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1 els in carbon monoxide-induced proarrhythmic early afterdepolarizations.
2 ent, which contributed to the development of early afterdepolarizations.
3 (+)-Ca(2+) exchanger activity and triggering early afterdepolarizations.
4 n of the action potential, and occurrence of early afterdepolarizations.
5 ed lability of repolarization and suppressed early afterdepolarizations.
6 n action potentials, calcium transients, and early afterdepolarizations.
7 d INa-L, abbreviated the APD, and suppressed early afterdepolarizations.
8 n potential duration (APD) and contribute to early afterdepolarizations.
9 iating the APD and reducing the frequency of early afterdepolarizations.
10 radient of APD and suppresses development of early afterdepolarizations.
11 DCT displayed prolonged repolarization with early afterdepolarizations.
12 olongation and development of arrhythmogenic early afterdepolarizations.
13 l shortening, predisposing the myocardium to early afterdepolarizations.
14 tion, hypokalemia, and quinidine resulted in early afterdepolarizations.
15 phase 2 of the SCS occasionally resulted in early afterdepolarizations.
16 ntly slow heart rate triggers arrhythmogenic early afterdepolarizations.
17 al prolongation and the induction of plateau early afterdepolarizations.
18 tubule loss led to altered LTCC function and early afterdepolarizations.
19 n (APD) and generate triggered activity from early afterdepolarizations.
21 fication of drug-induced arrhythmias such as early afterdepolarizations and delayed afterdepolarizati
22 dine, respectively, compared with negligible early afterdepolarizations and ectopic beats in untreate
23 with published studies using animal models, early afterdepolarizations and ectopic beats were observ
24 ay help to suppress arrhythmias initiated by early afterdepolarizations and premature beats in the ve
26 ties, marked arrhythmogenicity manifested by early afterdepolarizations and triggered arrhythmias, an
27 cular action potential duration, spontaneous early afterdepolarizations, and 2:1 atrioventricular blo
29 eft ventricle model, demonstrating that such early afterdepolarizations can propagate and initiate re
33 ially proarrhythmic effect, ie, by promoting early afterdepolarization (EAD) or delayed afterdepolari
34 ) pyramidal neurons in brain slices revealed early afterdepolarization (EAD)-like AP waveforms in CA1
36 f SHR hearts showed that VT was initiated by early afterdepolarization (EAD)-mediated triggered activ
38 Ranolazine (5 to 20 micromol/L) suppressed early afterdepolarizations (EADs) and reduced the increa
40 exogenous H(2)O(2) has been shown to induce early afterdepolarizations (EADs) and triggered activity
41 bbreviated action potential can give rise to early afterdepolarizations (EADs) and triggered arrhythm
48 lar precursor of lethal cardiac arrhythmias, early afterdepolarizations (EADs) during action potentia
51 M cells to the development of arrhythmogenic early afterdepolarizations (EADs) in isolated cells and
52 al duration (APD) prolongation and prominent early afterdepolarizations (EADs) in neonatal cardiomyoc
53 ion potential prolongation, multiple foci of early afterdepolarizations (EADs) result in beat to beat
54 reported both to suppress and to facilitate early afterdepolarizations (EADs) when repolarization re
55 WT mice, and TG cardiomyocytes had frequent early afterdepolarizations (EADs), a hypothesized mechan
56 cell membrane potential oscillations called early afterdepolarizations (EADs), and premature death i
57 action potential duration, Ca(2+) overload, early afterdepolarizations (EADs), and torsade de pointe
59 of intracellular Ca2+ (Ca2+i) in triggering early afterdepolarizations (EADs), the origins of EADs a
60 it abnormal electrical oscillations, such as early afterdepolarizations (EADs), which are associated
67 s in prolongation of APD and an incidence of early afterdepolarization equal to values previously rep
69 ecreased action potential duration, enhanced early afterdepolarization formation, and facilitated tri
73 m current is known to mediate arrhythmogenic early afterdepolarizations in heart, and these were simi
74 on potentials and to a higher probability of early afterdepolarizations in MLP-/- than in control myo
76 is consistent with the greater incidence of early afterdepolarizations induced in this region by dof
77 spose M cells and Purkinje fibers to develop early afterdepolarization-induced extrasystoles, which a
78 These results support the hypothesis that early afterdepolarization-induced triggered activity in
79 , suggesting that they might be initiated by early afterdepolarization-induced triggered activity in
83 ardium at the onset of focal activity showed early afterdepolarization-mediated triggered activity th
84 by spontaneous VF arising from the RV by an early afterdepolarization-mediated triggered activity.
85 12 CKD rats and 2 of 9 normal rats (P<0.05); early afterdepolarization occurred in two CKD rats but n
86 n potential duration and a high incidence of early afterdepolarizations on 1-Hz electric point stimul
87 rats, leading to increased vulnerability to early afterdepolarization, triggered activity, and ventr
88 oss-of-function increased [Ca2+]i and caused early afterdepolarizations under adrenergic stress, as o
89 At 10(-6) mol/L dofetilide, the incidence of early afterdepolarizations was 28% in DHT-treated and 55
90 de (cycle length=1 second), the incidence of early afterdepolarizations was: female, 67%; ORCH, 56%;
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