WordNet

very young; "at an early age"
before the usual time or the time expected; "she graduated early"; "the house was completed ahead of time" (同)ahead of time, too soon
in good time; "he awoke betimes that morning" (同)betimes
belonging to the distant past; "the early inhabitants of Europe"; "former generations"; "in other times" (同)former, other
at or near the beginning of a period of time or course of events or before the usual or expected time; "early morning"; "an early warning"; "early diagnosis"; "an early death"; "took early retirement"; "an early spring"; "early varieties of peas and tomatoes mature before most standard varieties"
being or occurring at an early stage of development; "in an early stage"; "early forms of life"; "early man"; "an early computer"
expected in the near future; "look for an early end to the negotiations"
of an early stage in the development of a language or literature; "the Early Hebrew alphabetical script is that used mainly from the 11th to the 6th centuries B.C."; "Early Modern English is represented in documents printed from 1476 to 1700"
fruiting spike of a cereal plant especially corn (同)spike, capitulum
attention to what is said; "he tried to get her ear"
good hearing; "he had a keen ear"; "a good ear for pitch"
the sense organ for hearing and equilibrium
a British peer ranking below a marquess and above a viscount

PrepTutorEJDIC

(時間・時期が)『早い』,『初期の』 / 昔の / (普通より,予定より)早い / 近い将来の / (時間・時期的に)『早く』 / (予定・ふだんより)早く
〈C〉『耳』 / 《単数形で》『聴覚』,聴力,音感 / 《単数形で》じっと聞くこと,傾聴 / 〈C〉耳の形をした物
(麦・とうもろこしなどの)穂
(英国の)伯爵

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/08/30 14:29:41」(JST)

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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

This article about a medical condition affecting the circulatory system is a stub. You can help Wikipedia by expanding it.

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English Journal

The link between abnormal calcium handling and electrical instability in acquired long QT syndrome - Does calcium precipitate arrhythmic storms?

Němec J1, Kim JJ1, Salama G2.
Progress in biophysics and molecular biology.Prog Biophys Mol Biol.2015 Nov 26. pii: S0079-6107(15)00206-0. doi: 10.1016/j.pbiomolbio.2015.11.003. [Epub ahead of print]
Release of Ca2+ ions from sarcoplasmic reticulum (SR) into myocyte cytoplasm and their binding to troponin C is the final signal form myocardial contraction. Synchronous contraction of ventricular myocytes is necessary for efficient cardiac pumping function. This requires both shuttling of Ca2+ betw
PMID 26631594

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

Forced fusion of human ventricular scar cells with cardiomyocytes suppresses arrhythmogenicity in a co-culture model.

Engels MC1, Askar SF1, Jangsangthong W1, Bingen BO1, Feola I1, Liu J1, Majumder R1, Versteegh MI2, Braun J2, Klautz RJ2, Ypey DL1, De Vries AA1, Pijnappels DA3.
Cardiovascular research.Cardiovasc Res.2015 Sep 1;107(4):601-12. doi: 10.1093/cvr/cvv191. Epub 2015 Jul 3.
AIMS: Fibrosis increases arrhythmogenicity in myocardial tissue by causing structural and functional disruptions in the cardiac syncytium. Forced fusion of fibroblastic cells with adjacent cardiomyocytes may theoretically resolve these disruptions. Therefore, the electrophysiological effects of such
PMID 26142215

Japanese Journal

Dexmedetomidine and Clonidine Inhibit Ventricular Tachyarrhythmias in a Rabbit Model of Acquired Long QT Syndrome

TSUTSUI Kenta,HAYAMI Noriyuki,KUNISHIMA Tomoyuki,SUGIURA Anna,MIKAMO Takashi,KANAMORI Kenta,YAMAGISHI Noboru,YAMAGISHI Satoshi,WATANABE Hidenori,AJIKI Kosuke,MURAKAWA Yuji
Circulation journal : official journal of the Japanese Circulation Society 76(10), 2343-2347, 2012-09-25
… To verify that VTs in this animal model are triggered by early afterdepolarization (EAD), the monophasic action potential on the left ventricular surface was recorded in 28 open-chest rabbits (Study 2). …
NAID 10030874645

Triggered Firing and Atrial Fibrillation in Transgenic Mice With Selective Atrial Fibrosis Induced by Overexpression of TGF-β1

CHOI Eue-Keun,CHANG Po-Cheng,LEE Young-Soo,LIN Shien-Fong,ZHU Wuqiang,MARUYAMA Mitsunori,FISHBEIN Michael C.,CHEN Zhenhui,RUBART-VON DER LOHE Michael,FIELD Loren J.,CHEN Peng-Sheng
Circulation journal : official journal of the Japanese Circulation Society 76(6), 1354-1362, 2012-05-25
… We hypothesized that CTTF underlies the mechanisms of early afterdepolarization (EAD) and spontaneous recurrent atrial fibrillation (AF) in transgenic (Tx) mice with overexpression of transforming growth factor β1 (TGF-β1). …
NAID 10030316001

Focal and Reentrant Mechanisms of Torsades de Pointes : EAD, Reentry, or Chimera?

MURAKAWA Yuji
Journal of arrhythmia 27(1), 28-37, 2011-01-25
… Although clinical and experimental studies suggested that TdP is triggered exclusively by early afterdepolarization, the reentrant mechanism seems to play a certain role in its maintenance. …
NAID 10029598592