BLOOD KETONE-BODIES IN CONGESTIVE-HEART-FAILURE

Objectives. The present study was designed to assess whether blood ket one 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 cac hexia. Increased mobilization of free fatty acids could, in theory, au gment ketogenesis, but whether patients with CHF are prone to ketosis remains unknown. Methods. Forty-five patients with chronic CHF (mean a ge [+/-SD] 57 +/- 13 years) and 14 control subjects free of CHF (mean age 53 +/- 13 years) underwent invasive and noninvasive cardiac studie s and determination of blood ketone bodies (acetoacetate plus beta-hyd roxybutyrate), circulating free fatty acids, glucose, lactate, insulin , glucagon, growth hormone, cortisol, norepinephrine, N-terminal proat rial natriuretic peptide, tumor necrosis factor-alpha and interleukin- 6 after an overnight fast. Results. Patients with CHF had elevated blo od ketone bodies (median 267 mu mol/liter, range 44 to 952) compared w ith control subjects (median 150 mu mol/liter, range 31 to 299, p < 0. 05). In the total study group, blood ketone bodies were related to pul monary artery wedge pressure (r(s) = 0.45, p < 0.001), left ventricula r ejection fraction (r(s) = -0.37, p < 0.01), right atrial pressure (r (s) = 0.36, p < 0.01) and circulating concentrations of free fatty aci ds (r(s) = 0.52, p < 0.001), glucose (r(s) = -0.39, p < 0.01), norepin ephrine (r(s) = 0.45, p < 0.001), growth hormone (r(s) = 0.30, p < 0.0 5) and interleukin-6 (r(s) = 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 car diac dysfunction and neurohormonal activation. This may be at least pa rtly attributable to increased free fatty acid mobilization in respons e to augmented neurohormonal stimulation. Additional studies are neede d to identify the detailed mechanisms and clinical implications of CHF ketosis.