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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...
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Mitral Regurgitation I: Introduction

Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...
Imbalances in Cardiac Output01:26

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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.
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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...
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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...
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Related Experiment Video

Updated: May 18, 2026

Magnetic Adjustment of Afterload in Engineered Heart Tissues
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Published on: May 5, 2020

Pressure overload induces early morphological changes in the heart.

Colby A Souders1, Thomas K Borg, Indroneal Banerjee

  • 1Department of Medicine, Cardiovascular Research Institute, Texas A&M Health Science Center, Temple, Texas 76504, USA.

The American Journal of Pathology
|September 8, 2012
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Summary

Early cardiac hypertrophy involves rapid remodeling, with increased collagen and fibroblasts appearing within 7 days after transverse aortic constriction (TAC). Capillary density initially drops but recovers, potentially mediated by pericytes.

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Published on: December 2, 2014

Area of Science:

  • Cardiovascular Biology
  • Cardiac Physiology
  • Pathology

Background:

  • Cardiac hypertrophy, both pathological and physiological, causes significant heart changes.
  • Early physiological hypertrophy's morphological and physiological shifts are understudied.
  • Pathological hypertrophy events are better documented than early physiological changes.

Purpose of the Study:

  • To define acute cardiac remodeling events following transverse aortic constriction (TAC).
  • To track temporal changes in hypertrophy, collagen, capillary density, and cell populations.
  • To understand the rapid morphological and physiological adaptations in the early stages of cardiac hypertrophy.

Main Methods:

  • Induction of cardiac hypertrophy via transverse aortic constriction (TAC) in mice.
  • Assessment of cardiac remodeling using heart weight, myocyte width, and wall thickness.
  • Analysis of collagen deposition (Picrosirius staining), cell populations (immunostaining, flow cytometry), and capillary density.

Main Results:

  • Cardiac hypertrophy was detected by day 2 and peaked by day 7 post-TAC.
  • Increased collagen deposition and fibroblast populations were observed by day 7.
  • Capillary density decreased at day 2 but recovered by day 7, with increased pericytes noted at day 2.
  • Gene expression indicated coordinated responses in growth, extracellular matrix, and angiogenic factors.

Conclusions:

  • Morphological changes in response to cardiovascular injury occur rapidly.
  • Early cardiac hypertrophy involves swift remodeling, including fibroblast proliferation and collagen deposition.
  • Pericytes may play a role in the angiogenic transition during early cardiac hypertrophy.