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 olarization effects, synthetic agents may be proarrhythmic.

5 onal wisdom holds that caffeinated coffee is proarrhythmic.

6 uch as QT prolonging drugs and female sex is proarrhythmic.

7 tive, often misclassifying safe compounds as proarrhythmic.

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

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

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

11 rug, and under unfortunate conditions may be proarrhythmic.

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

13 This suggests that ASA is not proarrhythmic.

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

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

16 to investigate the mechanistic link between proarrhythmic abnormalities, reduced contractility and d

17 ; e.g., through simulations, bepridil's more proarrhythmic action in adult cardiomyocytes compared to

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

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

20 rived bioactive metabolites that might exert proarrhythmic actions.

21 hondrial Ca(2+) uptake enhancer ezetimibe on proarrhythmic activity in atrial myocytes and on AF burd

22 Na current (I(Na)) may contribute to atrial proarrhythmic activity in patients with SDB.

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

24 Moreover, generation of proarrhythmic activity patterns within cerebral autonomi

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

26 V)1.5 results in dysregulation of I(Na) with proarrhythmic activity that was independent from preexis

27 on and CMR scar may identify a particularly "proarrhythmic" adaptation and may represent a potential

28 The oxa-iboga compounds lack the proarrhythmic adverse effects of ibogaine and noribogain

29 No life-threatening proarrhythmic adverse effects were reported.

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

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

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

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

34 ibrillation (AF) can be associated with both proarrhythmic and noncardiovascular toxicities.

35 Amiodarone is proarrhythmic and should be avoided in patients with ATS

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

37 classify risk to drugs in the comprehensive proarrhythmic assay initiative panels with very high acc

38 efforts, largely driven by the comprehensive proarrhythmic assay initiative, to develop more accurate

39 We hypothesised that the proarrhythmic background present between fibrillation ep

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

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

42 In multielectrode array recordings, proarrhythmic behavior arose when I(Kr) was reduced by t

43 hRNA, suggesting that co-knockdown mitigates proarrhythmic behavior expected from the selective reduc

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

45 evaluate risk of genetic mutations based-on proarrhythmic behavior in phenotypically variable popula

46 This proarrhythmic behavior is enhanced by disease-causing mu

47 st-graft electromechanical integration, less proarrhythmic behavior, and greater beneficial effects o

48 emodelling that underlies the Ca(2+) -driven proarrhythmic behaviour observed in atrial fibrillation

49 between TATS remodelling and Ca(2+) -driven proarrhythmic behaviour that probably reflects the arrhy

50 act of protein remodelling on Ca(2+) -driven proarrhythmic behaviour varied dramatically depending on

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

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

53 odazole displaced mitochondria and increased proarrhythmic Ca(2+) sparks, which were rescued by MitoT

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

55 an increased frequency of Ca(2+) sparks and proarrhythmic Ca(2+) waves, and RIalpha-icKO mice had an

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

57 en species (ROS) generation, which triggered proarrhythmic calcium-release events.

58 but it is unknown how NO donors modulate the proarrhythmic CaMKII to alter cardiac arrhythmia inciden

59 ular and organ behavior and the emergence of proarrhythmic cardiac phenotypes.

60 o the association between CKD and pathologic proarrhythmic cardiac remodeling.

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

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

63 Proarrhythmic changes in the heart were quantified from

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

65 A major proarrhythmic consequence is a pause-dependent potentiat

66 A proarrhythmic consequence of pulmonary vein (PV) isolati

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

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

69 phenotype and indicated an increased risk of proarrhythmic delayed afterdepolarizations in POAF subje

70 Oxidative stress in cardiac disease promotes proarrhythmic disturbances in Ca(2+) homeostasis, impair

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

72 s of the system, from the specific nature of proarrhythmic drug interaction with the hERG channel, to

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

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

75 f action potential morphology in response to proarrhythmic drugs improves prediction of torsadogenic

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

77 iPSC-CMs), we evaluated the effects of three proarrhythmic drugs: Ranolazine, Domperidone, and Sotalo

78 tion potential duration (APD) and triggering proarrhythmic early afterdepolarizations (EADs).

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

80 The proarrhythmic effect of ADS synchronized to normally con

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

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

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

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

85 mmed ventricular pacing, without significant proarrhythmic effect.

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

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

88 Proarrhythmic effects have been observed with the select

89 indications; however, given the undesirable proarrhythmic effects in the heart, selectivity for PDE3

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

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

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

93 The proarrhythmic effects of BPS were female specific; male

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

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

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

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

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

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

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

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

102 The proarrhythmic effects of SGK1 were linked to biochemical

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

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

105 myocyte electrical remodeling leading to the proarrhythmic effects that promote the development of AF

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

107 hmic potential without producing ventricular proarrhythmic effects.

108 There were no proarrhythmic effects.

109 atment of NRVMs with LUF7244 prevented these proarrhythmic effects.

110 ts resulting from hemodynamic, vascular, and proarrhythmic/electrophysiological consequences.

111 with significantly lower risk of ventricular proarrhythmic events (hazard ratio, 0.53 [95% CI, 0.38-0

112 associated with a lower risk of ventricular proarrhythmic events and conduction disorders while havi

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

114 rhythmic drugs were successful in minimizing proarrhythmic events.

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

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

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

118 1 reduces the sensitivity of HERG to classic proarrhythmic HERG blockers (sotalol, quinidine, dofetil

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

120 siology at high pacing rates are shown to be proarrhythmic in general.

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

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

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

124 man data, as well as increased propensity to proarrhythmic incidents such as early afterdepolarizatio

125 Our simulation data reveal that proarrhythmic incidents tend to occur in failing myocyte

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

127 cardiovascular risk prediction as potential proarrhythmic influencers.

128 Proarrhythmic ionic current remodeling in Pitx2(+/-) atr

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

130 D96V-CaM induced a proarrhythmic late Na+ current (INa) by impairing inacti

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

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

133 tify the effects of KCNQ1 mutations based on proarrhythmic markers.

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

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

136 The proarrhythmic mechanism of increased AF in contemporary

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

138 biochemistry were employed to elucidate the proarrhythmic mechanisms due to loss of cardiomyocyte FK

139 s transmit proinflammatory, profibrotic, and proarrhythmic molecules that induce atrial myopathy and

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

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

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

143 tify a potential molecular mechanism for the proarrhythmic NCX1 upregulation in chronic AF patients.

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

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

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

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

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

149 characteristics consistent with potentially proarrhythmic phenotypes.

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

151 Whether thiazolidinediones have proarrhythmic potential in clinical use requires further

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

153 While the anti and proarrhythmic potential of a sodium channel blocker is t

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

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

156 potential as an in vitro model to study the proarrhythmic potential of drugs, but insights from thes

157 comprehensive mechanistic assessment of the proarrhythmic potential of new drugs.

158 ings are an important step in evaluating the proarrhythmic potential of small molecules and are now r

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

160 rrhythmic activity, metabolic stability, and proarrhythmic potential.

161 eclinical screening tests to determine their proarrhythmic potential.

162 fy new and existing drugs according to their proarrhythmic potential.

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

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

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

166 hies in patients significantly increased the proarrhythmic propensity to certain intermediate and hig

167 ed a safety announcement about the potential proarrhythmic properties of lamotrigine.

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

169 F-termination effectiveness, and ventricular proarrhythmic properties.

170 serve as a novel molecular mechanism of the proarrhythmic reduction of ICa,L in cAF.

171 CKD is associated with atrial proarrhythmic remodeling and activation of the sympathet

172 arbonyl mediators of oxidative stress in the proarrhythmic remodeling and AF susceptibility that occu

173 n the setting of Pitx2 deficiency to promote proarrhythmic remodeling and AF.

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

175 ndidate compounds are extensively tested for proarrhythmic risk and in particular risk of Torsade de

176 APC datasets and improved safety margins and proarrhythmic risk assessments.

177 to K(v)11.1 and improve our understanding of proarrhythmic risk associated with compounds that block

178 t iPSC-CM computational model to predict the proarrhythmic risk of 40 KCNQ1 genetic variants.

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

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

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

182 f 12 blinded drugs (with different levels of proarrhythmic risk) against four human cardiac currents

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

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

185 essary to minimize a small but nonnegligible proarrhythmic risk.

186 elop more accurate methods for allocation of proarrhythmic risk.

187 s inputs for logistic regressions to predict proarrhythmic risk.

188 ther downregulate these channels and exhibit proarrhythmic risk.

189 (iAPs) are powerful biomarkers that predict proarrhythmic risks.

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

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

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

193 atrial specific effects may reduce limiting proarrhythmic side effects.

194 tively, our data affirm CaMKII as a critical proarrhythmic signal in diabetic AF and suggest ROS prim

195 arts, and calmodulin kinase II (CaMKII) is a proarrhythmic signal that may be activated by ROS (oxidi

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

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

198 istinctive proinflammatory, profibrotic, and proarrhythmic signature of eFat-EVs from patients with A

199 amplitude and SR Ca(2+) content, and reduced proarrhythmic spontaneous Ca(2+) waves in TAB VMs under

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

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

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

203 Ranolazine reduces proarrhythmic substrate and triggers such as early after

204 adipose tissue (inFAT) is a newly recognized proarrhythmic substrate for postinfarct ventricular tach

205 cardiomyocytes and fibroblasts may provide a proarrhythmic substrate in cardiac disease.

206 rtant for understanding the patient-specific proarrhythmic substrate of VTs and therapeutic planning.

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

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

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

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

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

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

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

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

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

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

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