Lommi J, Kupari M, Koskinen P, Näveri H, Leinonen H, Pulkki K, Härkönen M
Division of Cardiology (Department of Medicine), Helsinki University Central Hospital, Finland.
J Am Coll Cardiol. 1996 Sep;28(3):665-72. doi: 10.1016/0735-1097(96)00214-8.
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.
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.
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.
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.
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.
本研究旨在评估充血性心力衰竭（CHF）患者血酮体是否升高，以及酮血症是否与CHF的血流动力学和神经体液异常有关。
在CHF中，机体脂肪储备的消耗可能异常增加，导致心源性恶病质的发生。理论上，游离脂肪酸动员增加可能会增强酮体生成，但CHF患者是否易于发生酮症尚不清楚。
45例慢性CHF患者（平均年龄[±标准差]57±13岁）和14例无CHF的对照者（平均年龄53±13岁）在禁食过夜后接受了有创和无创心脏检查，并测定了血酮体（乙酰乙酸加β-羟基丁酸）、循环游离脂肪酸、葡萄糖、乳酸、胰岛素、胰高血糖素、生长激素、皮质醇、去甲肾上腺素、N末端前心钠素、肿瘤坏死因子-α和白细胞介素-6。
与对照者相比，CHF患者血酮体升高（中位数267μmol/升，范围44至952）（对照者中位数150μmol/升，范围31至299，p<0.05）。在整个研究组中，血酮体与肺动脉楔压（r5 = 0.45，p<0.001）、左心室射血分数（r3 = -0.37，p<0.01）、右心房压（r3 = 0.36，p<0.01）以及循环游离脂肪酸浓度（r5 = 0.52，p<0.001）、葡萄糖（r5 = -0.39，p<0.001）、去甲肾上腺素（r3 = 0.45，p<0.001）、生长激素（r5 = 0.30，p<0.05）和白细胞介素-6（r3 = 0.27，p<0.05）有关。多变量分析显示，左心室射血分数、血清游离脂肪酸和血清葡萄糖是酮血症的独立预测因素。
CHF患者血酮体升高，与心脏功能障碍和神经激素激活的严重程度成正比。这可能至少部分归因于对增强的神经激素刺激反应中游离脂肪酸动员增加。需要进一步研究以确定CHF酮症的详细机制和临床意义。
