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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.
12  may keep the [Ca]SR below the threshold for delayed afterdepolarizations and arrhythmia.
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
20                                          How delayed afterdepolarizations are synchronized to overcom
21                                              Delayed afterdepolarizations are thought to be due to sp
22 f Ca(2+) release have been shown to activate delayed afterdepolarizations as well as some cardiac arr
23                   This indicates that during delayed afterdepolarizations, Ca release units (CRUs) in
24                                              Delayed afterdepolarizations could be induced easily and
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
28        Early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs) are voltage oscillat
29                                              Delayed afterdepolarizations (DADs) carried by Na(+)-Ca(
30  acetylcholine (ACh) can elicit Ca2+-induced delayed afterdepolarizations (DADs) in atrial myocytes.
31                         How early (EADs) and delayed afterdepolarizations (DADs) overcome electrotoni
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
34 ytes leading to spontaneous Ca2+ release and delayed afterdepolarizations (DADs).
35 ing to Na(+)/Ca(2+)-exchanger activation and delayed afterdepolarizations (DADs).
36 cient Ca-sensitive inward currents to induce delayed afterdepolarizations (DADs).
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
39  Increasing [Na(+)]i monotonically increased delayed afterdepolarization frequency.
40  subunit gene expression, and an increase in delayed afterdepolarizations from 0/min to 12/min.
41 l recordings demonstrated the development of delayed afterdepolarizations in 69% of the CPVT-hiPSCs-C
42                    The mechanisms leading to delayed afterdepolarizations in AF patients have not bee
43 spontaneous Ca2+ release events that lead to delayed afterdepolarizations in affected patients.
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
46 lemia or hypokalemia in the long term, or by delayed afterdepolarizations in the short term.
47 eshold for AP firing, increased incidence of delayed afterdepolarizations, increased calcium transien
48                             Our data suggest delayed afterdepolarization-induced extrasystolic activi
49 rom RyR2/RyR2(R4496C) mouse hearts generated delayed afterdepolarization-induced triggered activity a
50                                              Delayed afterdepolarization-induced triggered beats that
51 eticulum; (6) greater Pcell vulnerability to delayed afterdepolarizations is attributable to higher s
52                         Mechanically induced delayed afterdepolarization-like events contributed to t
53                             It is clear that delayed afterdepolarization resulting from abnormal acti
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
60 lities that lead to focal ectopic firing via delayed afterdepolarizations/triggered activity.
61        Action-potential (AP) durations after delayed afterdepolarizations were significantly prolonge
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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