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1 uppress triggered activity due to delayed or early afterdepolarizations.
2 ntly slow heart rate triggers arrhythmogenic early afterdepolarizations.
3 al prolongation and the induction of plateau early afterdepolarizations.
4 n (APD) and generate triggered activity from early afterdepolarizations.
5 l remodeling and an increased propensity for early afterdepolarizations.
6 propagation), both lead to prolonged APs and early afterdepolarizations.
7 l, loss of giant AnkG results in delayed and early afterdepolarizations.
8 sms prolong the action potential and trigger early afterdepolarizations.
9 els in carbon monoxide-induced proarrhythmic early afterdepolarizations.
10 tubule loss led to altered LTCC function and early afterdepolarizations.
11 ent, which contributed to the development of early afterdepolarizations.
12 (+)-Ca(2+) exchanger activity and triggering early afterdepolarizations.
13 n of the action potential, and occurrence of early afterdepolarizations.
14 ed lability of repolarization and suppressed early afterdepolarizations.
15 n action potentials, calcium transients, and early afterdepolarizations.
16 d INa-L, abbreviated the APD, and suppressed early afterdepolarizations.
17 n potential duration (APD) and contribute to early afterdepolarizations.
18 repolarization and vulnerability to phase 3 early afterdepolarizations.
19 iating the APD and reducing the frequency of early afterdepolarizations.
20 radient of APD and suppresses development of early afterdepolarizations.
21 DCT displayed prolonged repolarization with early afterdepolarizations.
22 olongation and development of arrhythmogenic early afterdepolarizations.
23 l shortening, predisposing the myocardium to early afterdepolarizations.
24 tion, hypokalemia, and quinidine resulted in early afterdepolarizations.
25 phase 2 of the SCS occasionally resulted in early afterdepolarizations.
26 ion (696 9 ms, n=81, P<0.01) and caused more early afterdepolarizations (11.7%) compared with isogeni
28 Ps and of 14.5 mV in abnormal APs exhibiting early afterdepolarizations (72.5% of the emulated APs we
30 ropensity to proarrhythmic incidents such as early afterdepolarization and beat-to-beat alternans.
32 fication of drug-induced arrhythmias such as early afterdepolarizations and delayed afterdepolarizati
33 dine, respectively, compared with negligible early afterdepolarizations and ectopic beats in untreate
34 with published studies using animal models, early afterdepolarizations and ectopic beats were observ
35 he mutation endows DRG neurons with multiple early afterdepolarizations and leads to substantial prol
36 ls exhibited reduced excitability with fewer early afterdepolarizations and narrower action potential
37 ay help to suppress arrhythmias initiated by early afterdepolarizations and premature beats in the ve
39 ties, marked arrhythmogenicity manifested by early afterdepolarizations and triggered arrhythmias, an
40 cular action potential duration, spontaneous early afterdepolarizations, and 2:1 atrioventricular blo
42 c action potential duration and late phase 3 early afterdepolarizations associated with reduced sodiu
43 eft ventricle model, demonstrating that such early afterdepolarizations can propagate and initiate re
46 lated atrial myocytes additionally exhibited early afterdepolarizations during hypokalemia, associate
47 SN treatment also lowered the incidence of early afterdepolarizations during isoproterenol; an effe
49 ially proarrhythmic effect, ie, by promoting early afterdepolarization (EAD) or delayed afterdepolari
50 ) pyramidal neurons in brain slices revealed early afterdepolarization (EAD)-like AP waveforms in CA1
51 f SHR hearts showed that VT was initiated by early afterdepolarization (EAD)-mediated triggered activ
54 d with sudden cardiac death likely caused by early afterdepolarizations (EADs) and polymorphic ventri
55 Ranolazine (5 to 20 micromol/L) suppressed early afterdepolarizations (EADs) and reduced the increa
57 exogenous H(2)O(2) has been shown to induce early afterdepolarizations (EADs) and triggered activity
58 bbreviated action potential can give rise to early afterdepolarizations (EADs) and triggered arrhythm
64 ldwide, but it is unclear how arrhythmogenic early afterdepolarizations (EADs) are triggered in faili
67 lar precursor of lethal cardiac arrhythmias, early afterdepolarizations (EADs) during action potentia
70 M cells to the development of arrhythmogenic early afterdepolarizations (EADs) in isolated cells and
71 al duration (APD) prolongation and prominent early afterdepolarizations (EADs) in neonatal cardiomyoc
72 ion potential prolongation, multiple foci of early afterdepolarizations (EADs) result in beat to beat
73 ed even further by small oscillations called early afterdepolarizations (EADs) that can occur either
74 reported both to suppress and to facilitate early afterdepolarizations (EADs) when repolarization re
75 WT mice, and TG cardiomyocytes had frequent early afterdepolarizations (EADs), a hypothesized mechan
76 cell membrane potential oscillations called early afterdepolarizations (EADs), and premature death i
77 action potential duration, Ca(2+) overload, early afterdepolarizations (EADs), and torsade de pointe
79 of intracellular Ca2+ (Ca2+i) in triggering early afterdepolarizations (EADs), the origins of EADs a
80 is a circadian pattern in the occurrence of early afterdepolarizations (EADs), which are abnormal de
81 it abnormal electrical oscillations, such as early afterdepolarizations (EADs), which are associated
91 s in prolongation of APD and an incidence of early afterdepolarization equal to values previously rep
94 ecreased action potential duration, enhanced early afterdepolarization formation, and facilitated tri
95 es, or more generally to suppress delayed or early afterdepolarizations from any cause by overexpress
99 m current is known to mediate arrhythmogenic early afterdepolarizations in heart, and these were simi
100 on potentials and to a higher probability of early afterdepolarizations in MLP-/- than in control myo
103 is consistent with the greater incidence of early afterdepolarizations induced in this region by dof
104 spose M cells and Purkinje fibers to develop early afterdepolarization-induced extrasystoles, which a
105 These results support the hypothesis that early afterdepolarization-induced triggered activity in
106 , suggesting that they might be initiated by early afterdepolarization-induced triggered activity in
110 ardium at the onset of focal activity showed early afterdepolarization-mediated triggered activity th
111 by spontaneous VF arising from the RV by an early afterdepolarization-mediated triggered activity.
112 12 CKD rats and 2 of 9 normal rats (P<0.05); early afterdepolarization occurred in two CKD rats but n
113 n potential duration and a high incidence of early afterdepolarizations on 1-Hz electric point stimul
115 n showed frequent spontaneous development of early afterdepolarizations that occurred at phase 3 of a
116 rats, leading to increased vulnerability to early afterdepolarization, triggered activity, and ventr
117 oss-of-function increased [Ca2+]i and caused early afterdepolarizations under adrenergic stress, as o
118 At 10(-6) mol/L dofetilide, the incidence of early afterdepolarizations was 28% in DHT-treated and 55
119 de (cycle length=1 second), the incidence of early afterdepolarizations was: female, 67%; ORCH, 56%;