Wolfram Doehner and Stefan Anker

Summary

In advanced chronic heart failure (CHF), severe tissue wasting (i.e. cachexia) occurs, resulting from an overall anabolic failure and a catabolic / anabolic imbalance. Cardiac cachexia represents a serious complication of CHF associated with major pathophysiological alterations, increased morbidity, and a very poor prognosis. CHF represents a major medical and socio-economic burden of modern society with epidemic growth. As a matter of fact, CHF carries a worse prognosis than most malignant diseases. Despite substantial advances in the medical therapy of CHF, to date no therapeutic option has been developed to attenuate or even reverse the wasting process. The development of cardiac cachexia may follow a pathophysiologic pathway that is common to various other chronic cachectic diseases, such as for example chronic obstructive pulmonary disease (COPD). We will prospectively investigate metabolic pathways in fat and muscle tissue that may be involved in the development of cachexia.  The planned analyses include assessments at the whole body, interstitial fluid, tissue and sub-cellular (mitochondrial) levels.  Our aim is to identify mutual characteristics in metabolic, hormonal, and immune defects as a final common pathway to cachexia of cardiac and other origins.