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Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

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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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Heart Failure II: Pathophysiology01:29

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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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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...
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Myocarditis I: Introduction01:21

Myocarditis I: Introduction

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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...
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Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

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Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
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Pathophysiology of Cardiac Performance01:29

Pathophysiology of Cardiac Performance

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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...
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NETosis as a Pathogenic Factor for Heart Failure.

Shuang Ling1, Jin-Wen Xu1

  • 1Institute of Interdisciplinary Medical Science, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.

Oxidative Medicine and Cellular Longevity
|March 8, 2021
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Summary
This summary is machine-generated.

Neutrophil extracellular traps (NETs) contribute to heart failure by promoting inflammation and microvascular damage. Targeting NETs, particularly through inhibitors of myeloperoxidase (MPO) and peptidylarginine deiminase 4 (PAD4), shows therapeutic potential for heart failure.

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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Pathophysiology

Background:

  • Heart failure, particularly heart failure with preserved ejection fraction (HFpEF), is linked to chronic inflammation, endothelial dysfunction, and fibrosis.
  • Neutrophil extracellular traps (NETs), typically an immune defense, are implicated in noninfectious diseases, including cardiovascular conditions.
  • The precise role and mechanisms of NETs in heart failure pathogenesis remain largely unexplored.

Purpose of the Study:

  • To review the role of NETs in the initiation and progression of heart failure.
  • To elucidate the mechanisms by which damage-associated molecular patterns (DAMPs) and pattern recognition receptors (PRRs) induce NETosis in heart failure.
  • To explore NETs as a potential therapeutic target for heart failure.

Main Methods:

  • Literature review analyzing markers of heart failure and associated diseases (e.g., mitochondrial DNA, HMGB1, fibronectin EDA, galectin-3).
  • Investigation of PRRs (e.g., TLRs, RAGE, cGAS-STING, CXCR2) in NETosis activation.
  • Discussion of oxidative stress mechanisms, including thiol redox imbalance and MPO-derived HOCl, in NET production and potential coronary microvascular thrombosis.

Main Results:

  • DAMPs and PRRs are implicated in NET formation, contributing to inflammation and microvascular damage in heart failure.
  • Oxidative stress, particularly thiol redox imbalance and MPO activity, promotes NETosis and may trigger thrombosis.
  • Inhibition of myeloperoxidase (MPO) and peptidylarginine deiminase 4 (PAD4) has shown efficacy in related conditions like myocardial infarction and atherosclerosis.

Conclusions:

  • NETosis is a significant factor in heart failure development and progression, involving DAMPs, PRRs, and oxidative stress.
  • Targeting NET formation, specifically via MPO and PAD4 inhibition, represents a promising therapeutic strategy for heart failure.
  • Further research into NETosis mechanisms can unveil novel pathophysiological insights and therapeutic avenues for heart failure.