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Related Concept Videos

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...
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...
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...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
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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Related Experiment Video

Updated: Jul 6, 2026

Cell-based Therapy for Heart Failure in Rat: Double Thoracotomy for Myocardial Infarction and Epicardial Implantation of Cells and Biomatrix
09:11

Cell-based Therapy for Heart Failure in Rat: Double Thoracotomy for Myocardial Infarction and Epicardial Implantation of Cells and Biomatrix

Published on: September 22, 2014

Intracellular devastation in heart failure.

Federica Del Monte1, Roger J Hajjar

  • 1Cardiovascular Research, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215, USA. fdelmont@bidmc.harvard.edu

Heart Failure Reviews
|March 19, 2008
PubMed
Summary
This summary is machine-generated.

End-stage heart failure involves cellular changes like impaired calcium cycling and protein misfolding. Targeting these abnormalities offers potential therapeutic strategies for cardiac dysfunction.

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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

Published on: June 14, 2016

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Last Updated: Jul 6, 2026

Cell-based Therapy for Heart Failure in Rat: Double Thoracotomy for Myocardial Infarction and Epicardial Implantation of Cells and Biomatrix
09:11

Cell-based Therapy for Heart Failure in Rat: Double Thoracotomy for Myocardial Infarction and Epicardial Implantation of Cells and Biomatrix

Published on: September 22, 2014

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
10:21

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix

Published on: June 14, 2016

Area of Science:

  • Cardiology
  • Cellular Biology
  • Biochemistry

Background:

  • End-stage heart failure presents complex cellular abnormalities.
  • These include altered excitation-contraction coupling and signaling pathways.
  • While some changes are adaptive, many are detrimental to cardiac cells.

Purpose of the Study:

  • To review cellular calcium cycling changes in myopathic hearts.
  • To explore therapeutic targeting of these calcium cycling abnormalities.
  • To focus on the role of protein misfolding in cardiac dysfunction.

Main Methods:

  • Literature review of cellular mechanisms in heart failure.
  • Analysis of calcium cycling alterations in cardiac cells.
  • Examination of protein misfolding in myocardial disease.

Main Results:

  • Significant alterations in calcium cycling are observed in heart failure.
  • Protein misfolding contributes to cardiac dysfunction.
  • These cellular changes impact overall cardiac performance.

Conclusions:

  • Targeting aberrant calcium cycling presents a promising therapeutic avenue.
  • Addressing protein misfolding is crucial for managing cardiac dysfunction.
  • Understanding cellular changes is key to developing effective heart failure treatments.