afterdepolarization

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afterdepolarization

 [af″ter-de-po″lah-rĭ-za´shun]
an oscillation in membrane potential that is dependent upon a preceding action potential for its initiation, and which upon reaching threshold potential can induce arrhythmias that are said to be “triggered.” Early afterdepolarizations occur during phases 2 and 3 of repolarization; delayed afterdepolarizations follow full repolarization.

afterdepolarization

/af·ter·de·po·lar·iza·tion/ (af″ter-de-po″lar-ĭ-za´shun) a depolarizing afterpotential, frequently one of a series, sometimes occurring in tissues not normally excitable. It may occur before (early a.) or after (delayed a.) full repolarization.

afterdepolarization

[-dēpō′lərizā′shən]
a membrane potential depolarization that follows an action potential. In cardiac muscles, it may be early (during phases 2 and 3 of the action potential) or delayed (during phase 4), and it is thought to cause atrial and ventricular tachycardia, especially in the setting of a long Q-T interval or digitalis poisoning. Also called afterpotential.

afterdepolarization

in myocardial activity a polarization, sufficient to trigger a cardiac cycle, which results from a preceding impulse or series of impulses.
References in periodicals archive ?
a physician researcher and colleagues studied early afterdepolarizations (EADs), an abnormal depolarization during the plateau phase of the heart electrical activity (action potential) that can initiate arrhythmia, and a hallmark of LQTS.
Canine left ventricular hypertrophy predisposes to ventricular tachycardia induction by phase 2 early afterdepolarizations after administration of BAY K 8644.
Distinct patterns of calcium transients during early and delayed afterdepolarizations induced by isoproterenol in ventricular myocytes.
Mechanisms underlying early and delayed afterdepolarizations induced by catecholamines.
Afterdepolarizations as a mechanism for the long QT syndrome: electrophysiologic studies of a case.
Dietary fish oil reduces the occurrence of early afterdepolarizations in pig ventricular myocytes.
On the one hand, prolonged repolarization durations found at the LV apex and adjacent areas under LV overload may provoke early afterdepolarizations.
Therapeutic concentrations of ranolazine (2 uM to 6 uM) suppressed early afterdepolarizations and reduced dispersion, two important predictors of a drug's anti-arrhythmic potential.
currents, leading to the development of early afterdepolarizations (EADs) and slow response APs (4) observed in mXin[alpha]-/- myocytes.
Functional consequences of elimination of i(to,f) and i(to,s): early afterdepolarizations, atrioventricular block, and ventricular arrhythmias in mice lacking Kv1.
ATX-II elicits early afterdepolarizations (EADs) and ventricular tachycardia (VT) in these models by selective activation of the late sodium channel in the heart.
Early afterdepolarizations (EADs) are abnormal delays in the repolarization of the heart, and can initiate ventricular tachycardias (VT) in this model.