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Related Concept Videos

Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

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.
Disturbances in Heart Rhythm01:29

Disturbances in Heart Rhythm

Arrhythmia or dysrhythmia refers to an abnormal heart rhythm caused by a defect in the heart's conduction system. It can cause the heart to beat irregularly, too quickly, or too slowly, leading to symptoms like chest pain, shortness of breath, and fainting. Factors such as stress, caffeine, alcohol, nicotine, cocaine, certain drugs, congenital defects, diseases, and electrolyte abnormalities can trigger arrhythmias.
Arrhythmias are categorized by their speed, rhythm, and origin. A slow heart...
ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias01:25

ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias

Arrhythmia is a condition characterized by an irregular heart rhythm, with ECG changes that differ based on its origin and nature. The types of arrhythmias discussed below include atrial, junctional, and ventricular arrhythmias.Atrial ArrhythmiasPremature Atrial Complexes (PACs): PACs are early atrial beats caused by stress, caffeine, alcohol, electrolyte imbalances, hypoxia, hyperthyroidism, or certain medications (e.g., bronchodilators and decongestants). The ECG shows early P waves with an...
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
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...
ECG Interpretation of Arrhythmias I: Sinus Arrhythmias01:16

ECG Interpretation of Arrhythmias I: Sinus Arrhythmias

Arrhythmias are disturbances in the heart's rhythm that lead to abnormal heartbeats. These irregularities can originate from different parts of the heart and are classified based on their origin and nature.
Types of Arrhythmias
Sinus Node Arrhythmias
Sinus Bradycardia: Originating from the sinoatrial (SA) node, sinus bradycardia involves slower impulses, resulting in a heart rate of less than 60 beats per minute (bpm). Causes include sleep, vagal stimulation, beta-blockers, hypothyroidism, and...

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  3. Liver-to-atria Inflammatory Axis Driving Arrhythmia.
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  3. Liver-to-atria Inflammatory Axis Driving Arrhythmia.

Related Experiment Video

High-Resolution Endocardial and Epicardial Optical Mapping in a Sheep Model of Stretch-Induced Atrial Fibrillation
09:17

High-Resolution Endocardial and Epicardial Optical Mapping in a Sheep Model of Stretch-Induced Atrial Fibrillation

Published on: July 29, 2011

Liver-to-Atria Inflammatory Axis Driving Arrhythmia.

Yue Yuan, Shuyue Wang, Jifei Ding

    Biorxiv : the Preprint Server for Biology
    |June 4, 2026

    View abstract on PubMed

    Summary
    This summary is machine-generated.

    Metabolic dysfunction-associated steatohepatitis (MASH) increases atrial fibrillation (AF) risk via osteopontin, which recruits inflammatory macrophages to the atria. Targeting osteopontin or gasdermin D offers novel therapeutic strategies for liver disease-related AF.

    Related Experiment Videos

    High-Resolution Endocardial and Epicardial Optical Mapping in a Sheep Model of Stretch-Induced Atrial Fibrillation
    09:17

    High-Resolution Endocardial and Epicardial Optical Mapping in a Sheep Model of Stretch-Induced Atrial Fibrillation

    Published on: July 29, 2011

    Area of Science:

    • Cardiology
    • Hepatology
    • Immunology
    • Molecular Biology

    Background:

    • Metabolic dysfunction-associated steatohepatitis (MASH) is an emerging risk factor for cardiometabolic diseases, including atrial fibrillation (AF).
    • The liver, under metabolic stress, releases inflammatory mediators and hepatokines that may influence atrial remodeling and arrhythmogenesis.

    Purpose of the Study:

    • To investigate the association between liver fibrosis indicators and AF risk in a human cohort.
    • To elucidate the mechanisms by which MASH contributes to atrial remodeling and AF susceptibility in a murine model.
    • To identify therapeutic targets for MASH-associated atrial arrhythmogenesis.

    Main Methods:

    • Analysis of the Atherosclerosis Risk in Communities (ARIC) cohort to correlate FIB-4 index with AF incidence.
  • Induction of MASH in mice using a specific diet, followed by electrophysiological studies, echocardiography, and molecular analyses (proteomics, snRNA-seq).
  • Investigation of the role of hepatocyte-derived osteopontin (OPN) and inflammatory macrophages in MASH-induced atrial remodeling.

    • Main Results:

    • Higher FIB-4 indices were associated with increased AF incidence in the ARIC cohort.
    • MASH mice showed enhanced AF susceptibility, atrial enlargement, and fibrosis, linked to OPN-mediated recruitment of TGFBR1+ inflammatory macrophages.
    • These macrophages activated gasdermin D (GSDMD), promoting proarrhythmic atrial remodeling; interventions targeting OPN, CD44, or GSDMD mitigated these effects.

    Conclusions:

    • Hepatokine osteopontin plays a critical role in MASH-induced atrial remodeling and AF by driving inflammatory macrophage activation and recruitment.
    • The OPN-CD44-macrophage-GSDMD axis represents a novel pathway linking liver disease to atrial arrhythmogenesis.
    • Targeting osteopontin or GSDMD offers promising therapeutic strategies for preventing AF in patients with MASH.