Overview and Risk Factors  

Heart failure is the inability of the heart to deliver adequate oxygen to the body's peripheral tissues. Primarily a disease of elderly persons, heart failure affects more than 5 million Americans. It can develop in anyone with a history of hypertension, myocardial infarction (MI), coronary heart disease (CHD), valvular heart disease, or diabetes, among other disorders.

Heart failure may be right-sided or left-sided. Signs and symptoms of right-sided failure include increased jugular venous pressure, pleural effusions, right upper quadrant or abdominal discomfort, hepatomegaly, ascites and/or jaundice, and peripheral edema. Left-sided failure is characterized by dyspnea, orthopnea, and paroxysmal nocturnal dyspnea, attributable to elevated pulmonary pressure with or without pulmonary edema. Acute heart failure often causes prominent dyspnea, diaphoresis, tachycardia, and pale, cold extremities. 

Low-output heart failure is marked by decreased cardiac output, and is most often caused by hypertension, myocardial infarction, or chronic coronary artery disease. High-output heart failure is often caused by anemia or hyperthyroidism.

The most common proximate cause of heart failure is left-ventricular systolic dysfunction, which is marked by reduced myocardial contractility, resulting in low stroke volume. Diastolic dysfunction (myocardial stiffness and impaired relaxation) produces heart failure due to elevated ventricular filling pressure. It is usually due to hypertension and often occurs without associated systolic dysfunction. In some studies, diastolic dysfunction accounts for as many as half of heart failure diagnoses. It is more common in women.

Complications of heart failure include limiting symptoms, syncope, dysrhythmias (which may be lethal), progressive systolic or diastolic dysfunction, thromboembolism (usually strokes), and circulatory collapse.

Risk Factors 

Compared with white Americans, African Americans often experience worse outcomes from heart failure and are at greater risk of death. Other risk factors include:

Age. The likelihood of heart failure and left-ventricular dysfunction increases with age.

History of MI or CHD. Left ventricular dysfunction often results from ischemic injury to the myocardium.

History of cardiomyopathy. Family or personal history of dilated, hypertrophic, or restrictive cardiomyopathy.

History of rheumatic fever or valvular heart disease.

Pericardial disease.

Hypertension. Pulmonary hypertension generally leads to right-sided heart failure, whereas systemic hypertension leads to left-sided heart failure.

Obesity. Hypertension and left ventricular hypertrophy are commonly found in obese patients.

Diabetes. Diabetic cardiomyopathy causes left ventricular dysfunction.

Alcohol abuse. Alcohol toxicity may lead to dilated cardiomyopathy.

Diagnosis

The New York Heart Association classification system¹ describes the functional limitations of heart failure:

Class I: Symptoms (eg, fatigue, dyspnea, and palpitations) are experienced on heavy exertion.

Class II: Symptoms occur with mild-to-moderate levels of exertion.

Class III: Symptoms occur with less-than-ordinary exertion.

Class IV: Symptoms occur at rest.

Diagnostic Tools

2-D and Doppler echocardiogram is the most common imaging modality for assessing cardiac function. Echocardiography can evaluate left and right ventricular systolic function, diastolic function, valvular function, and cardiac chamber sizes. It also identifies possible heart failure etiologies, such as MI, valvular disease, and cardiomyopathies.

Chest x-ray can identify intrinsic pulmonary disease, pulmonary edema, and pleural effusions. It can also estimate the degree of cardiac enlargement, but is much less accurate than echocardiography. 

Electrocardiogram may reveal MI, dysrhythmias, conduction abnormalities, or left ventricular hypertrophy.             

Pulmonary artery catheterization may identify increased pulmonary capillary wedge pressure, decreased cardiac output, and increased systemic vascular resistance in low-output failure. However, this procedure entails some risk and usually adds little to a careful clinical assessment and echocardiogram.
Measurement of circulating concentrations of brain natriuretic peptide (BNP), which is produced by the heart, is increasingly used to assess the degree of heart failure and monitor treatment effects.

Treatment

Treatment of heart failure should target the underlying disorder: hypertension, coronary artery disease, diabetes, etc. See relevant chapters for specific information.

Oral Drugs

Diuretics are the first-line therapy for most heart failure patients, but are less useful (and may be contraindicated) for diastolic heart failure. Loop diuretics (eg, furosemide), thiazides (eg, hydrochlorothiazide), and potassium-sparing diuretics (eg, spironolactone) prevent volume overload and have favorable vascular effects.

Nitrates reduce cardiac preload through venous dilation.

Beta-blockers are a first-line treatment for all categories of heart failure, and are not limited to patients with coronary artery disease or hypertension. Carvedilol, metoprolol succinate, and bisoprolol have all been shown to decrease heart failure mortality.²

Angiotensin-converting enzyme inhibitors (ACEI) (eg, enalapril, lisinopril, ramipril) are also first-line heart failure treatments. They decrease mortality in a broad range of heart failure patients by decreasing afterload. 

Angiotensin II receptor blockers (ARB) (eg, losartan, candesartan, irbesartan) are generally equivalent to ACE inhibitors as first-line heart failure treatments, and they are often used if side effects (usually cough) limit ACEI use. Some patients benefit from combined use of ACEI and ARB, which more completely blocks the effects of angiotensin II.

Aldosterone blockers (eg, spironolactone, eplerenone) have been shown to decrease heart failure mortality when added to usual therapy,^3,4 but may be associated with risk for hyperkalemia.

Calcium channel blockers (eg, verapamil, diltiazem) may be used to treat myocardial ischemia and hypertension, but are not usual therapies for heart failure patients and are contraindicated for patients with significant systolic dysfunction.

Anticoagulants (eg, warfarin) can be used to prevent thromboembolism in heart failure, especially if systolic dysfunction is severe and/or sinus rhythm is absent. Benefit has not been clearly established for patients with less severe heart failure and sinus rhythm.

Digoxin is an oral inotropic agent that provides symptomatic relief in patients with decompensated heart failure, but it has not been shown to decrease mortality. It may be useful for patients who remain symptomatic despite optimal treatment with diuretics, ACEI or ARB, beta-blockers, and aldosterone blockers, especially if atrial fibrillation is present. Digoxin is not useful for diastolic dysfunction. Dosage must be adjusted for older patients or those with renal dysfunction, and in the presence of many drugs that influence digoxin serum levels. The therapeutic window for digoxin is narrow, and its use has become increasingly controversial as newer therapies have emerged.

Intravenous Medications

The following drugs are used for treatment of decompensation:

Nesiritide is administered intravenously for decompensated heart failure, often in an emergency or intensive care setting. Nesiritide has not been shown to improve 1-month or 6-month survival and is very expensive.

Dobutamine is an inotropic and vasoactive agent administered intravenously for symptom relief and systolic function improvement. It requires close monitoring, as it may produce dysrhythmias or abrupt blood pressure changes. It is sometimes used for home infusions after demonstrated acute efficacy, to relieve symptoms and decrease the need for hospitalization.

Phosphodiesterase inhibitors (eg, milrinone) increase contractility by modulating calcium influx into cardiac cells. They also facilitate both arterial and venous dilation, reducing preload and afterload. They are not used for chronic therapy, as this has resulted in increased mortality for heart failure patients.
In general, intravenous therapies for heart failure decompensation are intended to relieve symptoms and facilitate hospital discharge. They are not generally used for prolonging survival beyond the short term.

It is important to note that metformin and thiazolidinediones (eg, rosiglitazone) are contraindicated in patients with diabetes and concomitant heart failure. Thiazolidinediones may exacerbate heart failure by causing pulmonary and peripheral edema. Metformin increases the risk of lactic acidosis.

Surgical Procedures

Implantable cardioverter defibrillator (ICD) use has been shown to decrease mortality from lethal dysrhythmias for high-risk patients, particularly those with documented dysrhythmias and/or severe systolic dysfunction.

Intra-aortic balloon pump (IABP) is used to treat acute heart failure decompensation. IABP assists the heart by decreasing afterload and improving cardiac output. After insertion into the aorta via catheter, the balloon inflates at the beginning of diastole to enhance coronary perfusion. It deflates at the beginning of systole, thereby increasing cardiac output.

Cardiac transplant may be necessary for patients with end-stage heart failure. Left ventricular assist devices (LVAD) are used in extraordinary cases to bridge a severely ill patient to cardiac transplantation.

Other Treatments

Exercise conditioning, which should be approved by a physician and overseen by an exercise physiologist.

Leg elevation above the heart should be done during rest.

Compression stockings may help control leg edema and improve fluid removal. Results are variable, and a therapeutic trial will help determine usefulness for individual heart failure patients.

Prevention and treatment of heart failure also require lifestyle modifications, as described in Nutritional Considerations and Orders below.

Nutritional Considerations

Diet therapy for congestive heart failure chiefly involves restriction of excess sodium and fluid, which can overburden an already reduced ability to handle plasma volume due to weakening of the heart muscle. Because the condition is usually the result of long-term cardiovascular disease, treatment should also include diet therapy for CHD (see Coronary Heart Disease), along with adequate calories to prevent the excessive weight loss that may accompany this condition. The primary nutritional considerations are as follows:

Sodium reduction. A higher intake of dietary sodium is a strong and independent risk factor for heart failure in overweight persons.⁵ In patients with heart failure, sodium restriction is an important part of treatment and may reduce the need for diuretic therapy.⁶ Restriction of sodium to 2000 to 2400 mg per day, along with fluid restriction to 1.5 liters daily, improves functional class and reduces edema.⁷ The most commonly recommended limit is 2000 mg of sodium daily.⁸ Moderation in sodium intake is also important for the control and treatment of hypertension (see Hypertension), which increases risk for heart failure.⁹

Maintaining magnesium adequacy. About 30% of heart failure patients have magnesium deficiency, which can cause a positive sodium balance and negative potassium balance and is associated with a poorer prognosis.10

Thiamine supplements for patients treated with diuretics. Evidence of vitamin B1 deficiency has been found in 57% to 98% of patients treated with diuretics; the risk increases in a dose-related manner.11 Supplementation with high-dose thiamine (200 mg/day) improves both biochemical indicators of deficiency and left ventricular function.12,13

Dietary supplements as adjunctive treatments. A meta-analysis of controlled clinical trials with coenzyme Q10 found significant improvements in stroke volume, cardiac output, cardiac index, and end-diastolic volume in patients with heart failure, regardless of etiology (eg, idiopathic, dilated, ischemia, hypertension, valvular heart disease, and congenital heart disease).14 Amounts typically used range from 150 mg to 300 mg per day as a supplement to conventional treatment.

Other supplements, including L-carnitine, taurine, and the herb crataegus oxycantha L, are under investigation for possible roles in heart failure treatment.15-23 None of these is yet established as safe and effective.

Orders

Diet: Sodium less than 2 grams daily. When heart failure is the result of heart disease, a cardiovascular-specific diet should be ordered (see Coronary Heart Disease).

Fluid restriction as appropriate.

Nutrition consultation to help the patient adjust to the above diet.

Exercise physiologist, physical therapist, and occupational therapist consultations to prescribe exercise regimen and provide appropriate support for activities of daily living.

What to Tell the Family

Heart failure is a progressive disease. However, patients may be able to prolong survival, improve chronic symptoms, avoid repeated episodes of decompensation, and decrease the need for hospitalization by following a low-sodium diet, restricting fluids, and taking medications as prescribed. Exercise conditioning is also important, as it can help improve exercise tolerance and oxygen uptake. The family may need to provide physical support as the patient attempts to recondition, and help the patient comply with diet changes.

References

1. Hunt SA, Baker DW, Chin MH, et al. ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). Circulation. 2001;104:2996-3007.

2. Patel M, Gattis W. Which β²-blocker for heart failure? Am Heart J. 2004;147:238.

3. Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Engl J Med. 1999;341:709-717.

4. Pitt B, Remme W, Zannad F. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med. 2003;348:1309-1321.

5. He J, Ogden LG, Bazzano LA, Vupputuri S, Loria C, Whelton PK. Dietary sodium intake and incidence of congestive heart failure in overweight U.S. men and women: first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Arch Intern Med. 2002;162:1619-1624.

6. Futterman LG, Lemberg L. Heart failure: update on treatment and prognosis. Am J Crit Care. 2001;10:285-293.

7. Colin Ramirez E, Castillo Martinez L, Orea Tejeda A, Rebollar Gonzalez V, Narvaez David R, Asensio Lafuente E. Effects of a nutritional intervention on body composition, clinical status, and quality of life in patients with heart failure. Nutrition. 2004;20:890-895.

8. Chavey WE II, Blaum CS, Bleske BE, Harrison RV, Kesterson S, Nicklas JM, and the American Heart Association. Guideline for the management of heart failure caused by systolic dysfunction: part II. Treatment. Am Fam Physician. 2001;64:1045-1054.

9. Haider AW, Larson MG, Franklin SS, Levy D, for the Framingham Heart Study. Systolic blood pressure, diastolic blood pressure, and pulse pressure as predictors of risk for congestive heart failure in the Framingham Heart Study. Ann Intern Med. 2003;138:10-16.

10. Witte KK, Clark AL, Cleland JG. Chronic heart failure and micronutrients. J Am Coll Cardiol. 2001;37:1765-1774.

11. Zenuk C, Healey J, Donnelly J, Vaillancourt R, Almalki Y, Smith S. Thiamine deficiency in congestive heart failure patients receiving long-term furosemide therapy. Can J Clin Pharmacol. 2003;10:184-188.

12. Shimon I, Almog S, Vered Z, et al. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med. 1995;98:485-490.

13. Seligmann H, Halkin H, Rauchfleisch S, et al. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med. 1991;91:151-155.

14. Bhagavan HN, Chopra RK. Potential role of ubiquinone (coenzyme Q10) in pediatric cardiomyopathy. Clin Nutr. 2005;24:331-338.

15. Rizos I. Three-year survival of patients with heart failure caused by dilated cardiomyopathy and L-carnitine administration. Am Heart J. 2000;139 (pt 3):S120-S123.

16. Anand I, Chandrashekhan Y, De Giuli F, 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. 1998;12:291-299.

17. Kobayashi A, Masumura Y, Yamazaki N. L-carnitine treatment for congestive heart failure--experimental and clinical study. Jpn Circ J. 1992;56:86-94.

18. Azuma J, Sawamura A, Awata N. Usefulness of taurine in chronic congestive heart failure and its prospective application. Jpn Circ J. 1992;56:95-99.

19. Azuma J, Sawamura A, Awata N, et al. Therapeutic effect of taurine in congestive heart failure: a double-blind crossover trial. Clin Cardiol. 1985;8:276-282.

20. Azuma J, Hasegawa H, Sawamura A, Awata N, Ogura K, Harada H. Therapy of congestive heart failure with orally administered taurine. Clin Ther. 1983;5:398-408.

21. Pittler MH, Schmidt K, Ernst E. Hawthorn extract for treating chronic heart failure: meta-analysis of randomized trials. Am J Med. 2003;114:665-674.

22. Degenring FH, Suter A, Weber M, Saller R. A randomised double blind placebo controlled clinical trial of a standardised extract of fresh Crataegus berries (Crataegisan) in the treatment of patients with congestive heart failure NYHA II. Phytomedicine. 2003;10:363-369.

23. Tauchert M. Efficacy and safety of crataegus extract WS 1442 in comparison with placebo in patients with chronic stable New York Heart Association class-III heart failure. Am Heart J. 2002;143:910-915.