• Left-side heart failure: shortness of breath on exertion, cough, fatigue, enlargement of the heart
• Right-side heart failure: elevated venous pressure, enlargement of the liver, whole-body edema
• Both left and right ventricular failure: combinations of the above
Congestive heart failure (CHF) is an inability of the heart to effectively pump enough blood. Chronic CHF is most often due to long-term effects of high blood pressure, previous heart attack, disorder of a heart valve, disorder of the heart muscle (cardiomyopathy), or chronic lung disease. Factors that precipitate or worsen CHF are listed below.
One of the most serious consequences of CHF is reduction in blood flow to the kidneys. This results in a reduced filtration rate by the kidneys, which in turn leads to sodium and fluid retention. Adding more stress to the situation is the secretion of hormones by the kidneys to try to raise blood pressure by constricting blood vessels and increasing the fluid volume in the blood. In an attempt to compensate for the reduced output by the heart, the heart beats faster (tachycardia), the force of contraction increases, and the heart enlarges from the stress. Ultimately these factors severely worsen the picture.
Factors That Precipitate or Worsen Congestive Heart Failure
Low levels of essential fatty acids
Increased demand on the heart
High sodium intake
High environmental temperature
Chronic respiratory disease (such as asthma)
Nonsteroidal anti-inflammatory drugs
CHF is most effectively treated by natural measures in the early stages. Hence early diagnosis and prevention are imperative. The first symptom of CHF is usually shortness of breath. A chronic, nonproductive cough may also be the first presenting symptom. Anyone suspected of having CHF should have an extensive cardiovascular evaluation including a complete physical examination to look for the characteristic signs of CHF (e.g., peripheral signs of heart failure, enlarged and sustained left ventricular impulse, diminished first heart sound, gallop rhythm), electrocardiogram, and echocardiogram.
In the initial stages of CHF, natural measures designed to address the underlying cause (e.g., high blood pressure) or improve the metabolic functions of the heart muscle (described later, as well as measures described in the chapter “Angina”) are often quite effective. In later stages, however, medical treatment involving the use of diuretics, angiotensin-converting enzyme (ACE) inhibitors, or digitalis glycosides is indicated in most cases. The measures described here can be used as adjunctive therapy in these more severe cases. The New York Heart Association (NYHA) staging system for CHF (see the table below) can be used to help determine which patients are likely to respond to natural therapy alone. In general, excellent clinical results can be expected in stages (or classes) I and II with the use of the natural measures described below.
The natural approach focuses on improving energy production within the heart muscle (myocardium), as CHF is always characterized by impaired energy production within the myocardium. This impaired energy production is often the result of nutrient or coenzyme deficiency (e.g., magnesium, thiamine, coenzyme Q10, or carnitine deficiency). The dietary recommendations given in the chapter “High Blood Pressure” are appropriate for most patients with CHF, especially if the CHF is due to long-term high blood pressure (hypertension). Of particular importance is a diet low in sodium and high in potassium. A high intake of sodium greatly worsens CHF. Sodium intake should be restricted to less than 1.8 g per day. Furthermore, CHF patients are likely to have a low dietary intake of several nutrients, most notably magnesium, calcium, zinc, copper, manganese, energy, thiamine, riboflavin, and folic acid.1 A high-potency multivitamin and mineral formula is critical, especially if a person is on a diuretic.
Stages of Congestive Heart Failure as Defined by the New York Heart Association
Patient is symptom free at rest and with treatment.
Patient experiences impaired heart function with moderate physical effort. Shortness of breath with exertion is common. There are no symptoms at rest.
Even minor physical exertion results in shortness of breath and fatigue. There are no symptoms at rest.
Symptoms such as shortness of breath and signs such as lower-extremity edema are present when the patient is at rest.
Low magnesium level (particularly white blood cell magnesium) is a common finding in patients with CHF. This association is extremely significant, as magnesium levels have been shown to correlate directly with survival rates. In one study, CHF patients with normal levels of magnesium had one- and two-year survival rates of 71% and 61%, respectively, compared with rates of 45% and 42%, respectively, for patients with lower magnesium levels.2 In other words, magnesium level was a strong predictor of survival. These results are not surprising, considering that magnesium deficiency is associated with cardiac arrhythmias, reduced cardiovascular prognosis, worsened angina, lower mitochondrial energy production (critical for heart muscle health), and increased mortality due to heart attack (myocardial infarction).
The magnesium deficiency is probably due to a combination of inadequate intake and overactivation of the kidneys’ attempt to increase blood flow. It can also be the result of diuretics such as furosemide (Lasix).
In addition to providing benefits of its own in CHF, magnesium supplementation also prevents the magnesium depletion caused by conventional drug therapy for CHF (i.e., digitalis, diuretics, and vasodilators such as beta-blockers and calcium-channel blockers). Magnesium supplementation has even been shown to produce positive effects in CHF patients receiving conventional drug therapy, even if serum magnesium levels are normal.3 However, magnesium supplementation is not indicated in patients with kidney failure, as this condition predisposes them to elevations in magnesium in the blood (hypermagnesemia), which is a significant risk factor for death in these patients.4,5
Typical dosages are 200 to 300 mg one to three times per day of magnesium in the citrate form. Oral magnesium can be effective in raising white blood cell magnesium (and potassium) levels.6 Monitoring blood (serum) magnesium levels is critical to preventing hypermagnesemia in patients with kidney failure, as well as those on drugs such as digoxin. Magnesium significantly reduces the frequency and complexity of ventricular arrhythmias in digoxin-treated patients with CHF even without the presence of digoxin toxicity, but too much magnesium may interfere with digoxin.7
Interest has recently risen regarding the potential role of thiamine deficiency in CHF. Thiamine was the first B vitamin discovered, hence its designation as vitamin B1. It is well established that thiamine deficiency can result in “wet beriberi,” sodium retention, peripheral vasodilation, and heart failure. It is also well established that furosemide (Lasix), the most widely prescribed diuretic, has been shown to cause thiamine deficiency in animals and patients with CHF.
Although severe thiamine deficiency is relatively uncommon (except in alcoholics), many Americans do not consume the recommended dietary intake of 1.5 mg, especially elderly patients in hospitals or nursing homes. In an attempt to gauge the prevalence of thiamine deficiency in the geriatric population, 30 people visiting a university outpatient clinic in Tampa, Florida, were tested for thiamine levels. Depending on how the thiamine was measured, low levels were found in 57% and 33%, respectively.8
These results highlight the growing body of evidence that a significant percentage of the geriatric population is deficient in one or more of the B vitamins. Given the essential role of thiamine and other B vitamins in normal human physiology, especially cardiovascular and brain function, routine B vitamin supplementation appears to be worthwhile in this age group.
The association between thiamine deficiency and long-term furosemide use was discovered in 1980 when it was shown that after only four weeks of furosemide use, thiamine concentrations and the activity of the thiamine-dependent enzyme transketolase were significantly reduced. The first study looking at thiamine as a potential support aid in the treatment of CHF showed only modest benefits. However, several subsequent studies have shown that daily doses of 80 to 240 mg thiamine per day resulted in a 13% to 22% increase of left ventricular ejection fraction—a marker that tells us that thiamine improved the heart’s ability to perform.9,10 This increase is quite significant, as an increase in ejection fraction is associated with a greater survival rate in patients with CHF. In one study, biochemical evidence of severe thiamine deficiency was found in 98% of patients receiving at least 80 mg per day of furosemide and in 57% of patients taking 40 mg furosemide per day.11
Given the possible benefit, lack of risk, and low cost of thiamine supplementation, administration of 200 to 250 mg thiamine per day appears to be a wise recommendation in patients with CHF, especially if they are on furosemide.
Normal heart function is critically dependent on adequate concentrations of carnitine and CoQ10 (discussed later). These compounds are essential in the transport of fatty acids into the myocardium and mitochondria for energy production. Although the normal heart stores more carnitine and CoQ10 than it needs, if the heart does not have a good supply of oxygen, carnitine and CoQ10 levels quickly decrease. Both of these agents have shown benefit in the treatment of CHF.
Several double-blind clinical studies have shown carnitine supplementation to improve cardiac function in patients with CHF.12–14 In one double-blind study, only one month of treatment (500 mg three times per day) was needed to cause significant improvement in heart function.13 The longer carnitine was used, the more dramatic the improvement. After six months of use, the carnitine group demonstrated a 25.9% increase in maximum exercise time and a 13.6% increase in ventricular ejection fraction. In another double-blind study of similar patients, at the end of six months of treatment maximum exercise time on the treadmill increased by 16.4% and the ejection fraction increased by 12.1%.14
Even more obvious benefits were seen in a three-year study of 80 patients with moderate to severe heart failure (NYHA classification III to IV) caused by a condition known as dilated cardiomyopathy. After a period of stable cardiac function of up to three months, patients were randomly assigned to receive either carnitine (2 g per day orally) or a placebo. After a mean of 33.7 months of follow-up (range 10 to 54 months), 70 patients were in the study: 33 in the placebo group and 37 in the carnitine group. At the time of analysis, 63 patients were alive. Six deaths occurred in the placebo group, and one death in the carnitine group. Survival analysis showed that patients’ survival was statistically significant in favor of the carnitine group.15
Coenzyme Q10 (COQ10)
Numerous studies have shown CoQ10 supplementation to be extremely effective in the treatment of CHF. Most of these studies used CoQ10 as an adjunct to conventional drug therapy. In one of the early studies, 17 patients with mild CHF received 30 mg per day of CoQ10.16 All patients improved, and nine (53%) became asymptomatic after four weeks. In another early study, 20 patients with congestive heart failure due to either atherosclerosis or high blood pressure were treated with CoQ10 at a dosage of 30 mg per day for one to two months.17 Of these patients, 55% reported subjective improvement, 50% showed a decrease in NYHA classification, and 30% showed a “remarkable” decrease in chest congestion as seen on chest X-rays. Patients with mild disease were more likely to improve than those with more severe disease. Subjective improvements in how the patients felt were confirmed by various objective tests, including increased cardiac output, stroke volume, cardiac index, and ejection fraction. These results were consistent with CoQ10 producing an increased force of contraction similar to but less potent than that produced by digitalis.18,19
Three more studies have also shown CoQ10 to be effective in significantly improving heart function in patients with CHF. In a double-blind Scandinavian study of 80 patients, participants were given either CoQ10 (100 mg per day) or a placebo for three months and then crossed over to the other treatment. The improvements noted with CoQ10 were found to be more positive than those obtained from conventional drug therapy alone.20 In another double-blind study, 641 patients with CHF received either CoQ10 (2 mg/kg) or a placebo for one year.21 The number of patients requiring hospitalization or experiencing serious consequences due to CHF was significantly reduced in the CoQ10 group compared with the placebo group.
In the largest study to date, a total of 2,664 patients in NYHA classes II and III were enrolled in an open study in Italy.22 The daily dosage of CoQ10 was 50 to 150 mg orally for 90 days, with the majority of patients (78%) receiving 100 mg per day. After three months of CoQ10 treatment, the proportions of patients with improvement in clinical signs and symptoms were as follows:
• Cyanosis (extremities turning blue): 78.1%
• Edema (fluid retention): 78.6%
• Pulmonary edema: 77.8%
• Enlargement of liver area: 49.3%
• Venous congestion: 71.81%
• Shortness of breath: 52.7%
• Heart palpitations: 75.4%
• Sweating: 79.8%
• Subjective arrhythmia: 63.4%
• Insomnia: 66.2%
• Vertigo: 73.1%
• Nocturnal urination: 53.6%
Improvement of at least three symptoms occurred in 54% of patients, indicating a significantly improved quality of life with CoQ10 supplementation. The results also showed a low incidence of side effects—only 36 patients (1.5%) reported mild side effects attributed to CoQ10.
These positive results with CoQ10, however, were not seen in one clinical trial. In this double-blind study, 55 patients with CHF NYHA class III and IV, ejection fraction less than 40%, and peak oxygen consumption less than 50% during standard therapy were randomly assigned to receive CoQ10 (200 mg) or a placebo. Analysis indicated that there were no changes in ejection fraction, peak oxygen consumption, or exercise duration in either group. Possible explanations for failure to achieve a therapeutic benefit in this study may be that the CoQ10 was not strong enough to produce significant effects in more severe stages of CHF or that blood levels of CoQ10 did not reach sufficient values. Though the mean serum concentration of CoQ10 increased from 0.95 mcg/ml to 2.2 mcg/ml in 19 of 22 patients on CoQ10, blood levels were below the suggested threshold of 2.5 mcg/ml.23
An important consideration in patients with CHF, especially at the more advanced stages, is that they often fail to achieve adequate plasma CoQ10 levels (>2.5 mcg/ml) on supplemental ubiquinone (the common form of CoQ10) even at dosages up to 900 mg per day. These patients may respond better to highly absorbed forms of CoQ10 such as ubiquinol or emulsified ubiquinone. In one study, seven patients with advanced CHF who had average plasma CoQ10 levels of 1.6 mcg/ml on an average dose of 450 mg ubiquinone per day (range: 150–600 mg per day) were changed to an average of 580 mg per day of ubiquinol (range: 450–900 mg per day) with follow-up plasma CoQ10levels, clinical status, and ejection fraction measurements by echocardiography. Average plasma CoQ10 levels increased from 1.6 mcg/ml to 6.5 mcg/ml. The average ejection fraction improved from 22% (10–35%) to 39% (10–60%) and NYHA class improved from a mean of IV to a mean of II (range: I to III). In this study, ubiquinol dramatically improved absorption in patients with severe heart failure, and the improvement in plasma CoQ10 levels was correlated with both clinical improvement and improvement in measurement of left ventricular function.24
Cross Section of the Heart
Another amino acid of value in CHF is arginine, although its effects come by means of a totally different mechanism from other nutrients. One of the experimental findings in patients with CHF is that they are less able to achieve peripheral dilation of blood vessels during exercise due to dysfunction of the lining of the blood vessels (endothelium). Since the cells that line blood vessels make the natural blood vessel dilating compound nitric acid from arginine, several researchers have evaluated arginine’s effect in improving CHF. The first study of orally administered arginine showed promising results. In a randomized, double-blind, placebo-controlled study of 5.6 to 12.6 g per day of oral L-arginine, peripheral blood flow was found to increase by 29%, 6-minute walking distance increased by 8%, and arterial flexibility (compliance) increased by 19%.25 Subsequent studies have shown arginine supplementation to improve endothelial cell function and kidney function in patients with CHF.26,27 However, use of arginine requires caution in survivors of a heart attack, because in one study supplementation with arginine (9 g per day for six months) was associated with an increase in mortality compared with that in the placebo group (8.6% vs. 0%).28
• In the early stages of CHF, natural measures designed to address the underlying cause (e.g., high blood pressure) or improve the metabolic functions of the heart are often quite effective.
• In later stages, however, medical treatment involving the use of diuretics, angiotensin-converting enzyme (ACE) inhibitors, or digitalis glycosides is indicated in most cases.
• CHF is always characterized by impaired energy production within the heart muscle, often the result of nutrient or coenzyme deficiency (e.g., magnesium, thiamine, coenzyme Q10, carnitine).
• The level of magnesium is a strong predictor of survival in CHF.
• Magnesium supplementation has been shown to produce positive effects in CHF patients receiving conventional drug therapy, even if serum magnesium levels are normal.
• Studies have shown that doses of 80 to 240 mg thiamine per day produced a 13 to 22% increase in the heart’s ability to perform.
• Several double-blind clinical studies have shown carnitine supplementation to improve cardiac function in patients with CHF.
• Numerous studies have also shown CoQ10 supplementation to be extremely effective in the treatment of CHF.
• Patients with severe CHF may respond better with highly absorbable forms of CoQ10 such as ubiquinol or emulsified ubiquinone.
• Arginine supplementation improves blood vessel and kidney function in patients with CHF.
• Preparations of hawthorn appear to be quite useful in CHF, especially in the early stages as a sole agent and in the latter stages in combination with conventional medicines such as digitalis.
• Terminalia arjuna, a traditional ayurvedic medicine for cardiac failure, has recently been shown to be effective in a controlled clinical study.
Preparations of hawthorn (Crataegus oxyacantha) appear to be quite useful in CHF, in the early stages as a sole agent and in the latter stages in combination with conventional medicines such as digitalis. The effectiveness of hawthorn in CHF has been repeatedly demonstrated in double-blind studies.29–31 In one recent study, 30 patients with CHF (NYHA stage II) were assessed in a randomized, double-blind format.29 Treatment consisted of a hawthorn extract standardized to contain 15 mg proanthocyanidin oligomers per 80 mg capsule, taken twice a day. Treatment duration was eight weeks. The group receiving the hawthorn extract showed a statistically significant advantage over the group taking a placebo in terms of changes in heart function as determined by standard testing procedures. Systolic and diastolic blood pressures were also mildly reduced. As in all other studies with hawthorn extracts, no adverse reactions occurred.
In another study, 78 patients with CHF (NYHA stage II) were given either 600 mg standardized hawthorn extract or a placebo per day.30 The indicator used to measure effectiveness was the patient’s working capacity on a stationary bicycle. After 56 days of treatment, the hawthorn group had a mean increase of 25 watts compared with the placebo group’s increase of only 5 watts. In addition, the hawthorn group also experienced a mild but significant reduction in systolic blood pressure (from 171 to 164 mm Hg) and heart rate (115 to 110 beats/min). There was no change in blood pressure or heart rate with the placebo group.
In patients with NYHA stage III, hawthorn may not be sufficient to produce clinical effects. In a randomized, double-blind, placebo-controlled trial involving 120 ambulatory patients with NYHA class II-III CHF, all patients received conventional medical therapy, as tolerated, and were randomly assigned to receive either hawthorn 450 mg twice per day or a placebo for six months. The primary outcome was a change in the six-minute walk distance at six months and no significant effect was noted.31
Arjun Tree (Terminalia arjuna)
A traditional ayurvedic medicine for cardiac failure has recently been shown to be effective in a controlled clinical study. Twelve patients with severe refractory congestive heart failure (class IV NYHA) received an extract (500 mg every eight hours) from the bark of Terminalia arjuna or a placebo for two weeks. Those receiving the medicinal plant experienced, according to echocardiogram evaluation, statistically significant improvement in several indicators of cardiac function, such as end-systolic volume and left ventricular ejection fractions. A second, uncontrolled phase of the study using a combination of T. arjuna with conventional medication found that after two years, nine patients showed a remarkable improvement to NYHA class II, with the other three improving to class III.32
Treatment with diet and the natural agents mentioned earlier is effective in early stages of CHF (i.e., NYHA stages I and II). In later stages, adjunct drug therapy is usually necessary. Treatment is designed to address the underlying disease process and to improve heart function through improved energy production.
It is essential to achieve and maintain ideal body weight, restrict sodium intake (to below 1.8 g per day), increase consumption of plant foods, reduce the intake of saturated fat, and follow the other dietary guidelines for lowering blood pressure in the chapter “High Blood Pressure.”
• A high-potency multiple vitamin and mineral formula as described in the chapter “Supplementary Measures”
• Key individual nutrients:
Thiamine (vitamin B1): 200 to 250 mg per day
Vitamin B6: 25 to 50 mg per day
Folic acid: 800 to 2,000 mcg per day
Vitamin B12: 800 mcg per day
Vitamin C: 500 to 1,000 mg per day
Vitamin E (mixed tocopherols): 100 to 200 IU per day
Magnesium (bound to aspartate, citrate, fumarate, malate, or succinate): 200 to 300 mg three times per day
Vitamin D3: 2,000 to 4,000 IU per day (ideally, measure blood levels and adjust dosage accordingly)
• Fish oils: 1,000 mg EPA + DHA per day
• Specialty supplements:
L-carnitine: 500 to 1,000 mg three times per day
CoQ10: 100 to 200 mg three times per day
Arginine: 1,000 to 2,000 mg three times per day
• Hawthorn (Crataegus species) extract (1.8% vitexin-4-rhamnoside or 10% proanthocyanidin content): 200 to 300 mg three times per day
• T. arjuna extract: 500 mg three times per day