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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...
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...
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...
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 Cardiac Performance01:29

Pathophysiology of Cardiac Performance

Typical heart performance is influenced by heart rate, rhythm, myocardial contraction, and metabolism or blood flow. The cardiac muscle exhibits distinct electrophysiological features, including pacemaker activity and calcium channel control, which play a vital role in the heart's response to various drugs. The autonomic nervous system, comprising the sympathetic and parasympathetic branches, regulates heart rate. Sympathetic activation increases heart rate, while parasympathetic activation...
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: Jun 13, 2026

Surgically Induced Cardiac Volume Overload by Aortic Regurgitation in Mouse
08:12

Surgically Induced Cardiac Volume Overload by Aortic Regurgitation in Mouse

Published on: August 30, 2022

Gender differences in cardiac dysfunction and remodeling due to volume overload.

Melissa R Dent1, Paramjit S Tappia, Naranjan S Dhalla

  • 1Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.

Journal of Cardiac Failure
|May 8, 2010
PubMed
Summary

Sex differences in heart failure were studied using an arteriovenous (AV) shunt model. Estrogen protects female rats from cardiac dysfunction and adverse remodeling, highlighting gender-specific responses in heart disease.

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A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
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Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction
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Last Updated: Jun 13, 2026

Surgically Induced Cardiac Volume Overload by Aortic Regurgitation in Mouse
08:12

Surgically Induced Cardiac Volume Overload by Aortic Regurgitation in Mouse

Published on: August 30, 2022

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
07:13

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure

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Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction
09:20

Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction

Published on: February 13, 2021

Area of Science:

  • Cardiovascular Physiology
  • Endocrinology
  • Comparative Medicine

Background:

  • Investigates sex differences in cardiac remodeling and function following arteriovenous (AV) shunt induction.
  • Examines hypertrophied and failing hearts in male and female rats.

Purpose of the Study:

  • To elucidate gender-specific hemodynamic and echocardiographic changes in response to AV shunt.
  • To determine the role of estrogen in mitigating cardiac dysfunction in female rats.

Main Methods:

  • Induction of arteriovenous (AV) shunt in male and female rats.
  • Echocardiographic and hemodynamic assessments at 4 and 16 weeks post-AV shunt.
  • Analysis of ovariectomized females with and without estrogen treatment.

Main Results:

  • Both genders developed cardiac hypertrophy, with greater mass increase in females at 16 weeks.
  • Males exhibited impaired cardiac function (decreased fractional shortening, increased LVEDP) at 4 and 16 weeks.
  • Estrogen treatment in ovariectomized females normalized cardiac function but LVEDP remained elevated.

Conclusions:

  • Gender disparities in cardiac function are linked to differential cardiac remodeling post-AV shunt.
  • Estrogen plays a protective role against cardiac dysfunction and adverse ventricular remodeling in female rats.