Related Experiment Video

Updated: Aug 29, 2026

Methods for the Determination of Rates of Glucose and Fatty Acid Oxidation in the Isolated Working Rat Heart
12:24

Methods for the Determination of Rates of Glucose and Fatty Acid Oxidation in the Isolated Working Rat Heart

Published on: September 28, 2016

Blood ketone bodies in congestive heart failure

J Lommi1, M Kupari, P Koskinen

  • 1Division of Cardiology (Department of Medicine), Helsinki University Central Hospital, Finland.

Journal of the American College of Cardiology
|September 1, 1996
PubMed

Insights

Blood ketone bodies are elevated in congestive heart failure (CHF), correlating with disease severity and neurohormonal changes. This suggests increased free fatty acid mobilization contributes to ketosis in CHF patients.

Area of Science:

  • Cardiology
  • Metabolic Research
  • Biochemistry

Background:

  • Congestive heart failure (CHF) may involve increased fat store consumption and cardiac cachexia.
  • Elevated free fatty acid mobilization in CHF could theoretically increase ketogenesis.
  • The propensity for ketosis in CHF patients remains unestablished.

Purpose of the Study:

  • To determine if blood ketone bodies are elevated in patients with congestive heart failure (CHF).
  • To investigate the relationship between ketonemia and hemodynamic/neurohumoral abnormalities in CHF.

Main Methods:

  • Studied 45 chronic CHF patients and 14 controls, assessing blood ketone bodies, free fatty acids, glucose, and various hormones.
  • Utilized invasive and noninvasive cardiac function assessments.
  • Measurements were taken after an overnight fast.

Main Results:

  • CHF patients exhibited significantly higher blood ketone levels compared to controls (p < 0.05).
  • Ketonemia in CHF correlated with pulmonary artery wedge pressure, left ventricular ejection fraction, right atrial pressure, free fatty acids, glucose, norepinephrine, growth hormone, and interleukin-6.
  • Left ventricular ejection fraction, free fatty acids, and glucose were independent predictors of ketonemia.

Conclusions:

  • Elevated blood ketone bodies in CHF are proportional to cardiac dysfunction and neurohormonal activation.
  • Increased free fatty acid mobilization, driven by neurohormonal stimulation, likely contributes to CHF-related ketosis.
  • Further research is required to elucidate the precise mechanisms and clinical significance of ketosis in CHF.
Abstract

More Related Videos

Integration of Brain Tissue Saturation Monitoring in Cardiopulmonary Exercise Testing in Patients with Heart Failure04:20

Integration of Brain Tissue Saturation Monitoring in Cardiopulmonary Exercise Testing in Patients with Heart Failure

Published on: October 1, 2019

Cutoff Value of Phase Angle by Bioelectrical Impedance Analysis at Admission as a Prognostic Factor in Patients with Acute Heart Failure05:16

Cutoff Value of Phase Angle by Bioelectrical Impedance Analysis at Admission as a Prognostic Factor in Patients with Acute Heart Failure

Published on: June 10, 2025

Related Concept Videos

Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
Imbalances in Cardiac Output01:26

Imbalances in Cardiac Output

The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Heart Failure III: Clinical Manifestations01:26

Heart Failure III: Clinical Manifestations

Heart failure (HF) manifests primarily as dyspnea, fatigue, and fluid retention, resulting in peripheral and pulmonary edema. Symptoms may vary depending on which ventricle is more affected, left or right.Left-Sided Heart FailureAlso known as left ventricular failure, this condition results from the left ventricle's inability to fill or eject sufficient blood into the systemic circulation. It leads to pulmonary congestion, which occurs when the left ventricle fails to eject blood effectively...
Diabetic Ketoacidosis l: Introduction01:25

Diabetic Ketoacidosis l: Introduction

DefinitionDiabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus, characterized by a triad of hyperglycemia (blood glucose >250 mg/dL), ketonemia or ketonuria, and metabolic acidosis (arterial pH <7.30 and serum bicarbonate <18 mEq/L). It results from insulin deficiency combined with elevated levels of counterregulatory hormones—glucagon, catecholamines, cortisol, and growth hormone—leading to increased lipolysis, hepatic ketone production, and...
Diabetic Ketoacidosis ll: Pathophysiology01:22

Diabetic Ketoacidosis ll: Pathophysiology

Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...