ライフサイエンスコーパス: delayed afterdepolarization

1 eration of both spontaneous Ca(2+) waves and delayed afterdepolarizations.

2 duration, which facilitates the formation of delayed afterdepolarizations.

3 beats, leading to the formation of early and delayed afterdepolarizations.

4 nolazine reduced the occurrence of early and delayed afterdepolarizations.

5 hmias such as early afterdepolarizations and delayed afterdepolarizations.

6 nternal Ca(2+) stores in the pathogenesis of delayed afterdepolarizations.

7 t-term variability of AP repolarization, and delayed afterdepolarizations.

8 initiate by nonreentrant mechanisms such as delayed afterdepolarizations.

9 a significant increase in the occurrence of delayed afterdepolarizations.

10 en probability that resulted in formation of delayed afterdepolarizations.

11 tation of AP duration and provoked early and delayed afterdepolarizations.

12 predisposes the myocardium to arrhythmogenic delayed afterdepolarizations.

13 m that may be due to triggered activity from delayed afterdepolarizations.

14 mic membrane potential oscillations as early/delayed afterdepolarizations.

15 diated arrhythmia triggers such as early and delayed afterdepolarizations.

16 showed a greater tendency for calcium-driven delayed afterdepolarizations.

17 se and promotion of arrhythmogenic waves and delayed afterdepolarizations.

18 neous Ca(2+) waves underlying arrhythmogenic delayed afterdepolarizations.

19 or) leading to voltage instabilities through delayed afterdepolarizations.

20 e receptor 2)-mediated store Ca(2+) leak and delayed afterdepolarizations, a known mechanism of Ca(2+

21 may keep the [Ca]SR below the threshold for delayed afterdepolarizations and arrhythmia.

22 or by using Mg(2+) or flecainide eliminated delayed afterdepolarizations and decreased BVR independe

23 ker RyR2 inhibitor, did not reduce SCaEs and delayed afterdepolarizations and failed to prevent AF.

24 r the cardiomyocyte interior and also caused delayed afterdepolarizations and later cardiomyocyte dea

25 +), induced Na(+)/Ca(2+) exchanger-dependent delayed afterdepolarizations and spontaneous arrhythmias

26 spontaneous SR Ca release events, triggering delayed afterdepolarizations and spontaneous beats.

27 ed a significant reduction of arrhythmogenic delayed afterdepolarizations and spontaneous Ca(2+) wave

28 ay modulate the susceptibility threshold for delayed afterdepolarizations and the aftercontraction wa

29 michannel opening furthermore contributed to delayed afterdepolarizations and triggered action potent

30 ffectively (1) reduced isoproterenol-induced delayed afterdepolarizations and triggered activity in i

31 rent (IK1), which predisposes HF myocytes to delayed afterdepolarizations and triggered activity.

32 alter action potential duration, and caused delayed afterdepolarizations and triggered beats in inta

33 ard current (for a given SR Ca(2+) release), delayed afterdepolarizations, and nonreentrant initiatio

34 , and reduced the incidence of Ca(2+) waves, delayed afterdepolarizations, and spontaneous action pot

35 How delayed afterdepolarizations are synchronized to overcom

36 Delayed afterdepolarizations are thought to be due to sp

37 f Ca(2+) release have been shown to activate delayed afterdepolarizations as well as some cardiac arr

38 This indicates that during delayed afterdepolarizations, Ca release units (CRUs) in

39 of stretch-release to trigger suprathreshold delayed afterdepolarizations can be affected by heteroge

40 ration, higher mean diastolic potential, and delayed afterdepolarizations compared with controls.

41 Delayed afterdepolarizations could be induced easily and

42 promoting early afterdepolarization (EAD) or delayed afterdepolarization (DAD) or both, is unknown.

43 ontaneous sarcoplasmic reticulum Ca release, delayed afterdepolarization (DAD), and triggered activit

44 lease (SCR) from the sarcoplasmic reticulum, delayed-afterdepolarizations (DAD), and triggered activi

45 ng infusion of ISO in vivo, the incidence of delayed afterdepolarizations (DADs) and beat-to-beat var

46 al that the peri-infarct zone is a source of delayed afterdepolarizations (DADs) and has a high beat-

47 Early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs) are voltage oscillat

48 Delayed afterdepolarizations (DADs) carried by Na(+)-Ca(

49 acetylcholine (ACh) can elicit Ca2+-induced delayed afterdepolarizations (DADs) in atrial myocytes.

50 How early (EADs) and delayed afterdepolarizations (DADs) overcome electrotoni

51 cium (Ca) waves in cardiac myocytes underlie delayed afterdepolarizations (DADs) that trigger cardiac

52 plasmic reticulum (SR) Ca(2+) release causes delayed afterdepolarizations (DADs) via Ca(2+)-induced t

53 Females were more prone to delayed afterdepolarizations (DADs), whereas males were

54 ytes leading to spontaneous Ca2+ release and delayed afterdepolarizations (DADs).

55 ing to Na(+)/Ca(2+)-exchanger activation and delayed afterdepolarizations (DADs).

56 cient Ca-sensitive inward currents to induce delayed afterdepolarizations (DADs).

57 fect of ranolazine on late phase 3 early and delayed afterdepolarization (EAD and DAD)-induced trigge

58 ation of cardiomyocyte action potentials and delayed afterdepolarizations, factors that increase risk

59 Increasing [Na(+)]i monotonically increased delayed afterdepolarization frequency.

60 subunit gene expression, and an increase in delayed afterdepolarizations from 0/min to 12/min.

61 tial upstroke velocity, greater incidence of delayed afterdepolarizations, greater contraction force,

62 l recordings demonstrated the development of delayed afterdepolarizations in 69% of the CPVT-hiPSCs-C

63 The mechanisms leading to delayed afterdepolarizations in AF patients have not bee

64 spontaneous Ca2+ release events that lead to delayed afterdepolarizations in affected patients.

65 reduced frequency and amplitude of SCaEs and delayed afterdepolarizations in atrial myocytes and inta

66 s risk of AF by promoting regional SCaEs and delayed afterdepolarizations in atrial tissue, which can

67 uration prolongation and depressed early and delayed afterdepolarizations in cardiomyocytes isolated

68 otential duration and induction of early and delayed afterdepolarizations in myocytes superfused with

69 oplasmic reticulum Ca(2+) release events and delayed afterdepolarizations in NPR-B(+/-) atrial myocyt

70 indicated an increased risk of proarrhythmic delayed afterdepolarizations in POAF subjects in respons

71 lemia or hypokalemia in the long term, or by delayed afterdepolarizations in the short term.

72 eshold for AP firing, increased incidence of delayed afterdepolarizations, increased calcium transien

73 Our data suggest delayed afterdepolarization-induced extrasystolic activi

74 rom RyR2/RyR2(R4496C) mouse hearts generated delayed afterdepolarization-induced triggered activity a

75 Delayed afterdepolarization-induced triggered beats that

76 eticulum; (6) greater Pcell vulnerability to delayed afterdepolarizations is attributable to higher s

77 Mechanically induced delayed afterdepolarization-like events contributed to t

78 It is clear that delayed afterdepolarization resulting from abnormal acti

79 he presence of beta stimulation, we observed delayed afterdepolarizations, suggesting that accelerate

80 e likely to contribute to the arrhythmogenic delayed afterdepolarizations that occur in Ca2+-overload

81 he Na(+)/Ca(2+) exchange current inducing a "delayed afterdepolarization" that can in turn trigger an

82 current-clamp and Ca(2+) imaging, early and delayed afterdepolarizations trailed spontaneous Ca(2+)

83 ge coupling gain, causes AF-promoting atrial delayed afterdepolarizations/triggered activity in cAF p

84 ts accompanied by inward I(NCX) currents and delayed afterdepolarizations/triggered activity occurred

85 lities that lead to focal ectopic firing via delayed afterdepolarizations/triggered activity.

86 Action-potential (AP) durations after delayed afterdepolarizations were significantly prolonge

87 nity of the RyR increased the probability of delayed afterdepolarizations when heart failure was simu

88 Ca2+]i and membrane potential, with signs of delayed afterdepolarizations when undergoing periodic pa

89 eshold spontaneous Ca elevations (SCaEs) and delayed afterdepolarizations whenever the pacing train f

90 C overexpression, where high [Na(+)]i causes delayed afterdepolarizations, which can be prevented by

91 d that the elevated [Na(+)]i of PCs promoted delayed afterdepolarizations, which were always preceded