Shizuo Uno

Arterial ketone body ratio as a prognostic indicator in acute heart failure.

The arterial ketone body ratio (AKBR), an established clinical tool that reflects hepatic mitochondrial oxidation-reduction potential, predicts the outcome of patients with shock and multiple organ failure and the postoperative outcome in patients who have undergone major liver or heart surgery. The purpose of this study was to determine the prognostic significance of AKBR in patients with acute heart failure. The subjects of this study were 52 patients with acute heart failure. The following parameters were analyzed after Cox univariate hazard analysis was performed: AKBR, plasma norepinephrine, left ventricular ejection fraction, cardiac index, pulmonary arterial wedge pressure, sex, age, human atrial natriuretic peptide, endothelin-1, and cholesterol. The follow-up period was 30 weeks with cardiac death as the end point. Stepwise multivariate proportional hazard analysis revealed that AKBR was the most significant predictor of death, followed by norepinephrine and human atrial natriuretic peptide. Curve-fitting analysis revealed that the relationship between log (norepinephrine) and AKBR could best be described by two distinct lines, with their intersection at AKBR = 0.7 and norepinephrine = 418. With these results we conducted Kaplan-Meier analysis for AKBR > or = 0.7 and AKBR <0.7. The survival rate in patients with AKBR > or = 0.7 was 100%, whereas that in patients with AKBR <0.7 was 15% (p < 0.0001, log-rank analysis). These results indicate that AKBR is a novel independent predictor of death in heart failure.

Ketone body ratios of the superior and inferior vena cava and of pulmonary arterial blood compared to that of arterial blood: central venous ketone body ratio as a substitute for the arterial ketone body ratio.

To investigate the ketone body ratio (acetoacetate/3-hydroxybutyrate) of central venous blood compared to that of peripheral arterial blood, the acetoacetate and 3-hydroxybutyrate concentrations in paired peripheral arterial and central venous or pulmonary arterial blood were measured. The ketone body concentrations in superior and inferior vena cava blood were significantly (P < 0.0001) lower than those in peripheral arterial blood, whereas those in pulmonary arterial blood were almost the same as those in peripheral arterial blood. These results indicate that ketone bodies were metabolized in the muscles, which reduced their levels in vena cava blood, but ketone bodies newly produced by the liver were transported to the right side of the heart via the hepatic vein, giving concentrations in pulmonary arterial blood that were almost the same as those in peripheral arterial blood. On the other hand, the correlation coefficients (r2) of the arterial blood ketone body ratio to the ratio of superior and inferior vena cava and pulmonary arterial blood were 0.897, 0.767 and 0.882, respectively. The ratios of central venous ketone body ratio/arterial blood ketone body ratio were 0.89 +/- 0.15 in the superior vena cava, 0.64 +/- 0.18 in the inferior vena cava and 1.01 +/- 0.15 in the pulmonary artery.