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Related Concept Videos

Voltage-gated Ion Channels01:26

Voltage-gated Ion Channels

Voltage-gated ion channels are transmembrane proteins that open and close in response to changes in the membrane potential. They are present on the membranes of all electrically excitable cells such as neurons, heart, and muscle cells.
Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several types of...
Voltage-gated Ion Channels01:26

Voltage-gated Ion Channels

Voltage-gated ion channels are transmembrane proteins that open and close in response to changes in the membrane potential. They are present on the membranes of all electrically excitable cells such as neurons, heart, and muscle cells.
Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several types of...
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...
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
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.
Electrophysiology of Normal Cardiac Rhythm01:19

Electrophysiology of Normal Cardiac Rhythm

The normal cardiac rhythm is a synchronized electrical activity that facilitates the regular and coordinated contraction of the heart muscle. This process is essential for efficient blood circulation throughout the body. The fundamental elements involved in establishing and maintaining this rhythm include the unique electrical properties of cardiac muscle cells, the sinoatrial (SA) node's pacemaker function, the specialized conducting system, and the ionic mechanisms underlying each phase of...

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Updated: Jun 27, 2026

Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation
07:15

Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation

Published on: January 16, 2019

Genetic Na+ channelopathies and sinus node dysfunction.

Ming Lei1, Christopher L-H Huang, Yanmin Zhang

  • 1Cardiovascular Group, School of Clinical and Laboratory Sciences, The University of Manchester, Grafton Street, Manchester M13 9NT, UK. ming.lei@manchester.ac.uk

Progress in Biophysics and Molecular Biology
|November 26, 2008
PubMed
Summary
This summary is machine-generated.

Mutations in the SCN5A gene cause cardiac Na+ channelopathies, leading to arrhythmias like sick sinus syndrome (SSS). This review details SCN5A

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Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
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Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

Published on: July 5, 2021

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Genetics

Background:

  • Voltage-gated Na+ channels are crucial for cardiac action potential and rhythm.
  • Mutations in the SCN5A gene lead to cardiac Na+ channelopathies, including various arrhythmias.
  • Sick sinus syndrome (SSS) is a significant manifestation of SCN5A-related channelopathies.

Purpose of the Study:

  • To review the functional roles of cardiac Na+ currents in sino-atrial node pacemaker activity.
  • To explore the genetic basis of Na+ channelopathies and their link to sinus node dysfunction.
  • To summarize recent advancements in understanding SCN5A mutations and SSS.

Main Methods:

  • Literature review of functional studies on cardiac Na+ channels.
  • Analysis of genetic data from SCN5A mutation databases.
  • Synthesis of findings on genotype-phenotype correlations in Na+ channelopathies.

Main Results:

  • Specific Na+ currents play distinct roles in sino-atrial node function.
  • Over 200 SCN5A mutations identified, with at least 20 linked to sinus node dysfunction.
  • Genetic defects in SCN5A are a significant cause of inherited sinus node dysfunction.

Conclusions:

  • Understanding Na+ channel function is key to deciphering pacemaker activity.
  • SCN5A mutations are a major genetic cause of sick sinus syndrome and other arrhythmias.
  • Further research into SCN5A channelopathies can improve diagnosis and treatment of cardiac rhythm disorders.