ライフサイエンスコーパス: QT prolongation

1 tant before prescribing drugs known to cause QT prolongation.

2 inversely correlated with ibutilide-induced QT prolongation.

3 ng to frequent EADs and electrocardiographic QT prolongation.

4 a trigger to initiate the onset of TdP under QT prolongation.

5 o the need for careful predrug screening for QT prolongation.

6 long QT syndrome (LQTS) is characterized by QT prolongation.

7 lace during AVB with the bradycardia-induced QT prolongation.

8 effects of cardiac memory lead to excessive QT prolongation.

9 entricular fibrillation, but did not prevent QT prolongation.

10 , and the dose-limiting toxicity was grade 3 QT prolongation.

11 es the odds for mortality then those without QT prolongation.

12 icking of mutant proteins, thus exacerbating QT prolongation.

13 pertrophy, resulting in action potential and QT prolongation.

14 inding to this channel leads to drug-induced QT prolongation.

15 drugs may be an important aspect of acquired QT prolongation.

16 ir2.1 and hERG potassium channels, causal to QT prolongation.

17 otassium conductance, more commonly known as QT prolongation.

18 vely) and DHT-treated animals exhibited less QT prolongation (11.4 +/- 3.8% increase; P < .03).

19 nic exposure is consistently associated with QT prolongation, a risk factor for arrhythmia and sudden

20 Despite the absence of manifest QT prolongation, adolescent anorexic females have impair

21 by diffuse symmetrical T wave inversion and QT prolongation after recovery from an episode of cardio

22 ry edema may cause deep T wave inversion and QT prolongation after resolution of the symptoms.

23 ependently (1 to 100 micromol/L), leading to QT prolongation and an increase in TDR.

24 ed with baseline QT interval to drug-induced QT prolongation and arrhythmias is not known.

25 ise mechanism by which the mutations lead to QT prolongation and arrhythmias is uncertain, however.

26 ardiac hypertrophy, which is associated with QT prolongation and arrhythmias.

27 ssociated with acquired electrocardiographic QT prolongation and arrhythmic activity initiated by pre

28 resent study examines the cellular basis for QT prolongation and arrhythmogenesis after reversal of t

29 e IKs channel), who presented with excessive QT prolongation and high serum levels of norfluoxetine,

30 roportion of the variability in drug-induced QT prolongation and is a significant predictor of drug-i

31 ocyte ID are likely to provide insights into QT prolongation and its associated disorders.

32 ave implications regarding the definition of QT prolongation and its use in predicting arrhythmias an

33 normal resting QTc values and only developed QT prolongation and malignant arrhythmias after exposure

34 during AVB is independently associated with QT prolongation and may be arrhythmogenic during AVB.

35 e slow component of I(to) (I(to,s)), have no QT prolongation and no spontaneous arrhythmias, and (c)

36 keted drugs, and this inhibition may lead to QT prolongation and possibly fatal cardiac arrhythmia.

37 This review focuses on mechanisms underlying QT prolongation and proarrhythmia, risk factors, includi

38 The predictive values of QT prolongation and QTD were assessed in 1839 participan

39 ough V4, with either persistent or transient QT prolongation and severe disease expression of exercis

40 us results in a clinical phenotype combining QT prolongation and ST segment elevation, indicating a c

41 alpain may contribute to ischemia-associated QT prolongation and sudden cardiac death.

42 The clinical observation of QT prolongation and torsade de pointes found with astemi

43 We report the clinical observation of QT prolongation and torsade de pointes in a patient with

44 g of hERG channels to the cell surface cause QT prolongation and torsade de pointes in patients treat

45 e inhibitors could predispose individuals to QT prolongation and torsade de pointes.

46 iarrhythmic drugs are used for AF, excessive QT prolongation and torsades de pointes (TdP) often occu

47 Drug-induced QT prolongation and torsades de pointes remain significa

48 ncidence of serious adverse events including QT prolongation and torsades de pointes.

49 cell model, the KCNQ1-G589D mutation induced QT prolongation and transient afterdepolarizations, know

50 yndrome type 3 child experienced paradoxical QT prolongation and worsening of arrhythmias after mexil

51 ely used antibiotic that infrequently causes QT-prolongation and torsades de pointes cardiac arrhythm

52 T syndrome characterized by deafness, marked QT prolongation, and a high risk of sudden death.

53 with early childhood cardiac arrest, extreme QT prolongation, and a negative family history.

54 fects causing hypertension, thromboembolism, QT prolongation, and atrial fibrillation.

55 t lack both I(to,f) and I(to,s), have AP and QT prolongation, and spontaneous ventricular tachyarrhyt

56 Wide QRS/T angle, ECG-MI, and QT prolongation appeared as dominant predictors when eva

57 Indeed, progressive corrected QT prolongation, arrhythmias, and ischemic changes were

58 ociated systemic and pulmonary hypertension, QT prolongation, arrhythmias, pericardial disease, and r

59 se in HRV over 24h at 10 dpa, accompanied by QT prolongation as well as diurnal variations, followed

60 v4.2W362FxKv1.4(-/-) animals revealed marked QT prolongation, atrioventricular block, and ventricular

61 L1825P fails to generate QT prolongation because it does not reach the cell surfa

62 ischemia, hypotension, hypertension, edema, QT prolongation, bradyarrhythmia, and thromboembolism.

63 ent, I(to,f), have action potential (AP) and QT prolongation, but no spontaneous arrhythmias, (b) Kv1

64 menon occurs in the heart and contributes to QT prolongation by altering cardiac sodium current prope

65 747+/-36 ms (+40%, P<0.0001), similar to the QT prolongation by dofetilide (511+/-22 to 703+/-45 ms [

66 e hypothesis that the extent of drug-induced QT prolongation by dofetilide is greater in sinus rhythm

67 on of SR, there was increased sensitivity to QT prolongation by this I(Kr)-specific blocker.

68 8057 prevented action potential duration and QT prolongation caused by dofetilide.

69 owever, it is unclear whether to what extent QT prolongation coexisting with ECG-LVH can explain the

70 ivo telemetric recordings also reveal marked QT prolongation, consistent with a defect in ventricular

71 Underlying abnormalities include QT prolongation, delayed repolarization from downregulat

72 y cardiovascular liabilities associated with QT prolongation due to hERG activity or endothelial NOS

73 el antagonists will be useful in normalizing QT prolongation during As(2)O(3) therapy.

74 Consistent with QT prolongation, epileptic rats had longer ventricular a

75 Patients with QT prolongation had longer hospitalization (276 hrs vs.

76 Attenuation of ibutilide-induced QT prolongation has been observed in a small number of p

77 patients without structural heart disease or QT prolongation has been reported.

78 ever, innate susceptibility to PM-associated QT prolongation has not been characterized.

79 Acutely ill patients with QT prolongation have longer lengths of hospitalization a

80 ce, management, and clinical consequences of QT prolongation in a large cohort of patients treated wi

81 rize genetic susceptibility to PM-associated QT prolongation in a multi-racial/ethnic, genome-wide as

82 A case of QT prolongation in a patient receiving protease inhibito

83 Exercise testing is useful in unmasking QT prolongation in disorders associated with abnormal re

84 was to develop and validate a risk score for QT prolongation in hospitalized patients.

85 Danio rerio, we found that drugs that cause QT prolongation in humans consistently caused bradycardi

86 sis was conducted to determine the degree of QT prolongation in patients treated with arsenic trioxid

87 may alter susceptibility to PM10-associated QT prolongation in populations protected by the U.S. Env

88 The magnitude of QT prolongation in response to bradycardia, rather than

89 Predictors of QT prolongation in the acutely ill population are simila

90 olarization at the single cell level but not QT prolongation in the intact animal.

91 y associated with giant negative T waves and QT prolongation in the postevent electrocardiogram.

92 hERG inhibition (IC(50) = 44 muM for 7a) and QT prolongation in vivo.

93 th erythromycin caused significantly greater QT-prolongation in female rabbit hearts (mean [SD], 11.8

94 voltage, reduced heart rate variability, and QT prolongation (in the cardiovascular disease-free grou

95 ic ventricular tachycardia in the absence of QT prolongation, indicating a novel proarrhythmic syndro

96 er to initiate torsade de pointes (TdP) with QT prolongation induced by dl-sotalol and azimilide.

97 QT prolongation is a risk factor for ventricular arrhyth

98 udden death, and the increased prevalence of QT prolongation is an independent risk factor for cardio

99 QT prolongation is associated with increased risk of sud

100 QT prolongation is commonly associated with life-threate

101 Drug-induced QT prolongation is usually caused by block of human ethe

102 up, n=1 [1%]; imatinib group, n=1 [1%]), and QT prolongation (nilotinib group, n=1 [1%]; imatinib gro

103 These results provide a mechanism for the QT prolongation observed clinically with administration

104 QT prolongation occurred in 49 (3%) patients given nerat

105 ring intravenous tacrolimus infusion, marked QT prolongation occurred.

106 t AF at the time of drug discontinuation for QT prolongation (odds ratio 0.14, 95% confidence interva

107 pital mortality compared to patients without QT prolongation (odds ratio 2.99 95% confidence interval

108 e 4 thrombocytopenia [cohort 2], one grade 3 QT prolongation on electrocardiogram [cohort 3], and one

109 Although no clinical events due to QT prolongation on electrocardiography were observed, QT

110 Arrhythmias associated with QT prolongation on the ECG often lead to sudden unexpect

111 We identified 24 patients with QT prolongation or torsade de pointes, or both, associat

112 which is consistent with other findings that QT prolongation, per se, is insufficient to generate TdP

113 ater presence in men of a factor that blunts QT prolongation responses, especially at slow heart rate

114 creased action potential duration, mimicking QT prolongation seen in the index patient on mexiletine

115 are Na- and K-channel mutations in Mendelian QT prolongation syndromes.

116 e do not know why some patients develop more QT prolongation than others, despite similar bradycardia

117 de pointes may be less related to degree of QT prolongation than to drug effects on transmural dispe

118 , we report a mechanism for diabetes-induced QT prolongation that involves an increase in INaP caused

119 We find QT prolongation to be common (24%), with Torsade de Poin

120 Its clinical use is burdened by QT prolongation, torsade de pointes, and sudden cardiac

121 Cases of QT prolongation, torsades de pointes, and sudden death h

122 d the association of citalopram with cardiac QT prolongation, use of this agent to treat agitation ma

123 was also a prerequisite for aging-dependent QT prolongation, ventricular fibrillation and SCD immedi

124 at 0.10 mug/kg per minute and borderline if QT prolongation was 1 to 29 ms.

125 Electrocardiographic QT prolongation was common (63%).

126 e, new large or global T wave inversion with QT prolongation was observed after resolution of acute c

127 QT prolongation was present in 24%.

128 (AF) at the time of drug discontinuation for QT prolongation was protective despite similar heart rat

129 gation on electrocardiography were observed, QT prolongation was reported significantly more frequent

130 nt EADs in rabbits, in which more pronounced QT prolongation was seen.

131 events occurred in 26 (8%) of 329 patients; QT prolongation was the most common serious adverse even

132 Predictors of QT prolongation were female sex, QT-prolonging drugs, hy

133 Episodes of QT prolongation were manually over-read.

134 ade de pointes, in addition to the degree of QT prolongation, which is an imperfect predictor.

135 A wide array of drugs can cause marked QT prolongation with the associated risk of torsade de p

136 version to normal rhythm was associated with QT prolongation yet absent proarrhythmia markers for Tor