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 ?
2+] content, and an increased susceptibility to arrhythmias CPTV CMs Similar to above, but also evidence of early afterdepolarizations (EADs) CPTV CMs Aberrant [Ca.
Early afterdepolarizations (EADs) are triggered before the completion of repolarization [1] and associated with polymorphic ventricular tachyarrhythmia for long QT syndrome patients [2].
sup][15] have found that, in the rabbit models, Wenxin Keli suppressed early afterdepolarizations, delayed afterdepolarizations, and triggered ventricular arrhythmias via selective inhibition of the late I[sub]Na that is proved to contribute to arrhythmogenesis.
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.
This generates early afterdepolarizations and may initiate triggered activity at the end of repolarization.
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.
Divergent proarrhythmic potential of macrolide antibiotics despite similar QT prolongation: fast phase 3 repolarization prevents early afterdepolarizations and torsade de pointes.
It has been shown that ROS prolong action potential duration (APD) in rat and guinea pig myocytes and induce early afterdepolarizations (EADs) and delayed afterdepolarization (DADs) [27].
currents, leading to the development of early afterdepolarizations (EADs) and slow response APs (4) observed in mXin[alpha]-/- myocytes.