Treatment of Congestive Heart Failure
by Hans R. Larsen, MSc ChE
Heart failure is defined as the inability of the heart to supply sufficient blood flow to meet the needs of the body. The term "congestive heart failure" implies that the impaired blood flow is causing fluid retention in the lungs, legs, ankles or feet. Other common symptoms include shortness of breath when lying down or during exercise, fatigue and weakness, reduced exercise capacity, and rapid or irregular heartbeat.
Coronary artery disease (atherosclerosis) and heart attack are the most common causes of heart failure along with high blood pressure, faulty heart valves, damage to the heart muscle, inflammation (myocarditis), and congenital heart defects. Untreated chronic heart arrhythmias, especially atrial fibrillation, may also lead to heart failure as may the presence of diabetes, severe anemia and thyroid problems. Finally, there is evidence that heart failure is associated with a deficiency of thiamine (vitamin B1) which is exacerbated with the use of thiazide diuretics.
The primary diagnostic markers of heart failure are left ventricular ejection fraction of less than 40% and a blood (plasma) level of brain natriuretic peptide (BNP) in excess of 100 pg/mL. An elevated blood (serum) level of C-reactive protein is also associated with heart failure.
Regardless of the cause and manifestation of the disease (left-sided heart failure, right-sided heart failure, systolic heart failure or diastolic heart failure) the medications commonly prescribed for heart failure are as follows:
The most recent AHA/ACCF Guidelines for the Management of Heart Failure recommend the following treatment protocol for patients with structural heart disease (valve problems) and symptoms of heart failure:
The following comments in the guidelines regarding potassium are of particular interest:
"Patients with HF (heart failure) should be monitored carefully for changes in serum potassium, and every effort should be made to prevent the occurrence of either hypokalemia or hyperkalemia, both of which may adversely affect cardiac excitability and conduction and may lead to sudden death. Activation of both the sympathetic nervous system and renin-angiotensin system can lead to hypokalemia and most drugs used for the treatment of HF can alter serum potassium. Even modest decreases in serum potassium can increase the risks of using digitalis and antiarrhythmic drugs, and even modest increases in serum potassium may prevent the use of treatments known to prolong life. Hence, many experts believe that serum potassium concentrations should be targeted in the 4.0 to 5.0 mmol per liter range."
The goal of alternative and complementary therapies is to increase the pumping efficiency of the heart and to alleviate the adverse effects of conventional treatment. Several natural substances have been found effective in the treatment of heart failure. Substantial evidence of efficacy is available for the following:
Coenzyme Q10 supplementation is of extreme importance in heart failure patients on statin drugs. Research has shown that these drugs seriously impede the synthesis of coenzyme Q10 leading to such adverse effects asmyalgia (muscle pain), fatigue, breathing difficulties, memory loss, and peripheral neuropathy. Fortunately, supplementation with coenzyme Q10, preferably in conjunction with discontinuation of statin drugs, can completely reverse these effects.[11-14]
Well-functioning heart cell mitochondria are essential to heart health. Coenzyme Q10 is the "spark plug" that powers the mitochondria. Recently, a new supplement, pyrroloquinoline quinone (PQQ) has been developed which markedly increase the formation of new mitochondria.[15-17] Thus, it would seem that a protocol which combines ubiquinol (3 x 100 or 3 x 200 mg/day) with PQQ (20 mg/day) would be greatly beneficial.
Magnesium is of key importance to human health. It participates in over 300 enzymatic reactions in the body. A deficiency has been linked to conditions such as irregular heartbeat, asthma, emphysema, cardiovascular disease, high blood pressure, mitral valve prolapse, stroke and heart attack, diabetes, fibromyalgia, glaucoma, migraine, kidney stones, osteoporosis, and probably many more. About 99% of the body's magnesium stores are found in the bones and tissues and heart tissue is particularly rich in this important mineral. Only 1% of the body's magnesium is actually present in the blood so a standard blood analysis is a very poor way of determining overall magnesium status.
Magnesium deficiency is widespread in the general population and especially pronounced in atrial fibrillation and heart failure patients, especially if treated with loop diuretics (thiazides), digoxin and ACE inhibitors.[27,28] There is evidence that magnesium deficiency is associated with a much lower survival rate in heart failure patients. Fortunately, there is also evidence that replenishment of magnesium with oral supplementation, specially magnesium orotate, can markedly improve both clinical symptoms, survival and quality of life.
A growing body of evidence points to a close connection between magnesium deficiency and mitral valve prolapse and, perhaps even more importantly, clinical trials have shown that supplementation with magnesium can partially or fully eliminate the symptoms of mitral valve prolapse.[31,32]
Intramuscular injections of magnesium sulfate and oral supplementation with chelated magnesium (magnesium glycinate) are effective means of increasing magnesium level in heart cells.
Whichever protocol is used to achieve a potassium level between 4.5 and 5.5 mmol/L, it should be kept in mind that a low magnesium level (hypomagnesemia) increases potassium excretion, and it is very difficult to remedy hypokalemia without first attaining normal magnesium levels. One study found that 42% of people with low magnesium levels also had low potassium levels.[35,36]
The product most widely used in Germany is WS1442 which is an extract of hawthorn leaf and flower standardized to contain 18.75% of oligomeric procyanidins. A recent Cochrane review of 10 clinical trials evaluating the effect of hawthorn in heart failure patients concluded that supplementation with hawthorn (most likely 450 mg of WS1442 twice daily) improved exercise tolerance and significantly reduced symptoms such as shortness of breath and fatigue. Most of the clinical trials used hawthorn as an adjunct to standard medical treatment. Adverse effects were infrequent, mild and transient. The Cochrane researchers conclude that "there is a significant benefit in symptom control and physiologic outcomes from hawthorn extract as an adjunctive treatment for chronic heart failure".
Vitamin D deficiency is widespread and has been implicated in cancer, osteoporosis, hypertension, diabetes, rheumatoid arthritis and multiple sclerosis. Most researchers now consider a 25(OH)D level below 50 nmol/L (20 ng/mL) to be deficient and an optimum level to be about 75 nmol/L (30 ng/mL). A low vitamin D [25(OH)D] level is common among heart failure patients and is an indicator of a poor prognosis. Dutch researchers have found that heart failure-related mortality increases by 10% for each 10 nmol/L decrease in 25(OH)D level. Fortunately, it is relatively simple to correct a vitamin D deficiency. It can be achieved slowly through oral supplementation with 2000 to 4000 IU/day of cholecalciferol over a 6-month period, or quickly by using one-time doses as high as 500,000 IU.[45,46]
Taurine deficiency is common among heart failure patients; thus, it is not surprising that Japanese researchers, 30 years ago, reported that taurine supplementation (2-3 grams/day) is effective and entirely safe in the treatment of congestive heart failure.[51-54] More recent research has shown that taurine supplementation (500 mg three times daily) for 2 weeks significantly increases exercise capacity in heart failure patients. There is also evidence that taurine exerts an inotropic effect similar to that of digoxin (without the side effects), and that it has diuretic effects and counteracts the adverse effects of angiotensin II.[56,57] Thus taurine supplementation could potentially reduce the need for treatment with ACE inhibitors/angiotensin II receptor blockers and digoxin.
It is clear that heart failure patients are often deficient in nutrients crucial to proper heart function. In many cases, these deficiencies are exacerbated by drugs (digoxin, diuretics, statins and ACE inhibitors) prescribed as part of the standard medical treatment for heart failure. It is thus of utmost importance that patients