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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...
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...
Structure of Cardiac Muscles01:13

Structure of Cardiac Muscles

Cardiac muscle, or myocardium, is a specialized type of muscle found exclusively in the heart. Its unique structural and functional characteristics enable the heart to perform its vital role of pumping blood throughout the body continuously and rhythmically. The cardiac muscle cells, or cardiomyocytes, possess an endomysium and perimysium but do not have an epimysium.
Compared to skeletal muscles, cardiac muscle cells are small and mostly have a single nucleus. Additionally, they are usually...
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...
Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...

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Analysis of Cardiac Contractile Dysfunction and Ca2+ Transients in Rodent Myocytes
07:32

Analysis of Cardiac Contractile Dysfunction and Ca2+ Transients in Rodent Myocytes

Published on: May 25, 2022

Myocyte changes in heart failure.

Olga V Savinova1, A Martin Gerdes

  • 1Cardiovascular Health Research Center, Sanford Research, University of South Dakota, 2301 East 60th Street North, Sioux Falls, SD 57104, USA.

Heart Failure Clinics
|November 24, 2011
PubMed
Summary
This summary is machine-generated.

Heart failure involves structural remodeling, altering cardiomyocyte shape. Reversing these changes offers a promising therapeutic strategy to improve heart function.

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Area of Science:

  • Cardiology
  • Cell Biology
  • Pathophysiology

Background:

  • Structural remodeling is a key characteristic of heart failure, often preceding symptoms.
  • This remodeling involves changes in cardiomyocyte (heart muscle cell) morphology.
  • Abnormal myocyte growth, such as thickening (concentric hypertrophy) or lengthening (eccentric hypertrophy), alters heart structure.

Purpose of the Study:

  • To review the role of structural remodeling in heart failure.
  • To discuss the reversibility of myocyte morphology changes.
  • To highlight the therapeutic potential of reversing maladaptive cardiomyocyte remodeling.

Main Methods:

  • Review of human and animal studies on cardiac structural remodeling.
  • Analysis of the relationship between myocyte morphology and cardiac function.
  • Examination of the potential for therapeutic interventions targeting cardiomyocyte remodeling.

Main Results:

  • Pathological hypertrophy involves disproportional myocyte growth (thickening or lengthening).
  • These alterations in myocyte shape impact cardiac chamber geometry and wall stress.
  • Evidence suggests that changes in myocyte morphology are reversible.

Conclusions:

  • Reversing maladaptive cardiomyocyte remodeling is a potential therapeutic goal.
  • Such interventions may prevent disease progression or enhance cardiac function in heart failure.
  • Targeting structural remodeling offers a promising avenue for heart failure treatment.