• Weight (kg) [ Time Frame: 18 weeks ] [ Designated as safety issue: No ]
  
• Quality of Life [ Time Frame: 18 weeks ] [ Designated as safety issue: No ]
  

• Lean tissue content, total plus arms and legs separately, as assessed by dual X-ray absorptiometry (DEXA) [ Time Frame: 18 weeks ] [ Designated as safety issue: No ]
  
• Fat tissue content, total plus arms and legs separately, as assessed by dual X-ray absorptiometry (DEXA) [ Time Frame: 18 weeks ] [ Designated as safety issue: No ]
  
• Serum levels of inflammatory markers including tumor necrosis factor, its soluble receptors 1 and 2, and interleukin-6 [ Time Frame: 18 weeks ] [ Designated as safety issue: No ]
  
• Biochemistry markers including cholesterol, low density lipoprotein, high density lipoprotein [ Time Frame: 18 weeks ] [ Designated as safety issue: No ]
  
• Left ventricular ejection fraction as assessed by echocardiography [ Time Frame: 18 weeks ] [ Designated as safety issue: No ]
  
• Exercise testing using spiroergometry [ Time Frame: 18 weeks ] [ Designated as safety issue: No ]
  

Cardiac cachexia has been shown to be powerful independent predictor of mortality in patients with congestive heart failure (CHF). Unlike starvation, cachectic CHF patients present with a decrease of muscles and/or fat tissue. This probably depends, at least in part, on the level of inflammatory activation. Theoretically, it seems clear that nutritional status has to be improved in cardiac cachexia. It has been suggested that inflammatory activation in CHF may be due to endotoxin translocation through the edematous gut wall. Elevated endotoxin levels have been found in patients with acutely decompensated CHF, but these levels normalized with diuretic treatment. This finding may be of utmost importance. From one side it underscores the need for aggressive diuretic treatment to prevent translocation, from another side however, it suggests potential area for enteral treatment. Enteral route of nutrition may be highly beneficial by diminishing bacterial translocation from guts and/or endotoxin transfer, finally resulting in lower inflammatory activation Numerous experimental studies display that enteral feeding reduces bacterial translocation, endotoxin absorption and positively modulates function of local immune tissue.

A search of the literature shows that very little is known about the effectiveness of nutritional support on functional performance in cachectic CHF patients and actually no reports concern the influence of enteral feeding on immune activation of cachectic CHF patients. Recent information of some links existing between leptin, which is increased in CHF, and inflammatory activation in this syndrome speculate on a functional role of leptin in immune activation in CHF. As leptin is one of the most important hormones in the regulation of body energy metabolism, we think it is reasonable to look also into enteral feeding -induced changes of leptin and concomitant fluctuations of plasma cytokines.

During the last 12 months we have been using nutritional support in cachectic patients with CHF as an adjunct to standard therapy. We were surprised by a significant functional improvement that we observed in many instances. As most of these patients were subjected to aggressive multi-drug diuretic therapy as well, it was impossible to appreciate the role of enteral nutrition in this respect. We think, these observations are worth verification in more controlled prospective studies.