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Afterdepolarizations are abnormal depolarizations of cardiac myocytes that interrupt phase 2, phase 3, or phase 4 of the cardiac action potential in the electrical conduction system of the heart. Afterdepolarizations may lead to cardiac arrhythmias.

Early afterdepolarizations

Early afterdepolarizations (EADs) occur with abnormal depolarization during phase 2 or phase 3, and are caused by an increase in the frequency of abortive action potentials before normal repolarization is completed. Phase 2 may be interrupted due to augmented opening of calcium channels, while phase 3 interruptions are due to the opening of sodium channels. Early afterdepolarizations can result in torsades de pointes, tachycardia, and other arrhythmias.^[1]

Afterhyperpolarizations can also occur in cortical pyramidal neurons. There, they typically follow an action potential and are mediated by voltage gated sodium or chloride channels. This phenomenon requires potassium channels to close quickly to limit repolarization. It is responsible for the difference between regular spiking and intrinsically bursting pyramidal neurons.^[2]

Delayed afterdepolarizations

Delayed afterdepolarizations (DADs), on the other hand, begin during phase 4 - after repolarization is completed, but before another action potential would normally occur. They are due to elevated cytosolic calcium concentrations, as might be seen with digoxin toxicity.^[3]^[4] The overload of the sarcoplasmic reticulum may cause spontaneous Ca²⁺ release during repolarization, causing the released Ca²⁺ to exit the cell through the 3Na⁺/Ca²⁺-exchanger which results in a net depolarizing current.

References

^ Cranefield, PF: The Conduction of the Cardiac Impulse. New York, Future Publishing Co. 1975
^ Nelson Spruston, "Pyramidal Neurons: dendritic structure and synaptic integration", 2008. Nature Reviews. Neuroscience.
^ Katzung, B: Basic and Clinical Pharmacology (10th ed.), chapter 14: "Agents Used in Cardiac Arrhythmias", The McGraw-Hill Companies, 2007, ISBN 978-0-07-145153-6
^ Lilly, L: "Pathophysiology of Heart Disease", chapter 11: "Mechanisms of Cardiac Arrhthmias", Lippencott, Williams and Wilkens, 2007

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1. QT延長症候群の病態生理 pathophysiology of the long qt syndrome
2. 心室性期外収縮 ventricular premature beats
3. I群抗不整脈薬の主な副作用 major side effects of class i antiarrhythmic drugs
4. 限局性心房性頻拍 focal atrial tachycardia
5. カテコラミン誘発多形性心室頻拍および他のQT間隔正常の多形性心室頻拍 catecholaminergic polymorphic ventricular tachycardia and other polymorphic ventricular tachycardias with a normal qt interval

English Journal

Further insights into blood pressure induced premature beats: Transient depolarizations are associated with fast myocardial deformation upon pressure decline.

Haemers P1, Sutherland G1, Cikes M1, Jakus N1, Holemans P1, Sipido KR1, Willems R1, Claus P2.
Heart rhythm : the official journal of the Heart Rhythm Society.Heart Rhythm.2015 Nov;12(11):2305-15. doi: 10.1016/j.hrthm.2015.06.037. Epub 2015 Jun 30.
BACKGROUND: An acute increase in blood pressure is associated with the occurrence of premature ventricular complexes (PVCs).OBJECTIVE: We aimed to study the timing of these PVCs with respect to afterload-induced changes in myocardial deformation in a controlled, preclinically relevant, novel closed-
PMID 26142299

Suppression of Early and Late Afterdepolarizations by Heterozygous Knockout of the Na+/Ca2+ Exchanger in a Murine Model.

Bögeholz N1, Pauls P2, Bauer BK2, Schulte JS2, Dechering DG2, Frommeyer G2, Kirchhefer U2, Goldhaber JI2, Müller FU2, Eckardt L2, Pott C2.
Circulation. Arrhythmia and electrophysiology.Circ Arrhythm Electrophysiol.2015 Oct;8(5):1210-8. doi: 10.1161/CIRCEP.115.002927. Epub 2015 Sep 3.
BACKGROUND: The Na(+)/Ca(2+) exchanger (NCX) has been implied to cause arrhythmias. To date, information on the role of NCX in arrhythmogenesis derived from models with increased NCX expression, hypertrophy, and heart failure. Furthermore, the exact mechanism by which NCX exerts its potentially proa
PMID 26338832

Delayed afterdepolarizations generate both triggers and a vulnerable substrate promoting reentry in cardiac tissue.

Liu MB1, de Lange E2, Garfinkel A3, Weiss JN4, Qu Z5.
Heart rhythm : the official journal of the Heart Rhythm Society.Heart Rhythm.2015 Oct;12(10):2115-24. doi: 10.1016/j.hrthm.2015.06.019. Epub 2015 Jun 10.
BACKGROUND: Delayed afterdepolarizations (DADs) have been well characterized as arrhythmia triggers, but their role in generating a tissue substrate vulnerable to reentry is not well understood.OBJECTIVE: The purpose of this study was to test the hypothesis that random DADs can self-organize to gene
PMID 26072025

Japanese Journal

特発性心室細動，QT延長症候群と自律神経活動

心電図 36(1), 38-48, 2016
NAID 130005139493

電気的ストームにおける自律神経・イオンチャネルリモデリングの役割

心電図 34(1), 45-52, 2014
NAID 130005090810

心臓イオンチャネルに作用する薬物の効果に関するシステム論的理解

Drug Delivery System 29(5), 397-407, 2014
NAID 130004874239

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