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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]]

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{{Short description|A phenomenon in cardiac electrophysiology}}
{{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.

==Types==

===Early Afterdepolarizations (EADs)===
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)===
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==

The mechanisms underlying afterdepolarizations involve complex interactions between ionic currents and intracellular calcium handling.

===Ionic Currents===
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===
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==
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.

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

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

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

Afterdepolarization - Revision history

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