin
converting enzyme (ACE) inhibitors, angiotensin receptor blockers, beta blockers,
nitrates, antiarrhythmics and coumadine, were not altered unless there was a change in
clinical status. Not only did each of the seven patients experience a remarkable increase
in their plasma CoQ10 levels when supplemented with ubiquinol, but they also observed
improvements in their clinical status. Patients with Class IV heart failure have a very low
prognosis and high mortality rates. In this study however, six out of the seven
participants survived longer than they had expected and had remained stable between
Class I and Class III on ubiquinol for an average of 12 months. The clinical features at
the beginning were right and left heart failure with signs and symptoms of pulmonary
edema, ascites and leg edema. The authors postulated that the intestinal wall edema
associated with heart failure in these patients is interfering with CoQ10 absorption. This
leads to a continuous cycle where the decreased absorption of CoQ10 leads to worsening
of the heart failure, which worsens the symptoms (such as edema) which then again will
decrease CoQ10 absorption, leading to the decreased plasma concentrations that further
worsen heart failure. The authors believe that supplementation of ubiquinol will end this
cycle and that the best response to CoQ10 supplementation is when it is started in the
early stages of the disease.9
Several studies examined the effects of CoQ10 on exercise and quality of life and
found positive results. A different form of CoQ10 was used in a study by Fumagalli et al.
They conducted a controlled trial using a water-soluble, commercially available form
(CoQ10 terclatrate; Q-ter). They researched the effects on exercise tolerance and healthrelated quality of life and there results indicated significant improvements. Berman et al.
worked with patients awaiting heart transplantation and also represented that the
administration of CoQ10 resulted in significant improvements in their functional status,
clinical symptoms and quality of life. The patients had a significant reduction in fatigue
during usual activities of daily living, improvements in nocturia and dyspnea, and
improved results of a six minute walk test.10
Ejection fraction was also commonly examined in research studies. Belcaro et al.
looked at ejection fraction and distal edema in patients supplemented with CoQ10. The
participants in the study had a stable Class II or Class III level of heart failure within the
last six months. The patients that were treated with the supplement experienced an
increase in heart ejection faction by 22.4% and a significant decrease in distal edema. The
improvement in ejection fraction in this study further indicates the possibility of
supplementation as a therapeutic option for improving heart failure management.11
Although there have been several studies showing positive endpoints from
supplementation with CoQ10, there have been other randomized and blinded studies that
lacked an effect.12 Khatta et al. conducted a study on 46 patients who had heart failure
with Class III and Class IV symptoms to determine the effects of CoQ10 on peak oxygen
consumption, exercise duration, and ejection fraction. The patients received 200 mg/day
of CoQ10 or a placebo. The results did report an increase in serum concentrations,
however ejection fraction, peak oxygen consumption, and exercise duration remained
unchanged in both the treatment and placebo group.13Similarly, a study by Permanetter
and colleagues, did not detect an effect on coenzyme Q10 on ejection fraction. This
study was conducted on 25 patients that were classified in Class I, II and III. The lack of
an effect may be due to the minimal impairment of the patients in this study.14Other
explanations for the inability of these studies to show a therapeutic effect of
supplementation may be due to the time at which they were conducted. These studies
were older studies (1992 and 2000) and factors of the research process, such as patient
selection, dosing, and end point measurements, may have changed over the years.
Additionally, another concern with CoQ10 supplementation is adverse effects
and/or drug interactions. It has been commonly connected with gastrointestinal upset. It
has drug interactions with statin drugs and warfarin. If a patient is simultaneously taking
a statin drug, the levels of CoQ10 are reduced as a result of the inhibition of endogenous
CoQ10 production. Also, the anticoagulant effects of warfarin are reduced by CoQ10
because of similarity in structure between CoQ10 and vitamin K.15 However, there are
mixed findings in the results. Some studies report showing no adverse reactions with
CoQ10 therapy.16 In addition, CoQ10 may have a useful or clinical role as an adjunct or
alternative anti-hypertensive to conventional agents such as diuretics and ACE inhibitors
used to lower blood pressure.
A multitude of small observational studies have shown the benefits of coenzyme
Q10 in heart failure patients. Researchers have studied numerous endpoints such as
plasma concentration, ejection fraction, quality of life and exercise capacity. However
large, well-designed trials are lacking and end points such as mortality and HF
hospitalizations are limited.15 Also, there is a lack of a clear dose range in the literature
(amounts ranging from 60 mg/day to more than 200 mg/day). Due to conflicting data,
small sample sizes, and inconsistent dosing, it is difficult to make conclusive
recommendations. Current heart failure guidelines do not support the use of CoQ10 with
this condition.17
Since heart failure is a leading cause of morbidity in mortality, research is needed
on therapeutic agents that may benefit these patients. Caution should be taken when
interpreting the results due to the limitations. In order to make a widespread
recommendation, I feel as if larger studies focusing on optimal dosing, efficacy, adverse
side effects, as well as drug interactions are imperative. This research will help
determine whether or not CoQ10 may be successful in reducing hospital readmissions,
reducing the number of days that patients spend in the hospital, and improving the quality
of life scores in a heart failure patient in a safe manner.
References
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update. A report from the American Heart Association. J Am Heart Assoc. 2010;
121: e46-e215.
2. Mahan KL, Escott-Stump S, Raymond JL, Krause MV. Heart Failure. In:
Alexopoulos Y, ed. Krause's Food & the Nutrition Care Process. 13th ed. St. Louis,
MO: Elsevier/Saunders; 2012:769-777.
3. Witte KK, Clark AL, Cleland JG. Chronic heart failure and micronutrients. J Am Coll
Cardiol. 2001;37: 1765–1774.
4. Tarnopolsky MA. The mitochondrial cocktail: rationale for combine nutraceutical
therapy in mitochondrial cytopathies. Adv Drug Deliv Rev. 2008; 60(13-14): 1561-7.
5. Belardinelli R, Lancisi CR, Riuniti AO, et al. Oxidative stress, endothelial function
and coenzyme Q10. Biofactors. 2008; 32(1-4): 129-33
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Medsurg Nurs. 2012; 21(6): 367-71.
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supplementation on heart failure: a meta-analysis. Am J Clin Nutr. 2013; 97: 268-75.
8. Molyneux SL, Florkowski CM, George PM. Coenzyme Q 10: An independent
predictor of mortality in chronic heart failure. JACC Heart Fail. 2008; 52(18): 14351441.
9. Langsjoen PH, Langsjoen AM. Supplemental ubiquinol in patients with advanced
congestive heart failure. Biofactors. 2008; 32(1-4):119-28
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combination with coenzyme Q10 in heart failure patients (NYHA II/III). Panminerva
Med. 2010; 52: 21-5.
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464-472.
13. Khatta M, Alexander B, Krichten CM, et al. The effect of coenzyme Q10 in patients
with congestive heart failure. Ann Intern Med. 2000; 132:636-640.
14. Permanetter B, Rossy W, Klein G, Weingartner F, Seidl KF, Blomer H. Ubiquinone
(coenzyme Q10) in the long-term treatment of idiopathic dilated cardiomyopathy. Eur
Heart J. 1992; 13: 1528-33.
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micronutrients, macobenefit? Clin Cardiol. 2011; 34(4): 196-7.
16. Langsjoen PH, Langsjoen AM. Supplemental ubiquinol in patients with advanced
congestive heart failure. Biofactors. 2008; 32(1-4):119-28
17. Dunn SP, Bleske B, Dorsch M, et al. Nutrition and heart failure: impact of drug
therapies and management strategies. Nutr Clin Pract. 2009; 24(1): 60-75.