Protein kinetics in stable heart failure patients.

Heart failure (HF) is a slow progressive syndrome characterized by low cardiac output and peripheral metabolic, biochemical, and histological alterations. Protein loss and reduced protein turnover occur with aging, but the consequences of congestive HF (CHF) superimposed on the normal aging response are unknown. This study has two objectives: 1) to determine whether there was a difference between older age-matched controls and those with stable HF (i.e., ischemic pathology) in whole body protein turnover and 2) to determine whether protein metabolism in liver and skeletal muscle protein turnover is impacted by CHF. We measured the whole body protein synthesis rate with a U-N-15-labeled algal protein hydrolysate in 10 patients with CHF and in 10 age-matched controls. Muscle fractional synthesis rate of lateral vastus muscle was determined with [U-C-13]alanine on muscle biopsies obtained by a standard percutaneous needle biopsy technique. Fractional synthesis rates of five plasma proteins of hepatic origin (fibrinogen, complement C-3, ceruloplasmin, transferrin, and very low-density lipoprotein apoliprotein B-100) were determined by using H-2(5)-labeled L-phenylalanine as tracer. Results showed that whole body protein synthesis rate was reduced in CHF patients (3.09+/-0.19 vs. 2.25+/-0.71 g protein.kg(-1).day(-1), P<0.05) as was muscle fractional synthesis rate (3.02&PLUSMN;0.58 vs. 1.33&PLUSMN;0.71%/day, P<0.05) and very low-density lipoprotein apoliprotein B-100 (265+/-25 vs. 197 160%/day, P<0.05). CHF patients were hyperinsulinemic (9.6&PLUSMN;3.1 vs. 47.0&PLUSMN;7.8 μU/ml, P<0.01). The results were compared with those found with bed rest patients. In conclusion, protein turnover is depressed in CHF patients, and both skeletal muscle and liver are impacted. These results are similar to those found with bed rest, which suggests that inactivity is a factor in depressed protein metabolism.