BIOCHEMICAL-ANALYSIS OF MUSCLE BIOPSY IN OVERNIGHT FASTING PATIENTS WITH SEVERE CHRONIC HEART-FAILURE

Citation
C. Opasich et al., BIOCHEMICAL-ANALYSIS OF MUSCLE BIOPSY IN OVERNIGHT FASTING PATIENTS WITH SEVERE CHRONIC HEART-FAILURE, European heart journal, 17(11), 1996, pp. 1686-1693
Citations number
30
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0195668X
Volume
17
Issue
11
Year of publication
1996
Pages
1686 - 1693
Database
ISI
SICI code
0195-668X(1996)17:11<1686:BOMBIO>2.0.ZU;2-Q
Abstract
To better characterize the role of skeletal muscle in chronic heart fa ilure we studied energetic charge, metabolites and enzyme activity in the energy production pathway. We selected 15 males with severe chroni c heart failure (NYHA class III, stable clinical conditions and in nor mal nutritional status) and seven controls. Controls and patients were submitted to biopsy of the vastus lateralis muscle in resting and fas ting conditions. Hormone profiles were also evaluated. Our results sho wed near normal ATP, ADP and AMP concentrations, but there were substa ntially more reductions in glycogen (46 +/- 5 vs 77 +/- 6 mu moles gly cosidic units.g(-1) fresh tissue) and creatine phosphate (5 +/- 1 vs 1 3 +/- 1 mu moles.g(-1) fresh tissue) in patients than in controls. We also found a reduction in glycolytic activity (pyruvate kinase 1009 +/ - 79 vs 1625 +/- 26 nmoles.min(-1).mg protein(-1)), despite normal tri carboxylic acid cycle velocity, an increase in alanine aminotransferas e (964 +/- 79 vs 425 +/- 34 nmoles.min(-1).mg protein(-1)) and in aspa rtate aminotransferase (515 +/- 44 vs 291 +/- 56 nmoles.min(-1).mg pro tein(-1)). An increase was also observed in total NADH cytochrome c re ductase (128 +/- 14 vs 68 +/- 5 nmoles.min(-1).mg protein(-1)), while cytochrome oxidase activity was normal. The cortisol/insulin ratio was slightly elevated (77 +/- 4 vs 32 +/- 12). In conclusion. normonutrit ive patients with severe heart failure show an imbalance in the energy production/utilization ratio. The impairment is probably due both to a decrease in production and an increase in consumption of energy owin g to greater cellular workload and/or a hypercatabolic state.