title: Blood ketone bodies in congestive heart failure.
abstract: OBJECTIVE
  The present study was designed to assess whether blood ketone bodies are elevated in congestive heart failure (CHF) and whether ketonemia is related to the hemodynamic and neurohumoral abnormalities of CHF.
  
  
  BACKGROUND
  In CHF, consumption of the body's fat stores may become abnormally high, contributing to the development of cardiac cachexia. Increased mobilization of free fatty acids could, in theory, augment ketogenesis, but whether patients with CHF are prone to ketosis remains unknown.
  
  
  METHODS
  Forty-five patients with chronic CHF (mean age [+/- SD] 57 +/- 13 years) and 14 control subjects free of CHF (mean age 53 +/- 13 years) underwent invasive and noninvasive cardiac studies and determination of blood ketone bodies (acetoacetate plus beta-hydroxybutyrate), circulating free fatty acids, glucose, lactate, insulin, glucagon, growth hormone, cortisol, norepinephrine, N-terminal proatrial natriuretic peptide, tumor necrosis factor-alpha and interleukin-6 after an overnight fast.
  
  
  RESULTS
  Patients with CHF had elevated blood ketone bodies (median 267 mumol/liter, range 44 to 952) compared with control subjects (median 150 mumol/liter, range 31 to 299, p < 0.05). In the total study group, blood ketone bodies were related to pulmonary artery wedge pressure (r5 = 0.45, p < 0.001), left ventricular ejection fraction (r3 = -0.37, p < 0.01), right atrial pressure (r3 = 0.36, p < 0.01) and circulating concentrations of free fatty acids (r5 = 0.52, p < 0.001), glucose (r5 = -0.39, p < 0.001), norepinephrine (r3 = 0.45, p < 0.001), growth hormone (r5 = 0.30, p < 0.05) and interleukin-6 (r3 = 0.27, p < 0.05). In multivariate analysis, left ventricular ejection fraction, serum free fatty acids and serum glucose were independent predictors of ketonemia.
  
  
  CONCLUSIONS
  Blood ketone bodies are elevated in CHF in proportion to the severity of cardiac dysfunction and neurohormonal activation. This may be at least partly attributable to increased free fatty acid mobilization in response to augmented neurohormonal stimulation. Additional studies are needed to identify the detailed mechanisms and clinical implications of CHF ketosis.
authors.affiliation: Division of Cardiology (Department of Medicine), Helsinki University Central Hospital, Finland.
authors.forename: J
authors.initials: J
authors.lastname: Lommi
authors.forename: M
authors.initials: M
authors.lastname: Kupari
authors.forename: P
authors.initials: P
authors.lastname: Koskinen
authors.forename: H
authors.initials: H
authors.lastname: Näveri
authors.forename: H
authors.initials: H
authors.lastname: Leinonen
authors.forename: K
authors.initials: K
authors.lastname: Pulkki
authors.forename: M
authors.initials: M
authors.lastname: Härkönen
mesh_terms: D002153:Calorimetry, Indirect; D016207:Cytokines / Q000097:blood; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000503:physiopathology; D006439:Hemodynamics; D006728:Hormones / Q000097:blood; D006801:Humans; D007657:Ketone Bodies / Q000097:blood*; D008297:Male; D008875:Middle Aged
chemical_list: D016207:Cytokines; D005230:Fatty Acids, Nonesterified; D006728:Hormones; D007657:Ketone Bodies