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Related Concept Videos

Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

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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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Rheumatic Heart Disease I: Introduction01:23

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Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
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Myocarditis I: Introduction01:21

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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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Mechanism of Cardiac Arrhythmias01:28

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Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
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Related Experiment Video

Updated: Nov 19, 2025

Optimization of Transesophageal Atrial Pacing to Assess Atrial Fibrillation Susceptibility in Mice
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Enhanced Cardiomyocyte NLRP3 Inflammasome Signaling Promotes Atrial Fibrillation.

Chunxia Yao1,2,3, Tina Veleva4, Larry Scott1,2,5

  • 1Cardiovascular Research Institute (C.Y., L.S., S.C., P.J., X.P., Y.H.S., S.A.L., X.H.T.W., N.L.), Baylor College of Medicine, Houston, TX.

Circulation
|May 27, 2018
PubMed
Summary

Cardiomyocyte NLRP3 inflammasome activation drives atrial fibrillation (AF) by causing electrical and structural changes. Inhibiting NLRP3 offers a potential new therapy for AF.

Keywords:
AAV9NLRP3 inflammasomeatrial fibrillationelectrical remodeling

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Sterile Pericarditis in Aachener Minipigs As a Model for Atrial Myopathy and Atrial Fibrillation
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Isolation of Atrial Cardiomyocytes from a Rat Model of Metabolic Syndrome-related Heart Failure with Preserved Ejection Fraction
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Area of Science:

  • Cardiology
  • Immunology
  • Molecular Biology

Background:

  • Atrial fibrillation (AF) is linked to increased inflammation.
  • The NLRP3 inflammasome is known to activate immune cells but its role in cardiomyocytes (CMs) in AF is unclear.

Purpose of the Study:

  • To investigate the role of the cardiomyocyte NLRP3 inflammasome in the pathogenesis of atrial fibrillation.
  • To explore NLRP3 inflammasome inhibition as a potential therapeutic strategy for AF.

Main Methods:

  • Assessed NLRP3 inflammasome activation in atrial CMs from AF patients.
  • Created a cardiomyocyte-specific knockin mouse model (CM-KI) with active NLRP3.
  • Utilized in vivo electrophysiology, Ca2+ imaging, and genetic manipulation to study AF mechanisms in mice.

Main Results:

  • NLRP3 inflammasome activity was elevated in atrial CMs of AF patients.
  • CM-KI mice exhibited spontaneous arrhythmias and inducible AF, which MCC950 (NLRP3 inhibitor) attenuated.
  • Mice showed ectopic activity, abnormal Ca2+ handling, shortened refractory periods, and atrial hypertrophy.

Conclusions:

  • Cardiomyocyte NLRP3 inflammasome signaling is a novel factor in AF pathogenesis.
  • Targeting NLRP3 presents a potential therapeutic avenue for treating atrial fibrillation.