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1 beats, leading to the formation of early and delayed afterdepolarizations.
2 nolazine reduced the occurrence of early and delayed afterdepolarizations.
3 hmias such as early afterdepolarizations and delayed afterdepolarizations.
4 nternal Ca(2+) stores in the pathogenesis of delayed afterdepolarizations.
5 initiate by nonreentrant mechanisms such as delayed afterdepolarizations.
6 a significant increase in the occurrence of delayed afterdepolarizations.
7 en probability that resulted in formation of delayed afterdepolarizations.
8 tation of AP duration and provoked early and delayed afterdepolarizations.
9 predisposes the myocardium to arrhythmogenic delayed afterdepolarizations.
10 m that may be due to triggered activity from delayed afterdepolarizations.
11 duration, which facilitates the formation of delayed afterdepolarizations.
13 or by using Mg(2+) or flecainide eliminated delayed afterdepolarizations and decreased BVR independe
14 ker RyR2 inhibitor, did not reduce SCaEs and delayed afterdepolarizations and failed to prevent AF.
15 +), induced Na(+)/Ca(2+) exchanger-dependent delayed afterdepolarizations and spontaneous arrhythmias
16 ffectively (1) reduced isoproterenol-induced delayed afterdepolarizations and triggered activity in i
17 rent (IK1), which predisposes HF myocytes to delayed afterdepolarizations and triggered activity.
18 alter action potential duration, and caused delayed afterdepolarizations and triggered beats in inta
19 ard current (for a given SR Ca(2+) release), delayed afterdepolarizations, and nonreentrant initiatio
22 f Ca(2+) release have been shown to activate delayed afterdepolarizations as well as some cardiac arr
25 promoting early afterdepolarization (EAD) or delayed afterdepolarization (DAD) or both, is unknown.
26 ontaneous sarcoplasmic reticulum Ca release, delayed afterdepolarization (DAD), and triggered activit
27 lease (SCR) from the sarcoplasmic reticulum, delayed-afterdepolarizations (DAD), and triggered activi
30 acetylcholine (ACh) can elicit Ca2+-induced delayed afterdepolarizations (DADs) in atrial myocytes.
32 cium (Ca) waves in cardiac myocytes underlie delayed afterdepolarizations (DADs) that trigger cardiac
33 plasmic reticulum (SR) Ca(2+) release causes delayed afterdepolarizations (DADs) via Ca(2+)-induced t
37 fect of ranolazine on late phase 3 early and delayed afterdepolarization (EAD and DAD)-induced trigge
38 ation of cardiomyocyte action potentials and delayed afterdepolarizations, factors that increase risk
41 l recordings demonstrated the development of delayed afterdepolarizations in 69% of the CPVT-hiPSCs-C
44 reduced frequency and amplitude of SCaEs and delayed afterdepolarizations in atrial myocytes and inta
45 s risk of AF by promoting regional SCaEs and delayed afterdepolarizations in atrial tissue, which can
47 eshold for AP firing, increased incidence of delayed afterdepolarizations, increased calcium transien
49 rom RyR2/RyR2(R4496C) mouse hearts generated delayed afterdepolarization-induced triggered activity a
51 eticulum; (6) greater Pcell vulnerability to delayed afterdepolarizations is attributable to higher s
54 he presence of beta stimulation, we observed delayed afterdepolarizations, suggesting that accelerate
55 e likely to contribute to the arrhythmogenic delayed afterdepolarizations that occur in Ca2+-overload
56 he Na(+)/Ca(2+) exchange current inducing a "delayed afterdepolarization" that can in turn trigger an
57 current-clamp and Ca(2+) imaging, early and delayed afterdepolarizations trailed spontaneous Ca(2+)
58 ge coupling gain, causes AF-promoting atrial delayed afterdepolarizations/triggered activity in cAF p
59 ts accompanied by inward I(NCX) currents and delayed afterdepolarizations/triggered activity occurred
62 nity of the RyR increased the probability of delayed afterdepolarizations when heart failure was simu
63 Ca2+]i and membrane potential, with signs of delayed afterdepolarizations when undergoing periodic pa
64 eshold spontaneous Ca elevations (SCaEs) and delayed afterdepolarizations whenever the pacing train f
65 C overexpression, where high [Na(+)]i causes delayed afterdepolarizations, which can be prevented by
66 d that the elevated [Na(+)]i of PCs promoted delayed afterdepolarizations, which were always preceded
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