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Related Concept Videos

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...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Heart Failure I: Introduction01:27

Heart Failure I: Introduction

Heart failure refers to a clinical syndrome caused by structural or functional cardiac disorders that prevent the heart from pumping an adequate amount of blood to meet the body's metabolic needs. This condition often arises from myocardial infarction or ischemia, leading to decreased cardiac output, reduced tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.Heart failure can result from disruptions in the mechanisms that regulate cardiac output...

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Related Experiment Video

Updated: May 11, 2026

A Surgical Model of Heart Failure with Preserved Ejection Fraction in Tibetan Minipigs
07:09

A Surgical Model of Heart Failure with Preserved Ejection Fraction in Tibetan Minipigs

Published on: February 18, 2022

Galectin-3 in heart failure with preserved ejection fraction.

Rudolf A de Boer1, Frank Edelmann, Alain Cohen-Solal

  • 1University Medical Center Groningen, Department of Cardiology, University of Groningen, Hanzeplein 1, 9700RB, Groningen.

European Journal of Heart Failure
|May 8, 2013
PubMed
Summary

Galectin-3 shows promise as a biomarker and therapeutic target for heart failure with preserved ejection fraction (HFpEF), particularly in managing myocardial fibrosis and related comorbidities. Further research is needed to validate its role in HFpEF diagnosis and treatment.

Keywords:
BiomarkerFibrosisGalectin-3Heart failure

Related Experiment Videos

Last Updated: May 11, 2026

A Surgical Model of Heart Failure with Preserved Ejection Fraction in Tibetan Minipigs
07:09

A Surgical Model of Heart Failure with Preserved Ejection Fraction in Tibetan Minipigs

Published on: February 18, 2022

Area of Science:

  • Cardiology
  • Biomarkers
  • Fibrosis Research

Background:

  • Heart failure with preserved ejection fraction (HFpEF) presents diagnostic and therapeutic challenges.
  • Galectin-3 is implicated in heart failure pathophysiology, including fibrosis and comorbidities like renal disease and diabetes.
  • These HFpEF traits align with known galectin-3 roles, suggesting its importance in this condition.

Purpose of the Study:

  • To review the role of galectin-3 in myocardial fibrosis within heart failure (HF) and HFpEF models.
  • To explore galectin-3 as a potential biomarker and therapeutic target for HFpEF.
  • To discuss galectin-3's clinical relevance in HFpEF development and management.

Main Methods:

  • Review of experimental studies on galectin-3 in HF and HFpEF fibrosis models.
  • Analysis of clinical data linking galectin-3 levels to HFpEF correlates and outcomes.
  • Examination of galectin-3's interaction with aldosterone and aldosterone blockers.

Main Results:

  • Experimental studies indicate galectin-3's role in fibrosis and suggest it as a therapeutic target in HFpEF.
  • Aldosterone's detrimental effects may be mediated by galectin-3, with aldosterone blockers showing greater benefit in high galectin-3 patients.
  • Elevated galectin-3 levels correlate with new-onset HF, mortality, and are associated with established HFpEF.

Conclusions:

  • Galectin-3 may serve as a valuable tool for early detection, phenotyping, and risk stratification in HFpEF.
  • Targeting galectin-3 could be a therapeutic strategy for HFpEF, especially when fibrosis is a key factor.
  • Further research is essential to confirm galectin-3's definitive role in HFpEF management.