Cardiac Cachexia*

A Syndrome With Impaired Survival and Immune and Neuroendocrine Activation

  1. Stefan D. Anker, MD, PhD and
  2. Andrew J. S. Coats, DM
  1. *From the Department of Cardiac Medicine (Dr. Anker and Mr. Coats), National Heart & Lung Institute, London, UK; and the Franz-Volhard-Klinik am Max Delbrück Centrum (Dr. Anker), Charité, Campus Berlin-Buch, Berlin, Germany.

Abstract

Chronic heart failure (CHF) is a complex syndrome affecting many body systems. Body wasting (ie, cardiac cachexia) is a serious complication of CHF long known but little investigated. Although no specific diagnostic criteria have been established, we have suggested that cardiac cachexia be defined on the basis of the presence of documented nonintentional and nonedematous weight loss > 7.5% of the premorbid normal weight, occurring over a time period of > 6 months. Using this definition, 16% of an unselected CHF outpatient population was found to be cachectic. The cachectic state is predictive of impaired prognosis independently of age, functional disease classification, left ventricular ejection fraction, and peak oxygen consumption. The mortality in the cachectic cohort is 50% at 18 months. Analyzing body composition in detail, it has been found that patients with cardiac cachexia suffer from a general loss of fat tissue (ie, energy reserves), lean tissue (ie, skeletal muscle), and bone tissue (ie, osteoporosis). Cachectic CHF patients are weaker and fatigue earlier, which is due to both reduced skeletal muscle mass and impaired muscle quality. The pathophysiologic alterations leading to cardiac cachexia remain unclear, but initial cross-sectional studies have suggested that humoral neuroendocrine and immunologic abnormalities are linked, independently of established heart failure severity markers, to the presence of body wasting. Comparing the features of cachectic and noncachectic CHF patients with those of healthy control subjects, it is mainly the cachectic CHF patients who show raised plasma levels of epinephrine, norepinephrine, and cortisol; the highest plasma renin activity and aldosterone plasma concentrations; and the lowest plasma sodium level. Several studies have shown that cardiac cachexia is linked to raised plasma levels of tumor necrosis factor-α. The degree of body wasting is strongly correlated with neurohormonal and immune abnormalities. The available evidence suggests that cardiac cachexia is a multifactorial neuroendocrine and metabolic disorder with a poor prognosis. A complex imbalance of different body systems may cause the development of body wasting.

Abbreviations: ACE = angiotensin-converting enzyme; CHF = chronic heart failure; LVEF = left ventricular ejection fraction; NYHA = New York Heart Association; TNF-α = tumor necrosis factor-α; V̇o2 = oxygen consumption

Footnotes

  • For related material see page 708.

  • Dr. Anker is supported with a postgraduate fellowship of the Max Delbrück Centrum für Melekulare Medizin.

  • Correspondence to: Stefan D. Anker, MD, PhD, Department of Cardiac Medicine, National Heart & Lung Institute London, Dovehouse St, London SW3 6LY, UK; e-mail: s.anker@ic.ac.uk

    • Accepted September 15, 1998.
    • Received September 11, 1998.
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