Afterdepolarization: Difference between revisions

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{{Short description|A phenomenon in cardiac electrophysiology}}
== Afterdepolarization ==
{{Use dmy dates|date=October 2023}}


'''Afterdepolarization''' refers to a phenomenon in cardiac electrophysiology where abnormal depolarizations occur during or after the repolarization phase of the cardiac action potential. These can lead to [[cardiac arrhythmias]] and are classified into early and delayed afterdepolarizations.
[[File:Mechanisms_of_arrhythmia.jpg|thumb|right|Illustration of mechanisms of arrhythmia, including afterdepolarization.]]


==Types==
'''Afterdepolarization''' refers to a phenomenon in cardiac electrophysiology where an abnormal depolarization occurs during or after the repolarization phase of the cardiac action potential. These afterdepolarizations can lead to [[cardiac arrhythmias]] if they reach the threshold potential and trigger additional action potentials.


===Early Afterdepolarizations (EADs)===
== Types of Afterdepolarization ==
Early afterdepolarizations occur during the repolarization phase of the [[cardiac action potential]], specifically during phases 2 or 3. They are often associated with conditions that prolong the [[action potential duration]], such as [[long QT syndrome]]. EADs can lead to [[torsades de pointes]], a type of polymorphic ventricular tachycardia.


===Delayed Afterdepolarizations (DADs)===
Afterdepolarizations are classified into two main types based on their timing relative to the cardiac action potential:
Delayed afterdepolarizations occur after the completion of repolarization, during phase 4 of the cardiac action potential. They are typically associated with increased intracellular [[calcium]] levels and can be triggered by conditions such as [[digitalis toxicity]] or [[catecholaminergic polymorphic ventricular tachycardia]].


==Mechanisms==
=== Early Afterdepolarization (EAD) ===


The mechanisms underlying afterdepolarizations involve complex interactions between ionic currents and intracellular calcium handling.  
Early afterdepolarizations occur during the repolarization phase of the action potential, specifically during phases 2 or 3. They are often associated with conditions that prolong the [[action potential duration]], such as [[long QT syndrome]]. EADs can lead to [[torsades de pointes]], a type of polymorphic ventricular tachycardia.


===Ionic Currents===
=== Delayed Afterdepolarization (DAD) ===
In EADs, the reactivation of [[L-type calcium channels]] or persistent [[sodium channels]] can contribute to the depolarization. In DADs, the spontaneous release of calcium from the [[sarcoplasmic reticulum]] can activate the [[sodium-calcium exchanger]], leading to depolarization.


===Calcium Handling===
Delayed afterdepolarizations occur after the completion of repolarization, during phase 4 of the action potential. They are typically associated with increased intracellular calcium levels and can be triggered by conditions such as [[digitalis toxicity]] or [[catecholaminergic polymorphic ventricular tachycardia]].
Abnormal calcium handling plays a crucial role in both EADs and DADs. In DADs, the overload of calcium in the sarcoplasmic reticulum can lead to spontaneous calcium release, which then triggers depolarization through the sodium-calcium exchanger.


==Clinical Significance==
== Mechanisms ==
Afterdepolarizations are significant because they can lead to [[arrhythmias]], which are abnormal heart rhythms that can be life-threatening. Understanding the mechanisms of afterdepolarizations is important for developing treatments for arrhythmias.
 
The mechanisms underlying afterdepolarizations involve complex interactions between ionic currents and intracellular calcium handling. Key factors include:
 
* '''Calcium Overload:''' Excessive intracellular calcium can lead to spontaneous calcium release from the [[sarcoplasmic reticulum]], triggering DADs.
* '''Ion Channel Dysfunction:''' Abnormalities in ion channels, such as [[sodium channels]] or [[potassium channels]], can contribute to EADs by prolonging the action potential.
* '''Electrophysiological Remodeling:''' Changes in the expression or function of ion channels and transporters can predispose cardiac cells to afterdepolarizations.
 
== Clinical Significance ==
 
Afterdepolarizations are significant because they can initiate [[arrhythmias]] that may lead to [[sudden cardiac death]]. Understanding the mechanisms of afterdepolarizations is crucial for developing therapeutic strategies to prevent and treat arrhythmias.
 
== Related Pages ==


==Related pages==
* [[Cardiac action potential]]
* [[Cardiac action potential]]
* [[Arrhythmia]]
* [[Arrhythmia]]
* [[Long QT syndrome]]
* [[Long QT syndrome]]
* [[Torsades de pointes]]
* [[Torsades de pointes]]
* [[Digitalis]]


==Gallery==
{{Cardiology}}
<gallery>
File:Mechanisms_of_arrhythmia.jpg|Illustration of mechanisms of arrhythmia, including afterdepolarizations.
</gallery>


[[Category:Cardiac electrophysiology]]
[[Category:Cardiac electrophysiology]]
[[Category:Cardiac arrhythmia]]
[[Category:Arrhythmology]]

Latest revision as of 16:25, 16 February 2025

Afterdepolarization[edit]

Illustration of mechanisms of arrhythmia, including afterdepolarization.

Afterdepolarization refers to a phenomenon in cardiac electrophysiology where an abnormal depolarization occurs during or after the repolarization phase of the cardiac action potential. These afterdepolarizations can lead to cardiac arrhythmias if they reach the threshold potential and trigger additional action potentials.

Types of Afterdepolarization[edit]

Afterdepolarizations are classified into two main types based on their timing relative to the cardiac action potential:

Early Afterdepolarization (EAD)[edit]

Early afterdepolarizations occur during the repolarization phase of the action potential, specifically during phases 2 or 3. They are often associated with conditions that prolong the action potential duration, such as long QT syndrome. EADs can lead to torsades de pointes, a type of polymorphic ventricular tachycardia.

Delayed Afterdepolarization (DAD)[edit]

Delayed afterdepolarizations occur after the completion of repolarization, during phase 4 of the action potential. They are typically associated with increased intracellular calcium levels and can be triggered by conditions such as digitalis toxicity or catecholaminergic polymorphic ventricular tachycardia.

Mechanisms[edit]

The mechanisms underlying afterdepolarizations involve complex interactions between ionic currents and intracellular calcium handling. Key factors include:

  • Calcium Overload: Excessive intracellular calcium can lead to spontaneous calcium release from the sarcoplasmic reticulum, triggering DADs.
  • Ion Channel Dysfunction: Abnormalities in ion channels, such as sodium channels or potassium channels, can contribute to EADs by prolonging the action potential.
  • Electrophysiological Remodeling: Changes in the expression or function of ion channels and transporters can predispose cardiac cells to afterdepolarizations.

Clinical Significance[edit]

Afterdepolarizations are significant because they can initiate arrhythmias that may lead to sudden cardiac death. Understanding the mechanisms of afterdepolarizations is crucial for developing therapeutic strategies to prevent and treat arrhythmias.

Related Pages[edit]



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