ライフサイエンスコーパス: proarrhythmic

1 llation by 50-V shocks, which were otherwise proarrhythmic.

2 animals, whereas regional d-sotalol was not proarrhythmic.

3 duction block may be both antiarrhythmic and proarrhythmic.

4 on of repolarization, which is thought to be proarrhythmic.

5 herapy for long QT syndrome, but can also be proarrhythmic.

6 r cMSC/SkM1) were neither antiarrhythmic nor proarrhythmic.

7 rug, and under unfortunate conditions may be proarrhythmic.

8 ariability of repolarization (BVR) of APD is proarrhythmic.

9 This suggests that ASA is not proarrhythmic.

10 esentation of cardiac function predictive of proarrhythmic abnormalities in cardiac repolarization.

11 teralized asymmetry in midbrain activity and proarrhythmic abnormalities of cardiac repolarization (a

12 ifferentiation) commonly displayed immature, proarrhythmic action potential properties such as high d

13 more importantly, completely ablated all the proarrhythmic action potential traits, rendering the ele

14 ty and metabolic stability and was devoid of proarrhythmic activity in the rabbit model.

15 Moreover, generation of proarrhythmic activity patterns within cerebral autonomi

16 The S-enantiomers generally had less proarrhythmic activity than the corresponding racemates.

17 No life-threatening proarrhythmic adverse effects were reported.

18 of the heart in situ and determine both the proarrhythmic and antiarrhythmic actions of the drug.

19 Although several macrolide antibiotics are proarrhythmic and associated with an increased risk of s

20 eased SR Ca(2+) leak may contribute to AMT's proarrhythmic and cardiotoxic effects, which may be coun

21 ntiarrhythmic drugs should be avoided due to proarrhythmic and negative inotropic effects that may be

22 ole in altered Ca2+ homeostasis which drives proarrhythmic APD alternans in patients with AF.

23 valve, the superior transseptal incision, is proarrhythmic because of extensive atriotomies.

24 however, the mechanisms responsible for this proarrhythmic behavior are incompletely understood.

25 egulated intracellular calcium handling, and proarrhythmic behavior in isolated Purkinje cells.

26 This proarrhythmic behavior is enhanced by disease-causing mu

27 arization reserve at slow heart rate, but is proarrhythmic by steepening the slope of APDR curve, whi

28 ing that A(1)AR activation subtly mediates a proarrhythmic Ca(2+) entry through TRPC3-encoded ROC by

29 We have previously shown that proarrhythmic Ca(2+) waves during beta-AR stimulation te

30 leak to the critical level that can trigger proarrhythmic Ca(2+) waves.

31 asmic reticulum (SR) as a potential cause of proarrhythmic cellular ectopic (triggered) activity in A

32 rrhythmogenesis in long QT syndrome, whereas proarrhythmic changes in intracellular Ca(2+) handling r

33 Proarrhythmic changes in the heart were quantified from

34 toplasmic loop is a critical nodal point for proarrhythmic changes to Na(v)1.5 in congenital and acqu

35 A major proarrhythmic consequence is a pause-dependent potentiat

36 A proarrhythmic consequence of pulmonary vein (PV) isolati

37 M) coculture system to investigate potential proarrhythmic consequences of MSC transplantation into t

38 hese parameters, and their antiarrhythmic or proarrhythmic consequences, were investigated.

39 o HERG, may limit the sensitivity of HERG to proarrhythmic drug blockade and may be a rational target

40 torsade de pointes after dofetilide (a known proarrhythmic drug) and was associated with disproportio

41 dependent kinetics of block and unblock of a proarrhythmic drug, cisapride, to KV11.1.

42 Furthermore, sensitivity to proarrhythmic drugs was strongly enhanced in JLNS-CMs bu

43 .1) K(+) channels in carbon monoxide-induced proarrhythmic early afterdepolarizations.

44 The proarrhythmic effect of ADS synchronized to normally con

45 The potential ventricular proarrhythmic effect of atrial defibrillation shocks (AD

46 current (late I(Na)) attenuates the RRD and proarrhythmic effect of I(Kr) inhibition.

47 ic science and clinical studies have shown a proarrhythmic effect of reversing the direction of activ

48 echanism by which NCX exerts its potentially proarrhythmic effect, ie, by promoting early afterdepola

49 S(2)) insufficient to induce reentry produce proarrhythmic effects (proarrhythmic preconditioning) th

50 Electroporation is not associated with proarrhythmic effects and is associated with a reduction

51 Proarrhythmic effects have been observed with the select

52 he electrophysiological, antiarrhythmic, and proarrhythmic effects of a clinically relevant concentra

53 idence of sudden death and susceptibility to proarrhythmic effects of antiarrhythmic agents.

54 We investigated the electrophysiological and proarrhythmic effects of AZD1305 versus dofetilide in do

55 The proarrhythmic effects of BPS were female specific; male

56 Our data indicate that the proarrhythmic effects of CO arise from activation of NO

57 All proarrhythmic effects of CO were abolished by the NO syn

58 The lack of efficacy and the proarrhythmic effects of drugs catalyzed the development

59 Together, these findings demonstrate proarrhythmic effects of flecainide in WT and Scn5a+/- m

60 ssue, where hMSC PS protected from potential proarrhythmic effects of HC at various levels of engraft

61 zole intake may principally be caused by the proarrhythmic effects of its metabolite desmethylastemiz

62 d may be a rational target for modifying the proarrhythmic effects of otherwise clinically useful com

63 roughput preclinical tests for assessing the proarrhythmic effects of QT prolonging drugs.

64 The proarrhythmic effects of SGK1 were linked to biochemical

65 n cardiac death, yet the mechanism for AMT's proarrhythmic effects remains incompletely understood.

66 ity, but most sodium channel activators have proarrhythmic effects that limit their clinical use.

67 hmic potential without producing ventricular proarrhythmic effects.

68 There were no proarrhythmic effects.

69 atment of NRVMs with LUF7244 prevented these proarrhythmic effects.

70 on but also suggest that stem cells may have proarrhythmic effects.

71 This study examined the risk of proarrhythmic events in patients receiving antiarrhythmi

72 rhythmic drugs were successful in minimizing proarrhythmic events.

73 pendent contribution of Ca(2+) dynamics as a proarrhythmic factor in the heart.

74 chyarrhythmia (ERAT) may be due to transient proarrhythmic factors.

75 ssing pathway of cardiac ion channels may be proarrhythmic for similar reasons.

76 1 reduces the sensitivity of HERG to classic proarrhythmic HERG blockers (sotalol, quinidine, dofetil

77 Rapid exposure to low-dose BPS showed proarrhythmic impact on female rat hearts; these effects

78 Disopyramide therapy does not appear to be proarrhythmic in HCM and should be considered before pro

79 normal repolarization and that loss of 1b is proarrhythmic in human cardiac cells.

80 ise concern that biventricular pacing may be proarrhythmic in select cases, particularly when associa

81 Evidence of the proarrhythmic influence of behavioral stress has been fu

82 on of channel mRNA and protein, which may be proarrhythmic, is recapitulated with cultured neonatal r

83 These proarrhythmic manifestations, related to Ca(2+) /calmodu

84 bility of repolarization duration (BVR) is a proarrhythmic marker.

85 However, not all drugs that block KV11.1 are proarrhythmic, meaning that screening on the basis of eq

86 We hypothesized that CaMKII is a part of the proarrhythmic mechanism in TS.

87 This is a novel proarrhythmic mechanism that can increase arrhythmia sus

88 eneral, the changes proved to be pivotal for proarrhythmic myofibroblast-cardiomyocyte crosstalk in v

89 ts and cardiomyocytes and whether it affects proarrhythmic myofibroblast-cardiomyocyte crosstalk obse

90 ergistic functional effects of flecainide, a proarrhythmic Na+ channel blocker, and oxidative stress.

91 drug); 1 sudden cardiac death, classified as proarrhythmic, occurred on day 8 (0.4% of all patients g

92 her reduced heart rate variability itself is proarrhythmic or if it simply correlates with the severi

93 rdial ischaemia as it is the most strikingly proarrhythmic pathology, and the most common cause of co

94 es exhibited increased CaMKII activity and a proarrhythmic phenotype that included action potential p

95 tion, leading to diastolic Ca(2+) leak and a proarrhythmic phenotype.

96 characteristics consistent with potentially proarrhythmic phenotypes.

97 ugs were associated with minimal ventricular proarrhythmic potential and terminated AF in 33% of simu

98 Whether thiazolidinediones have proarrhythmic potential in clinical use requires further

99 tion instability and has a lower ventricular proarrhythmic potential in the remodeled dog heart.

100 In recent years, the limited efficacy and proarrhythmic potential of classic antiarrhythmic drugs

101 phosphoinositide 3-kinase inhibition-derived proarrhythmic potential of drugs and provide a mechanism

102 eutic approach may mitigate side-effects and proarrhythmic potential plaguing CPVT pharmacological ma

103 rrhythmic activity, metabolic stability, and proarrhythmic potential.

104 rmination rates of 100% with low ventricular proarrhythmic potential.

105 est that it is possible to track the dynamic proarrhythmic preconditioning of single premature depola

106 nduce reentry produce proarrhythmic effects (proarrhythmic preconditioning) that are measurable by us

107 Whether this increase is related to the proarrhythmic properties of methadone is unclear.

108 F-termination effectiveness, and ventricular proarrhythmic properties.

109 es, differences in arrhythmic substrates and proarrhythmic responses to antiarrhythmic drugs may have

110 Advances in understanding the proarrhythmic risk of antiarrhythmic drugs has led to de

111 Here, we investigated whether the proarrhythmic risk of existing drugs could be reduced by

112 strain in silico models that may be used for proarrhythmic risk prediction.

113 ion of the QT interval is considered free of proarrhythmic risk.

114 essary to minimize a small but nonnegligible proarrhythmic risk.

115 s in order to maximize efficacy and minimize proarrhythmic risk.

116 ver, concern has been raised that ASA may be proarrhythmic secondary to the iatrogenic scar created d

117 ovide a mechanistic rationale for predicting proarrhythmic sensitivity to flecainide based on the ide

118 defects in LQT3 and Brugada syndrome elicit proarrhythmic sensitivity to flecainide.

119 atrial specific effects may reduce limiting proarrhythmic side effects.

120 erged as a reactive oxygen species-activated proarrhythmic signal, so we hypothesized that oxidized C

121 ings support the hypothesis that CaMKII is a proarrhythmic signaling molecule in cardiac hypertrophy

122 d brain activity, using H2(15)O PET, and the proarrhythmic state of the heart, using ECG, during ment

123 greatly increased risk of arrhythmia, i.e. a proarrhythmic state.

124 al in the left temporal region reflected the proarrhythmic status of the heart (inhomogeneity of left

125 Ranolazine reduces proarrhythmic substrate and triggers such as early after

126 complication after cardiac surgery, but the proarrhythmic substrate underlying the development of po

127 ventricular fibrillation (VF), generating a proarrhythmic substrate.

128 pling, slowing of impulse propagation, and a proarrhythmic substrate.

129 um current and a potentially lethal BrS-like proarrhythmic substrate.

130 Instead, KCNE2 variants may confer proarrhythmic susceptibility when provoked by additional

131 sence of QT prolongation, indicating a novel proarrhythmic syndrome.

132 effects are often poorly tolerated and their proarrhythmic tendencies increase mortality.

133 of tissue, which become enhanced and, hence, proarrhythmic the higher the overall level of connexin40

134 channel activity can cause the nucleation of proarrhythmic traveling Ca(2+) waves.

135 reatment of acute promyelocytic leukemia, is proarrhythmic via two separate mechanisms: a well charac

136 cardiac ischemia, sympathetic activation is proarrhythmic, whereas parasympathetic activation is ant