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Related Concept Videos

Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

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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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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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Heart Failure Drugs: Inotropic Agents01:26

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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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Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

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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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Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

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Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of...
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Disturbances in Heart Rhythm01:29

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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.
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Hypochlorite-Modified LDL Induces Arrhythmia and Contractile Dysfunction in Cardiomyocytes.

Chintan N Koyani1,2, Susanne Scheruebel3, Ge Jin2,4

  • 1Division of Molecular Biology and Biochemistry, Gottfried Schatz Research Center, Medical University of Graz, 8010 Graz, Austria.

Antioxidants (Basel, Switzerland)
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Summary

Hypochlorous acid-modified low-density lipoprotein (HOCl-LDL) disrupts cardiac ion channels, leading to arrhythmias and impaired contractility. This oxidative damage contributes to cardiovascular disease progression, especially in patients with high myeloperoxidase levels.

Keywords:
MPO-H2O2-Cl- systemaction potentialcalcium transientcardiomyocytescardiovascular diseasehypochlorite/hypochlorous acidion channellow-density lipoproteinredox imbalancescavenger receptor

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Area of Science:

  • Cardiovascular Biology
  • Oxidative Stress
  • Molecular Cardiology

Background:

  • Neutrophil myeloperoxidase (MPO) and hypochlorous acid (HOCl) are implicated in cardiac damage.
  • Cardiomyocytes produce low-density lipoprotein (LDL)-like particles, suggesting potential interactions with oxidized LDL.

Purpose of the Study:

  • To identify the presence and impact of proatherogenic HOCl-modified LDL (HOCl-LDL) in human infarcted myocardium.
  • To investigate the effects of HOCl-LDL on cardiomyocyte electrophysiology, contractility, and underlying molecular mechanisms.

Main Methods:

  • Immunohistochemistry for MPO and HOCl-LDL in human myocardial tissue.
  • Electrophysiological and contractility studies in primary and HL-1 cardiomyocytes.
  • Immunoblotting, qPCR, and gene silencing to explore molecular pathways.

Main Results:

  • HOCl-LDL altered ion channel function (reduced ICa,L, IK1; increased INaL), causing action potential abnormalities and arrhythmias.
  • HOCl-LDL impaired contractility and calcium homeostasis by affecting CaV1.2, RyR2, NCX1, and SERCA2a.
  • LOX-1 signaling mediated increased superoxide and CaMKII oxidation by HOCl-LDL.

Conclusions:

  • HOCl-LDL contributes significantly to cardiac dysfunction and remodeling in infarcted hearts.
  • HOCl-LDL exerts detrimental effects on cardiac electrophysiology and contractility through oxidative stress and altered ion channel function.
  • Targeting CaMKII and INaL may offer therapeutic strategies for HOCl-LDL-induced cardiac damage.