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Related Concept Videos

Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

4.1K
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...
4.1K
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

1.1K
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...
1.1K
Heart Failure I: Introduction01:27

Heart Failure I: Introduction

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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...
1.0K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

534
Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
534
Heart Failure VI: Adjunct Therapies01:22

Heart Failure VI: Adjunct Therapies

466
Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.
466

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Related Experiment Video

Updated: Feb 26, 2026

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
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Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix

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Cell-Specific Pathways Supporting Persistent Fibrosis in Heart Failure.

Stephen D Farris1, Creighton Don1, Deri Helterline1

  • 1University of Washington, Department of Medicine, Division of Cardiology, Seattle, Washington.

Journal of the American College of Cardiology
|July 15, 2017
PubMed
Summary

Left ventricular assist device (LVAD) therapy unloads the heart but does not improve capillary density or fibrosis in end-stage heart failure (HF). However, LVADs decrease fibroblast collagen expression and alter macrophage signaling, suggesting ongoing inflammation may impede myocardial recovery.

Keywords:
collagenleft ventricular assist devicemyocardial biologyremodelingtranslational studies

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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Isolation and Characterization of Adult Cardiac Fibroblasts and Myofibroblasts
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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Isolation and Characterization of Adult Cardiac Fibroblasts and Myofibroblasts
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Isolation and Characterization of Adult Cardiac Fibroblasts and Myofibroblasts

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Area of Science:

  • Cardiology
  • Biomedical Engineering
  • Translational Medicine

Background:

  • Limited data exist on human myocardium histology and noncardiomyocyte function in end-stage heart failure (HF).
  • Understanding cellular changes post-left ventricular assist device (LVAD) is crucial for identifying recovery mechanisms.

Purpose of the Study:

  • To investigate noncardiomyocyte cellular activity in end-stage HF patients after LVAD-induced cardiac remodeling.
  • To identify mechanisms that may impede myocardial recovery despite LVAD support.

Main Methods:

  • Myocardium samples were collected from patients undergoing LVAD placement and/or heart transplantation.
  • Histological analyses and quantitative reverse transcription polymerase chain reaction (RT-PCR) were performed on isolated mononuclear cells.
  • Echocardiographic and catheterization data were acquired during routine care.

Main Results:

  • LVAD unloading for 8 months did not alter capillary density, cardiac fibrosis, or macrophage density.
  • Fibroblast-specific collagen expression significantly decreased (16.7-fold) post-LVAD.
  • A shift in macrophage signaling away from pro-fibrotic pathways was observed.

Conclusions:

  • Despite effective LVAD unloading, key structural components like capillary density and fibrosis remain unchanged.
  • Decreased fibroblast collagen expression and altered macrophage polarization may be linked to reduced mechanical stretch and inflammation.
  • Persistent myocardial dysfunction in HF may stem from ongoing inflammation and inadequate extracellular matrix remodeling, highlighting targets for future therapies.