Related Experiment Video
Updated: Sep 3, 2025

09:20
Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction
Published on: February 13, 2021
6.6K
Endothelial Dysfunction in Heart Failure With Preserved Ejection Fraction: What are the Experimental Proofs?
Lauriane Cornuault1, Paul Rouault1, Cécile Duplàa1
1Univ. Bordeaux, INSERM, Biology of Cardiovascular Diseases, U1034, Pessac, France.
Frontiers in Physiology
|July 25, 2022
Summary
Heart failure with preserved ejection fraction (HFpEF) is a major unmet need. Endothelial dysfunction, impacting small cardiac vessels, is increasingly recognized as a key factor in HFpEF development and severity.
Area of Science:
- Cardiovascular Medicine
- Pathophysiology
- Medical Research
Background:
- Heart failure with preserved ejection fraction (HFpEF) presents a significant challenge in cardiovascular medicine due to high morbidity and mortality.
- The prevalence of HFpEF is rising with an aging population and increasing comorbidities.
- Current understanding of HFpEF pathophysiology remains incomplete, lacking defined therapeutic targets.
Purpose of the Study:
- To review evidence supporting the causal role of endothelial dysfunction in the pathophysiology of HFpEF.
- To explore the proposed link between cardiovascular risk factors, systemic inflammation, and cardiac microvascular dysfunction in HFpEF.
- To discuss the implications of impaired coronary microvascular function in HFpEF patients.
Main Methods:
- Review of existing literature on HFpEF pathophysiology.
- Analysis of human and experimental models investigating endothelial cells (EC) and coronary microvascular dysfunction.
- Examination of studies correlating microvascular dysfunction with HFpEF severity.
Main Results:
- HFpEF patients exhibit decreased cardiac microvascular density and systemic endothelial dysfunction.
- A lower mean coronary flow reserve is observed in HFpEF patients.
- Impaired coronary microvascular function is associated with the severity of heart failure.
Conclusions:
- Endothelial dysfunction is a critical component in the pathophysiology of HFpEF.
- Cardiac small vessel disease, triggered by systemic inflammation from risk factors, may cause cardiac wall stiffening and diastolic dysfunction.
- Further research into endothelial dysfunction could reveal novel therapeutic targets for HFpEF.
Keywords:
animal modelscardiomyocytesdiastolic dysfunctionendothelial cellsheart failureintercellular crosstalkpathophysiologyMore Related Videos
Related Concept Videos
Pathophysiology of Heart Failure
1.8K
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...
1.8K
Heart Failure II: Pathophysiology
31
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...
31
Heart Failure I: Introduction
46
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...
46

