Encyclopedia of Behavioral Medicine

Living Edition
| Editors: Marc Gellman

Congestive Heart Failure

  • William WhangEmail author
Living reference work entry
DOI: https://doi.org/10.1007/978-1-4614-6439-6_1255-2



Congestive heart failure is a condition in which the heart cannot provide enough cardiac output for the metabolic demands of the body. The prevalence of heart failure has been estimated at 2% and is expected to grow due to improved survival of people with cardiac conditions (Mann 2008). The lifetime risk of developing heart failure has been estimated at 20%. Coronary artery disease is the most frequent cause of heart failure (60–75%) (Lloyd-Jones et al. 2002). Etiologies for heart failure aside from coronary artery disease include viral inflammation of the heart, also known as myocarditis; alcohol toxicity; or genetic mutations.

One way to classify heart failure is according to left ventricular ejection fraction, a measure of contractile function. “Systolic heart failure” is defined by the presence of reduced left ventricular ejection fraction, usually <40%. About half of patients with heart failure may still have preserved left ventricular ejection fraction, so-called heart failure with normal ejection fraction (HFNEF) (Maeder and Kaye 2009). This is often thought to be due to impaired left ventricular relaxation, or “diastolic dysfunction,” but can also occur in the setting of other conditions such as anemia or renal dysfunction.

Symptoms of this condition can include shortness of breath, peripheral edema, and fatigue. Worse symptomatology has been associated with greater mortality risk. New York Heart Association class is one way to indicate the symptom severity of someone with heart failure (Mann 2008):
  • Class I – no symptoms and no limitation in ordinary physical activity

  • Class II – slight limitation during ordinary activity

  • Class III – marked limitation in activity due to symptoms, even during less-than-ordinary activity

  • Class IV – symptoms even while at rest, mostly bedbound patients

The prevailing view of pathogenesis of systolic heart failure involves a neurohormonal hypothesis. After an initial insult that results in damage to heart muscle, a number of compensatory systems are activated, mainly involving overactivity of the sympathetic nervous system. Activation of the renin-angiotensin-aldosterone system results in salt and water retention, as well as constriction of peripheral blood vessels. This short-term adaptation leads to detrimental increases in left ventricular size and wall thinning, also referred to as remodeling.

The overall prognosis in patients with heart failure is poor, with 1-year mortality as high as 30–40% without treatment (Mann 2008). Depression has been estimated by a meta-analysis to occur in about 21% of heart failure patients, and its presence is associated with worse cardiovascular outcomes and higher overall mortality (Rutledge et al. 2006).

The hallmark of pharmacologic therapy for heart failure involves treatment with angiotensin-converting enzyme (ACE) inhibitors and beta blockers, which are known to improve long-term mortality. Of note, there is a relative lack of evidence for therapies for treatment of heart failure with normal ejection fraction, although blood pressure control is thought to play an important role in treatment.

Behavioral interventions for heart failure may include cessation of tobacco/alcohol use, reduction in salt intake, and exercise in selected patients. The Heart Failure: A Controlled Trial Investigating Outcomes of Exercise TraiNing (HF-ACTION) trial was performed in 2331 ambulatory patients with heart failure and reduced left ventricular ejection fraction (average 0.25) (O’Connor et al. 2009). The intervention consisted of a group-based, supervised exercise program for 3 months with transition to home exercise. During a median follow-up duration of 30 months, a nonsignificant reduction in the primary endpoint of all-cause mortality or hospitalization was achieved (HR 0.93, 95% CI 0.84–1.02. p = 0.13). Exercise training was also found to be relatively safe in the intervention group.

References and Further Reading

  1. Lloyd-Jones, D. M., Larson, M. G., Leip, E. P., Beiser, A., D’Agostino, R. B., Kannel, W. B., et al. (2002). Lifetime risk for developing congestive heart failure: The Framingham heart study. Circulation, 106(24), 3068–3072.CrossRefGoogle Scholar
  2. Maeder, M. T., & Kaye, D. M. (2009). Heart failure with normal left ventricular ejection fraction. Journal of the American College of Cardiology, 53(11), 905–918.CrossRefGoogle Scholar
  3. Mann, D. L. (2008). Chapter 227: Heart failure and cor pulmonale. In A. S. Fauci, E. Braunwald, D. L. Kasper, S. L. Hauser, D. L. Longo, J. L. Jameson, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (Vol. 17e). New York: McGraw-Hill.Google Scholar
  4. O’Connor, C. M., Whellan, D. J., Lee, K. L., Keteyian, S. J., Cooper, L. S., Ellis, S. J., et al. (2009). Efficacy and safety of exercise training in patients with chronic heart failure: HF-ACTION randomized controlled trial. Journal of the American Medical Association, 301(14), 1439–1450.CrossRefGoogle Scholar
  5. Rutledge, T., Reis, V. A., Linke, S. E., Greenberg, B. H., & Mills, P. J. (2006). Depression in heart failure a meta-analytic review of prevalence, intervention effects, and associations with clinical outcomes. Journal of the American College of Cardiology, 48(8), 1527–1537.CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  1. 1.Division of CardiologyColumbia University Medical CenterNew YorkUSA

Section editors and affiliations

  • Linda C. Baumann
    • 1
  1. 1.School of NursingUniversity of Wisconsin-MadisonMadisonUSA