Congestive Heart Failure (CHF)


Heart failure is a pathophysiological state in which the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the body. (1) Some clinicians now prefer to use the term heart failure rather than congestive heart failure because a patient can have the clinical syndrome of heart failure without having symptoms of congestion. Heart failure is not a specific disease entity, but rather a clinical syndrome that may be caused by numerous different cardiac disorders. (2)

Congestive heart failure has been described as low-output heart failure in which the heart is unable to pump all the blood with which it is presented. For example, a normal ejection fraction (EF) is greater than 60 percent; however, a patient with severe CHF may have an EF as low as 20-30 percent. Increased cardiac workload (preload, afterload, contractility, heart rate) and decreased myocardial contractility are factors, which contribute to the development of CHF.

To review; cardiac output (CO) is defined as the volume of blood ejected per unit of time (L/min) and can be determined by multiplying heart rate times stroke volume (CO=HR x SV). Stroke volume is the volume of blood ejected during systole, and is dependent on preload, afterload, and contractility. Preload occurs on the venous side of circulation. As the volume of blood returning to the left ventricle increases, pressure increases and causes an increase in wall tension. The fibers or sarcomeres are stretched, resulting in an increased force of contraction. Left ventricular end diastolic volume (LVEDV) is the primary determinant of preload. Afterload can be viewed as the sum of forces preventing active forward ejection of blood by the ventricle.

Contractility is the intrinsic property of cardiac muscle describing fiber shortening and tension development. The terms contractility and inotropic state are used synonymously. Myocardial contractility is decreased when myocardial fibers are diminished or poorly functioning. This often occurs with myocardial infarction, coronary artery disease, rheumatic heart disease, and persistent arrhythmias. Cardiomyopathy, a generalized term used to describe a deterioration of cardiac muscle function, may also produce CHF. Occasionally, drugs such as beta-blockers or daunorubicin induce CHF by decreasing myocardial contractility. (3)

The heart uses several compensatory mechanisms to maintain adequate cardiac output as cardiac function decreases. One of those mechanisms is tachycardia and increased contractility. When cardiac output decreases, there is decreased perfusion of tissues. The decreased perfusion signals the sympathetic autonomic nervous system to release norepinephrine. The effect of this release is increased inotropy and chronotropy (heart rate), which may initially maintain the cardiac output at near normal. This will preserve perfusion of the myocardium and CNS. The release of norepinephrine also acts to cause vasoconstriction in the skin, GI tract, and kidney, decreasing perfusion in these organs.

When the tachycardia and increased contractility occur, it is important to understand that the time ratio of systole: diastole decreases. The time it takes for systole to occur remains relatively the same; however, in tachycardia, the length of time of diastole, or the resting state, is decreased. Diastolic filling becomes compromised at approximately 170-200 beats per minute in the normal heart; however, in a heart with preexisting or acute diastolic dysfunction, the ventricle’s need for a longer diastolic filling results in reduction of effective preload at significantly lower heart rates. Increasing heart rate also increases myocardial oxygen demand. Shortened diastolic time also causes an increase in intracellular calcium levels, since calcium is pumped out of the sarcoplasmic reticulum and into the cells during diastole, increasing actin-myosin interaction and ultimately reducing lusitropy (relaxation) of heart fibers.

Another compensatory response is described as the Frank-Starling mechanism, where an increase in preload results in an increased stroke volume. As the cardiac output decreases, blood is shunted away from renal circulation and redirected to the myocardium and CNS. The kidney interprets this activity as a decrease in blood volume and acts to retain sodium and water. Renin is also released by the kidney in response to decreased perfusion. Renin is responsible for the conversion of angiotensin to angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme.

This process has two effects favoring water and sodium retention: its vasoconstricting effects further reduce glomerular filtration rates, and it also stimulates the release of aldosterone, further enhancing sodium and water retention. The process causes a net increase of intravascular fluid volume, which causes a left ventricular volume and pressure increase (preload). This causes sarcomeres to be stretched and enhances the force of ventricular contraction. While the preload response is the primary compensatory mechanism in normal hearts, the chronically failing heart has usually exhausted its preload reserve. When shown graphically, a point can be seen when this mechanism has reached the limit of its effectiveness. As the response curve begins to flatten, the effect seen is not an increase in stroke volume, but rather a point where increases in preload will only produce pulmonary or systemic congestion. This may, in turn, cause an increase in afterload, since increasing ventricular radius elevates wall tension.

The third compensatory mechanism used by the heart to increase cardiac output is vasoconstriction. This process has already been partially described as that which redirects blood to the cerebral and myocardial circulation and away from nonessential organs. There are a number of neurohormones likely to contribute to the vasoconstrictive process, including norepinephrine, angiotensin II, endothelin-I, and arginine vasopressin. In the normal heart, this mechanism helps to maintain blood pressure that may drop as a result of a decrease in cardiac output. In the failing heart, it only serves to further increase resistance against which the ventricle must pump (afterload). This may potentiate a vicious cycle of continued worsening and downward spiraling of the heart failure state.

Ventricular hypertrophy is a long-term adaptation to increased diastolic volume, and represents an increase in myocardial muscle mass. The cascade that creates this long- term response is complicated, and the specific type of hypertrophy (increased chamber size or increase in ventricular wall thickness) may result from specific stressors. Thus, while ventricular hypertrophy is designed to be an important compensatory response in heart failure, it often leads to abnormal myocardial stiffness and systolic and diastolic dysfunction.


World Health Organization, 1995.

  • More than 22 million people worldwide suffer from congestive heart failure (CHF).

National Heart Association of Malaysia, 2007.

  • Heart failure accounts for 10% of medical admissions in Malaysia.

National Heart, Lung & Blood Institute, National Institute of Health Data Fact Sheet, 1996.

    It is estimated that 4.8 million Americans have CHF. 1/2 the patients diagnosed with CHF will die within 5 yrs. The annual number of deaths from CHF increased from 10,000 in 1968 to 42,000 in 1993,with another 219,000 deaths related to CHF. CHF is the first-listed diagnosis in 875,000 hospitalizations and the most common diagnosis in hospital patients age 65 yrs. and older.

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

The most frequent signs of heart failure are those of systemic and/or pulmonary congestion. Congestion forms behind the failing ventricle, with left ventricular failure causing pulmonary congestion, and right-sided failure causing systemic congestion. Most patients initially have left sided failure; however, since the ventricles share a septal wall, and left ventricle failure increases the work of the right ventricle, both ventricles eventually fail. Many heart failure patients will present with symptoms of both right and left ventricular failure. (4)

As has been previously discussed, when a ventricle fails, it is unable to eject all the blood with which it is presented. In left ventricular failure, this causes pulmonary venous and capillary pressure to rise. The rise in pressure causes interstitial and bronchial edema, dyspnea, and increased airway resistance.

Symptoms include dyspnea upon exertion, or a feeling of breathlessness after normal exertion such as stair climbing or running the sweeper. Other types of dyspnea frequently seen are orthopnea and paroxysmal nocturnal dyspnea. Both of these types are seen when the patient is in a recumbent position. Orthopnea usually occurs within minutes of lying down, and is thought to be due to decreased pooling of blood in the abdomen and lower extremities. It can be relieved almost immediately upon sitting upright. Patients often have to sleep on several pillows to prevent orthopnea. A change in the number of pillows needed usually represents a worsening of heart failure. Paroxysmal nocturnal dyspnea occurs generally two to four hours after the patient is asleep. This is thought to be caused not only by decreased pooling of blood in the abdomen and lower extremities, but also by slow resorption of interstitial fluids seen in dependent edema, the normal reduction of sympathetic activity the occurs during sleep, and a normal depression in respiratory drive seen during sleep. The patient awakens with a feeling of suffocation. The patient may have to sit up as long as 30 minutes for symptoms to subside.

Pulmonary edema is the most severe form of pulmonary congestion and can be terrifying for patients, causing a feeling of suffocating, or drowning. A cough is often present with hemoptysis. Signs upon examination may include bibasilar rales, pulmonary edema, S3 gallop, pleural effusion, and Cheyne-Stokes respiration.

Signs and symptoms of right ventricular failure are the result of systemic venous congestion. The cardinal sign is peripheral edema, and is usually seen in a dependent part of the body. In the ambulatory patient, it appears as pedal or ankle edema; in the bedridden patient, as sacral edema. Adults may typically have a 10-pound weight gain before edema is even noticed. Symptoms of right ventricular failure are less common than those seen with left-sided failure, and are associated with hepatic and intestinal congestion. They may include abdominal pain, anorexia, nausea, bloating, and constipation. Upon examination, peripheral edema can be noted, as well as jugular venous distention, hepatojugular reflex (increase in jugular venous pressure when pressure is applied to the abdomen), and hepatomegaly.

Weakness, fatigue, and exercise intolerance are present in most patients with heart failure. Chest x-rays may show cardiomegaly, although this finding is considered non-specific. There are no specific electrocardiographic changes in heart failure; however, many patients will show left ventricular hypertrophy. Peripheral vasoconstriction may result in pallor, cool extremities, or cyanosis of the digits. Nocturia is frequently noted because of decreased sympathetic activity and reduction of cardiac output demands at night. Consequently, renal vasoconstriction diminishes, increasing renal blood flow and urine formation.

The most frequently used system in classifying degree of heart failure is the New York Heart Association Functional Classification, described below:

  • Class I Patients with cardiac disease, but without limitations of physical activity. Ordinary physical activity does not cause undue fatigue, dyspnea, or palpitations.
  • Class II Patients with cardiac disease that results in slight limitations of physical activity. Ordinary physical activity results in fatigue, dyspnea, palpitations, or angina. Class III Patients with cardiac disease that results in marked limitation of physical activity. Although patients are comfortable at rest, less than ordinary activity will lead to symptoms. Class IV Patients with cardiac disease that results in an inability to carry on physical activity without discomfort. Symptoms of congestive heart failure are present even at rest. With any physical activity, discomfort is experienced.

General Symptoms

    Weakness Fatigue Exercise intolerance Nocturia Tachycardia Pallor Cyanosis of digits Cardiomegaly

Left Ventricular Failure

    Dyspnea upon exertion Orthopnea Paroxysmal nocturnal dyspnea Tachypnea Cough with hemoptysis Bibasilar rales Pulmonary edema S3 gallop Pleural effusion Cheyne-Stokes respiration

Right Ventricular Failure

    Abdominal pain Anorexia Nausea Bloating Constipation Ascites Peripheral edema Jugular venous distention Hepato-jugular reflex Hepatomegaly

Treatment Options


The first step in treatment of heart failure is to determine the etiology and/or precipitating factors. Restriction of physical activity reduces cardiac workload and is recommended for virtually all patients with acute heart failure. Once the patient is stabilized and excess fluid removed, restrictions on physical activity are discouraged. In fact, recent data suggest low intensity exercise training programs in stable heart failure patients improve exercise tolerance and functional capacity. (5)

Another important nonpharmacological intervention is reduction of sodium in the diet, since the major compensatory mechanism in heart failure is retention of sodium and water. The typical American diet contains 3 to 6 grams of sodium per day. General recommendations are to cut that amount in half. Further sodium restriction is possible by removing all salt from cooking; however, patients find the food unpalatable and have a greater tendency to be non-compliant.

The goals of therapy in the management of chronic heart failure patients are to improve the patient’s quality of life and reduce symptoms, reduce hospitalizations, slow the disease process, and prolong survival.

Clinical practice guidelines have been published by three independent groups. Guidelines for the management of left ventricular systolic dysfunction were published by the Agency for Health Care Policy and Research (AHCPR) through the U.S. Public Health Service in 1994. (6) These include not only pharmacologic therapy guidelines, but also include patient assessment and evaluation, patient and family education, outcomes assessment, and role of revascularization. In 1995, the American College of Cardiology and the American Heart Association published practice guidelines for the evaluation and management of heart failure. (7) These guidelines are more comprehensive than the AHCPR guidelines and include both acute and chronic heart failure, and systolic and diastolic dysfunction. The Canadian Cardiovascular Society’s publication is largely in agreement with other publications; however, it is less detailed.

According to published guidelines, the first line drugs of choice in chronic heart failure that have been clinically shown to affect one or more of the goals of therapy include vasodilators (especially ACE inhibitors and hydralazine/nitrite combinations), diuretics, digoxin, and carvedilol.

The vasodilators represent the cornerstone of therapy, having been documented to positively impact all therapeutic goals in heart failure. ACE inhibitors cause dilation in both arterial and venous circulation, reducing preload and afterload. They act to reduce activation of angiotensin II, a potent vasoconstrictor, and also reduce the breakdown of bradykinin, a vasodilator. ACE inhibitors approved for use in heart failure are captopril, enalapril, lisinopril, quinapril, and ramipril. They are now considered the first drug of choice in treating heart failure.

Nitrates act on enzymes to increase cyclic guanosine monophosphate in vascular smooth muscle. This causes a vasodilatory effect in the venous beds. Hemodynamically, this acts to reduce preload, although a mild decrease in systemic vascular resistance may also be seen. Nitrates are often given in combination with hydralazine, which is a direct acting vasodilator affecting arterial smooth muscle. This causes a significant reduction in SVR, increasing stroke volume and cardiac output. The drugs together reduce both preload and afterload. Since adverse effects with both drugs are common, the use has been primarily limited to either patients who cannot take ACE inhibitors, or those who remain symptomatic on optimal doses of ACE inhibitors.

A very common component of therapy in the treatment of heart failures is the use of diuretics. As has been previously discussed, the body’s compensatory mechanisms in decreased cardiac output include the retention of sodium and water. This often leads to pulmonary and systemic congestion. The loop diuretics are of value because they act at the ascending loop of Henle where 20-25 percent of sodium is normally reabsorbed. The loop diuretics most frequently used are furosemide and bumetanide. Although thiazide diuretics may be used, they act in the proximal convoluted tubules (which are responsible for reabsorbing only 5-8 percent of sodium) and are considered weak diuretics and used infrequently in heart failure.

Diuretics cause a variety of side effects, most of which are directly dependent upon the potency of the diuretic being used. Probably the side effect of greatest consequence is that of hypokalemia. This is particularly worrisome in heart failure since it can precipitate ventricular arrhythmias, a common mode of death in CHF. Digitalis-associated arrhythmias are also more common with concurrent hypokalemia. Serum potassium should be monitored closely in heart failure patients and supplemented appropriately as needed.

Digitalis glycosides have been used clinically for over 200 years, and their efficacy in heart failure patients with supraventricular tachyarrhythmias such as atrial fibrillation has been well established. By far, the most frequently used digitalis glycoside is digoxin. Its use in the pharmacotherapy of chronic heart failure has been summarized as follows. In patients with left ventricular systolic dysfunction and supraventricular tachyarrhythmias such as atrial fibrillation, it should be considered early in therapy to control ventricular response rate. For patients in normal sinus rhythm, digoxin is not first line therapy because it does not improve survival. Its positive inotropic effects, symptom reduction, and quality of life improvement may be most evident in patients with moderate to severe left ventricular dysfunction. Thus, digoxin is recommended in patients in sinus rhythm who remain symptomatic after optimization of therapies known to improve survival.

Beta-blockers have been listed as drugs that can be used as first line therapy in heart failure patients and have also been listed as drugs that may exacerbate heart failure. This may seem paradoxical; however, it is true. When administered in normal doses, beta-blockers can lead to symptomatic worsening; however, there is mounting clinical evidence that if stable patients are initiated on low doses with upward titration over several weeks, they may derive significant benefits. (8) Although many different agents have been studied, over half were in enrolled in studies using carvedilol, the first beta-blocker approved by the FDA to treat heart failure. Carvedilol is indicated in patients with NYHA class II-III heart failure, added to standard therapy to reduce the progression of the disease, decrease hospitalizations, reduce the need to adjustment other heart failure medications, and decrease heart transplants.

Alternative drug treatments also include the use of angiotensin II receptor antagonists, antiarrhythmic therapy, and the use of second-generation calcium channel blockers.(amlodipine and felodipine).

Angiotensin II can be formed in a number of tissues, including the heart, through non-ACE dependent pathways. Therefore, the use of ACE inhibitors may not cause complete blockade. The angiotensin II receptor antagonists losartan and valsartan block the detrimental effects of angiotensin II regardless of its origin. The results of prospective mortality trials (ELITE-II) are needed before angiotensin II blockers can be considered first line therapy for heart failure. Until then, they may be most useful in patients intolerant to ACE inhibitors due to severe cough, or those with persistent symptoms and/or hypertension despite maximal ACE inhibitor use.

Both the use of class III antiarrhythmics and the use of second generation dihydropyridine calcium channel blocking agents are currently under investigation; however, current data fail to support their use specifically to treat heart failure.

Nutritional Supplementation

Coenzyme Q10 (CO-Q10)

Coenzyme Q10 (CoQ10) is a naturally occurring vitamin-like nutrient now being considered as an important nutrient for cardiac function and in the treatment of CHF. Conversely, a deficiency of coenzyme Q10 may be a contributing factor in the development of congestive heart failure. Clinical studies indicate that coenzyme Q10 can improve the quality of life, decrease the incidence of hospitalizations and life threatening cardiac complications, and reduce the need for pharmaceutical drugs. CoQ10 is a vital fat-soluble antioxidant that helps protect the heart and cardiovascular system against free radical-induced aging damage. The production of energy within the mitochondria also requires adequate supplies of coenzyme Q10.

Since the heart is the most energy-demanding muscle in the human body, a deficiency of coenzyme Q10 can begin to weaken the heart muscle energetics. When the heart cannot generate adequate levels of energy, it cannot adequately pump fluids through the vascular system.

In one study, patients with CHF were treated with CoQ10, 100mg daily. At this dosage level, 69 percent of patients with cardiomyopathy and 43 percent of patients with ischemic heart disease had good clinical response. These results were so impressive that the authors of the study called coenzyme Q10, "A scientific breakthrough in the management of chronic heart failure." (9) Another study provided equally impressive results. Patients with congestive heart failure were evaluated in a large multicenter double-blind, placebo controlled trial over the period of one year. Patients treated with coenzyme Q10 experienced a 37.4 percent decline in hospitalizations due to life threatening arrhythmias, a 60 percent decline in pulmonary edema, and a 50.6 percent decline in cardiac-induced asthma. (10)

CoQ10 has been studied in regard to hypertension. Studies conclude that coenzyme Q10 has the potential for strengthening heart muscle and could play a key role in the future treatment of congestive heart failure and other forms of cardiovascular disease. An attending physician must monitor this type of therapy because as heart muscle is strengthened, physicians will have to gradually decrease, and in many cases, eliminate some medications. Some categories of prescription drugs inhibit the body’s ability to synthesize coenzyme Q10, which may partially explain why congestive heart disease and other forms of cardiovascular disease are so prevalent.


In general, magnesium plays a critical role in regulating cardiovascular hemodynamics and electrophysiologic function. Deficiency frequently occurs in patients with congestive heart failure, which can result in cardiac arrhythmias. It has also been determined that a magnesium deficiency can lead to a coronary artery spasm, which is a heart attack that frequently causes death. (11) Magnesium influences many aspects of cardiovascular activity and functions similarly to many of the most frequently used cardiovascular drugs.

Studies have documented the fact that oral administration of magnesium to patients with CHF results in a significant rise in serum magnesium and potassium levels, which provides cardioprotective benefits. (12) , (13) This research reports that the use of magnesium supplements may be beneficial for treating and preventing many of the life-threatening conditions associated with congestive heart failure. Magnesium supplements can be administered safely either orally or parenterally depending on the situation. Many nutritionally oriented physicians advise patients with cardiovascular disease to take 300 to 600mg of magnesium daily. It should be noted that many common cardiovascular drugs deplete magnesium as well as CoQ10.


Carnitine is a cofactor in the intermediary metabolism of cellular heart function, and carnitine deficiency has been associated with congestive heart failure. One of the problems associated with congestive heart failure is an insufficiency in the supply of oxygen, which can damage the heart. Carnitine aids in fatty acid metabolism, which can make more energy available to the cells of the heart muscle. In one study, treatment with carnitine resulted in increased peak oxygen consumption by 45 percent, exercise time by 21 percent, and peak exercise heart rate by 12 percent. There was also a concomitant reduction of pulmonary artery pressure. (14)

L-carnitine is capable of reversing the inhibition of adenine nucleotide translocase and thus, can restore the fatty acid oxidation mechanism, which constitutes the main energy source for the myocardium. (15) Thus, carnitine helps to increase oxygen and energy in the heart. These results indicate that L-carnitine is a useful therapeutic agent for the treatment of congestive heart failure that can be used in combination with traditional cardiovascular drugs.


Taurine is an amino acid that helps to protect cardiac myocytes from a variety of damaging conditions. Studies have reported some success in treating congestive heart failure with oral taurine. (16) , (17) Taurine seems to act like a mild cardiac glycoside to raise intracellular sodium. If intracellular taurine levels were raised, calcium release from the sarcoplasmic reticulum would increase, calcium sensitivity of the contractile proteins would increase, and there would be a change in the action potential associated with the actions of taurine on calcium channels. It has also been suggested that increasing intracellular taurine levels in the hearts of patients before they go to cardiac surgery may be warranted. This would reduce the rise in ionizable sodium and the loss of amino acids and might aid in tissue preservation. (18)


Potassium loss occurs frequently in patients with congestive heart failure. Potassium can modify both the mechanical and electrical properties of the heart, exert diuretic effects, and reduce the frequency and complexity of potentially lethal ventricular tachyarrhythmias. (19) Commonly prescribed cardiovascular drugs, such as the loop diuretics, thiazide diuretics, and some of the calcium channel blocking drugs, are known to cause potassium depletion. (20) , (21) , (22)


Arginine is an amino acid that helps to regulate some aspects of cardiovascular function. Arginine is required for the production of nitric oxide, which acts as a vasodilator to increase blood flow. In fact, it is now known that a decrease in synthetic activity of the L-arginine-NO metabolic pathway contributes to decreased endothelium-dependent vasodilation in patients with congestive heart failure. (23) , (24) Infusion of L-arginine in patients with congestive heart failure results in increased production of nitric oxide, peripheral vasodilation, and increased cardiac output, suggesting a beneficial hemodynamic and possibly therapeutic profile. (25)

Herbal Supplementation


Hawthorn is used as a vasodilator and circulatory stimulant. (26) It has been used extensively by doctors in Europe in its standardized form in various cardiovascular and peripheral circulatory conditions. Its combination of effects on the heart leads to its use as a tonic, especially for the elderly, where mitral stenosis and minor heart failure may be present. Studies have reported a reduction in blood pressure due to arteriosclerosis and chronic nephritis with the use of hawthorn. (27) It is also used for peripheral vascular diseases such as Raynaud’s disease. Hawthorn is used in Europe by physicians to help maintain digoxin levels, while decreasing the need for the pharmaceutical medication. Hawthorn is reported to have the ability to regulate both low and high blood pressure. Its bioflavonoids reportedly dilate both peripheral and coronary blood vessels. (28) This leads to its use in decreasing angina attacks. The proanthocyanidin (PCO) content is claimed to support the spasmolytic effects. (29) The PCO content is also thought to be responsible for the coronary circulatory effects, increasing the amplitude of the heartbeat. (30) Hawthorn’s glycoside component reportedly increases the vagal tone of the heartbeat. (31) It is also thought that hawthorn inhibits angiotensin-converting enzyme. (32) It has a slight diuretic effect, which may help lower high blood pressure. Laboratory studies have reported that proanthocyanidins may actually aid in reversing atherosclerotic plaque. (33)


Cordyceps is a unique black mushroom that extracts nutrients from and grows only on a caterpillar found in the high altitudes of Tibet and China. Cordyceps is one of the most valued medicinal agents in the Chinese Materia Medica. Cordyceps has been used in traditional Chinese medicine as the herb of choice in lung and kidney problems, and as a general tonic for promoting longevity, vitality, and endurance. (34) Cordyceps is beneficial in helping individuals with decreased energy restore their capacity to function at a greater level of activity. Cordyceps has been used in humans for centuries as a tonic for improving performance and vitality, with the proposed mechanism of action being improved oxygen consumption by the cardiopulmonary system under stress and increased tissue "steady state" energy levels. Cordyceps may modulate immune function and optimize endocrine systems, increasing physical strength and endurance. (35) , (36)

Cordyceps has traditionally been used for its improvement in respiration and in individuals with decreased lung function, such as asthma and bronchitis, by increasing oxygenation (improving VO2 max by 9-15%). (37) Cordyceps has been reported to have anticancer effects by decreasing proliferation and differentiation of cancerous cells and has immunomodulatory effects. (38) , (39) , (40) Cordyceps has been used for decreasing the renal toxicity of aminoglycosides and cyclosporine (41) , (42) and in individuals with chronic renal failure. (43) Kidney protection is claimed to be due to: protecting tubular cell sodium pump activity; attenuating tubular cell lysosome overfunction stimulated by phagocytosis of aminoglycoside; and decreasing tubular cell lipoperoxidation in response to toxic injury. (44) Cordyceps was also reported to protect stem cells and red blood cells during chemotherapy and radiation. (45)

Cordyceps has been reported to increase sexual vitality in both men and women and decrease male impotence. This may be due to an increase in sex hormones, or by directly acting on the sexual center of the brain and sex organs in parallel with the hypothalamo-pituitary-adrenocortical axis. (46) It may also reverse drug-induced impotence. (47)

Dandelion Leaf

Dandelion has historically been used as a food and medicinal agent. The leaf contains a high content of vitamins and minerals, including: vitamin A (14,000 IU/100gm fresh leaf) and potassium (297mg/100gm dried leaf). (48) , (49) Dandelion leaf is reported to posses diuretic properties, and has potassium sparing qualities. (50) There have not been human clinical studies to support these uses, but many years of positive use by physicians around the world warrant further research. In experiments on laboratory animals, a fluidextract (1:1w/v) of dandelion leaf (corresponding to 8gm of dried leaf/kg body weight) was reported to posses diuretic activity comparable to that of furosemide (80mg/kg body weight). (51) A most promising point of this study was that the usual potassium loss seen in many conventional diuretics was not seen in dandelion’s use, due to the high potassium content in the leaves.

Acupuncture & Acupressure

In treating chronic cardiac insufficiency, Shi, et al. became aware that some patients complained about spasm and pain in the toes after being treated with digitalis. Calcium was not a viable remedy for these patients as it would enhance the related toxicity of digitalis. Therefore, they used acupuncture as an alternative. In their acupuncture treatment, the acupoints Taichong (Liv 3), Sanyinjiao (Sp 6), and Hegu (LI 4) were treated by the reinforcing method. The results: 29 cases were significantly improved after one session, 2 cases were significantly improved after two sessions, and one case was significantly improved after three sessions; the total effective rate was 100%. (52)

Hu treated 15 cases of acute left heart failure by needling the acupoints Lieque (Lu 7) and Neiguan (P 6). The results: all clinical symptoms disappeared; 14 cases had their heart rate decreased by 20 beats/minute, and the remaining one case had the heart rate decreased by 10 beats/minute. (53)

Traditional Chinese Medicine

Congestive Heart Failure (CHF)

Extensive information regarding the treatment of this health condition using Traditional Chinese Medicine is available through the link above.

Diet & Lifestyle

    Reduce foods that are high in sodium. Increase intake of fresh fruits and vegetables.

Clinical Lab Assessment

Some of the following laboratory testing can provide information necessary for the diagnosis and treatment of Congestive Heart Failure. In addition, the tests listed may also give insight to functional metabolism and functional nutrient status in the body.

Chemistry Profile (Blood)

The enzymes alanine amino transferase (ALT, SGPT), aspartate aminotransferase (AST, SGOT) and lactate dehydrogenase (LD, LDH), usually components of even basic chemistry profiles, are all useful in assessing cardiac damage. The enzymes are released from cardiac muscle in the event of myocardial injury. Along with creatine kinase (CK), these values can aid in differential diagnosis of various cardiovascular-related pathologies. Such a differential diagnostic approach generally employs a more specific assessment of LD and CK as isoenzyme fractions. Serum creatine kinase activity is not a reliable marker for muscle damage in conditions associated with low extracellular glutathione concentration. (54) Several of these values can be used in a correlative analysis to monitor trends in functional abnormality long before pathology becomes clearly apparent. ALT, AST, and LD irregularities can demonstrate abnormalities other than those from cardiac etiologies.

CoEnzyme Q-10, Vitamin E, and other antioxidants

The significance of oxidant stress in CHF has been established, and antioxidants have been suggested in intervention for CHF. (55) Considerable study has confirmed a useful role for CoQ10 in CHF (56) , (57) , (58) vitamin C, (59) and many studies correlate improved cardiovascular function with vitamin E intake.

Electrolytes, Plasma, Serum, or Urine

These values are monitored, especially when medications are being used. Many diuretics deplete potassium. Antihypertensive medications can produce elevations of uric acid and glucose. Low serum potassium (with or without alkalosis) is indication for further renal function study.


This androgen functions primarily as a reproductive hormone; however, evidence suggests it plays a significant role in bone health through its influence on maintaining a positive balance of potassium of sodium, potassium, calcium, and phosphorus.

Magnesium Level

There is considerable attention in the scientific community to the significance of magnesium in cardiovascular function. (60) , (61) , (62) .

Clinical Notes

Supplementation with magnesium, coenzyme Q10, and carnitine can provide benefits in some patients with improvement in quality of life with very little risk. Hawthorn should also be considered for CHF patients; however, note that ACE inhibitors and digoxin effects may be potentiated.


  1. Colucci WS, Braunwald E. Pathophysiology of congestive heart failure. In Braunwald E, ed. Heart Disease, A Textbook of Cardiovascular medicine. Philadelphia: Saunders; 1997:394-420.
  2. Johnson JA, Parker RB, Geraci SA, Heart Failure In DiPiro JT, et al, eds. Pharmacotherapy, A Pathophysiologic Approach 4th edition. Stamford, Conn: Appleton and Lange; 1999:153-181.
  3. Kradjan WA, Congestive Heart Failure, in Koda-Kimble, et al, eds. Applied therapeutics, the Clinical Use of Drugs, 5th edition. Vancouver, WA: Applied therapeutics; 1992:9-1to9-37.
  4. Braunwald E, Colucci WS, Grossman W. Clinical Aspects of Heart Failure: High output failure; pulmonary edema. In: Braunwald E, ed. Heart Disease, A Textbook of Cardiovascular Medicine. Philadelphia: Saunders; 1997:445-470.
  5. View Abstract: Belardinelli R, Deorgiou D, Scocco V, et al. Low intensity exercise training in patients with chronic heart failure. J AM Coll Cardiol. 1995;26:975-982.
  6. Konstam M, Dracup K, Baker D, et al. Heart Failure: Evaluation and care of patients with left ventricular systolic dysfunction. Clinical Practice Guideline #11. Rockville, MD: Agency for Health Care Policy and Research Publication; #94-0612.
  7. American College of Cardiology. American Heart Association Task force on Practice Guidelines. Guidelines for the evaluation and management of heart failure. Circulation. 1995;92:2764-84.
  8. View Abstract: Doughty RN, Sharpe N. b-adrenergic blocking agents in treatment of congestive heart failure: Mechanisms and clinical results. Annu Rev Med. 1997;48:103-114.
  9. View Abstract: Mortensen SA, et al. Coenzyme Q10: clinical benefits with biochemical correlates suggesting a scientific breakthrough in the management of chronic heart failure. Int J Tissue React. 1990;12(3):155-62.
  10. View Abstract: Morisco C, et al. Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study. Clin Investig. 1993;71(8 Suppl):S134-6.
  11. View Abstract: Siembab L, et al. Current views on the clinical significance of coronary artery spasm. Przegl Lek. 1995;52(8):395-9.
  12. View Abstract: Cohen N, et al. Metabolic and clinical effects of oral magnesium supplementation in furosemide-treated patients with severe congestive heart failure. Clin Cardiol. Jun2000;23(6):433-6.
  13. View Abstract: Bashir Y, et al. Effects of long-term oral magnesium chloride replacement in congestive heart failure secondary to coronary artery disease. Am J Cardiol. Nov1993;72(15):1156-62.
  14. View Abstract: Anand I, et al. Acute and chronic effects of propionyl-L-carnitine on the hemodynamics, exercise capacity, and hormones in patients with congestive heart failure. Cardiovasc Drugs Ther. Jul1998;12(3):291-9.
  15. View Abstract: Kobayashi A, et al. L-carnitine treatment for congestive heart failure--experimental and clinical study. Jpn Circ J. Jan1992;56(1):86-94.
  16. Azuma J. Long-term effect of taurine in congestive heart failure: preliminary report. Heart Failure Research with Taurine Group. Adv Exp Med Biol. 1994;359:425-33.
  17. View Abstract: Azuma J, et al. Usefulness of taurine in chronic congestive heart failure and its prospective application. Jpn Circ J. Jan1992;56(1):95-9.
  18. Chapman RA, et al. Taurine and the Heart. Cardiovascular Research. 1993:27:358-363.
  19. View Abstract: Packer M. Potential role of potassium as a determinant of morbidity and mortality in patients with systemic hypertension and congestive heart failure. Am J Cardiol. Mar1990;65(10):45E-52E.
  20. View Abstract: Lindeman RD. Hypokalemia: Causes, Consequences and Correction. Am J Med Sci. Aug 1976;272(1):5-17.
  21. View Abstract: Petri M, et al. The Metabolic Effects of Thiazide Therapy in the Elderly: A Population Study. Age Ageing. May1986;15(3):151-55.
  22. View Abstract: Tishler M, Armon S. Nifedipine-induced Hypokalemia. Drug Intell Clin Pharm. May 1986;20(5):370-71.
  23. View Abstract: Katz SD, et al. Decreased activity of the L-arginine-nitric oxide metabolic pathway in patients with congestive heart failure. Circulation. Apr1999;99(16):2113-7.
  24. View Abstract: Bednarz B, Jaxa-Chamiec T, Gebalska J, Herbaczynska-Cedro K, Ceremuzynski L. L-arginine supplementation prolongs duration of exercise in congestive heart failure. Kardiol Pol. Apr2004;60(4):348-53.
  25. View Abstract: Koifman B, et al. Improvement of cardiac performance by intravenous infusion of L-arginine in patients with moderate congestive heart failure. J Am Coll Cardiol. Nov1995;26(5):1251-6.
  26. View Abstract: Petkov V. Plants and Hypotensive, Antiatheromatous and Coronarodilatating Action. Am J Chinese Med. 1979;7:197-236.
  27. Racz-Kotilla E, et al. Salidiuretic and Hypotensive Action of Ribes-Leaves. Planta Medica. 1980;29:110-14.
  28. Wagner H, et al. Cardioactive Drugs IV. Cardiotonic Amines from Crataegus oxyacantha. Planta Medica. 1982;45:99-101.
  29. Rewerski W, et al. Some Pharmacological Properties of Flavan Polymers Isolated from Hawthorn. Arzneim-Forsch/Drug Res. 1967;17:490-91.
  30. View Abstract: Taskov M. On the Coronary and Cardiotonic Action of Crataemon. Acta Physiol Pharmacol Bulg. 1977;3(4):53-57.
  31. Petkov E, et al. Inhibitory Effect of Some Flavonoids and Flavonoid Mixtures on Cyclic AMP Phosphodiesterase Activity of Rat Heart. Planta Medica. 1981;43:183-86.
  32. View Abstract: Uchida S, et al. Inhibitory Effects of Condensed Tannins on Angiotensin Converting Enzyme. Jap J Pharmacol. 1987;43(2): 242-46.
  33. View Abstract: Wegrowski J, et al. The Effect of Procyanidolic Oligomers on the Composition of Normal and Hypercholesterolemic Rabbit Aortas. Biochem Pharm. 1984;33:3491-97.
  34. Sun YH. Cordyceps sinensis and Cultured Mycelia. Chung Yao Tung Pao. Dec1985;10(12):3-5.
  35. Bao TT, et al. Pharmacological actions of Cordyceps sinensis. Chung Hsi I Chieh Ho Tsa Chih. Jun1988;8(6):352-54.
  36. Chen YP. Studies on Immunological Actions of Cordyceps sinensis. I. Effect on Cellular Immunity. Chung Yao Tung Pao. Sep1983;8(5):33-35.
  37. View Abstract: Lei J, et al. Pharmacological Study on Cordyceps sinensis (Berk.) Sacc. and ze-e Cordyceps. Chung Kuo Chung Yao Tsa Chih. Jun1992;17(6):364-66.
  38. View Abstract: Zhou DH, et al. Effect of Jinshuibao Capsule on the Immunological Function of 36 Patients with Advanced Cancer. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih. Aug1995;15(8):476-78.
  39. View Abstract: Chen YJ, et al. Effect of Cordyceps sinensis on the Proliferation and Differentiation of Human Leukemic U937 Cells. Life Sci. 1997;60(25):2349-59.
  40. View Abstract: Yoshida J, et al. Antitumor Activity of an Extract of Cordyceps sinensis (Berk.) Sacc. against Murine Tumor Cell Lines. Jpn J Exp Med. Aug1989;59(4):157-61.
  41. View Abstract: Bao ZD, et al. Amelioration of Aminoglycoside Nephrotoxicity by Cordyceps sinensis in Old Patients. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih. May1994;14(5):271-73.
  42. View Abstract: Zhao X, et al. Cordyceps sinensis in Protection of the Kidney from Cyclosporine A Nephrotoxicity. Chung Hua I Hsueh Tsa Chih. Jul1993;73(7):410-12.
  43. View Abstract: Guan YJ, et al. Effect of Cordyceps sinesis on T-lymphocyte Subsets in Chronic Renal Failure. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih. Jun1992;12(6):338-39.
  44. View Abstract: Zhen F, et al. Mechanisms and Therapeutic Effect of Cordyceps sinensis (CS) on Aminoglycoside Induced Acute Renal Failure (ARF) in Rats. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih. May1992;12(5):288-91.
  45. Zhu J, et al. CordyMax Cs-4: A Scientific Product Review. Pharmanex Phytoscience Review Series. 1997.
  46. Zhu J, et al. CordyMax Cs-4: A Scientific Product Review. Pharmanex Phytoscience Review Series. 1997.
  47. Deng X, et al. Clinical study of fermentation product of cordyceps sinensis on thretment of hyposexuality. J Administration Traditional Chinese Med. 1995;5(supp):23-24.
  48. Bradley PR, ed. British Herbal Compendium, vol 1. Bournemouth: British Herbal Medicine Association; 1992:73-74.
  49. Popov AL, et al. Mineral Components of Dandelion Leaves. Vopr Pitan. 1993;3:57-58.
  50. Newall CA, et al. Herbal Medicines: A Guide for Health Care Professionals. London: The Pharmaceutical Press; 1996:96-97.
  51. Racz-Kotilla E, et al. The Action of Taraxacum officinale Extracts On the Body Weight and Diuresis of Laboratory Animals. Planta Med. Nov1974;26(3):212-17.
  52. Shi You Qi, et al. Journal of Acupuncture. 1989;9(5):35.
  53. Hu Yang Wu. Hunan TCM News. 1997;3(2-3):102.
  54. View Abstract: Gunst JJ, Langlois MR, Delanghe JR, De Buyzere ML, Leroux-Roels GG. Serum creatine kinase activity is not a reliable marker for muscle damage in conditions associated with low extracellular glutathione concentration. Clin Chem (United States). May1998;44(5):939-43, 905.
  55. View Abstract: Keith M, Geranmayegan A, Sole MJ, Kurian R, Robinson A, Omran AS, Jeejeebhoy KN. Increased oxidative stress in patients with congestive heart failure. J Am Coll Cardiol. May1998;31(6):1352-6.
  56. View Abstract: Sanbe A, Tanonaka K, Niwano Y, Takeo S. Improvement of cardiac function and myocardial energy metabolism of rats with chronic heart failure by long-term coenzyme Q10 treatment. J Pharmacol Exp Ther. Apr1994;269(1):51-6.
  57. View Abstract: Soja AM, Mortensen SA. Treatment of congestive heart failure with coenzyme Q10 illuminated by meta-analyses of clinical trials. Mol Aspects Med. 1997;18 Suppl:S159-68.
  58. View Abstract: Sinatra ST. Refractory congestive heart failure successfully managed with high dose coenzyme Q10 administration. Mol Aspects Med. 1997;18 Suppl:S299-305.
  59. View Abstract: Hornig B, Arakawa N, Kohler C, Drexler H. Vitamin C improves endothelial function of conduit arteries in patients with chronic heart failure. Circulation. Feb1998;97(4):363-8.
  60. View Abstract: Eisenberg MJ. Magnesium deficiency and sudden death. Am Heart J. 1992;124:544-549.
  61. VII International Symposium On Magnesium. Presented by John Hopkins Department of Cardiology and IntraCellular Diagnostics, Inc. Athens, Greece. 1997.
  62. View Abstract: Haigney MC, Berger R, Schulman S, Gerstenblith G, et al. Tissue Magnesium Levels and the Arrhythmic Substrate in Humans. J Cardiovasc Electrophysiol. Sep1997;8(9):980-6.