ライフサイエンスコーパス: SVT

1 SVT does not affect the transcription of CBP/p300, but r

2 SVT recurred in 19% of patients on digoxin and 31% of pa

3 SVT resulted in more than one third of therapies in both

4 SVT was also a prognostic factor for survival in patient

5 SVT was associated with only moderate signal amplitude e

6 SVTs free rates were 80.4%, 82.4%, and 75.8%, respective

7 icantly different (none [14.2%], AE [17.0%], SVT [11.8%], AF [14.8%], p = 0.50).

8 n functional classes III and IV) (p = 0.04); SVT occurred more commonly in patients with outflow obst

9 nate arrhythmias or discriminate between 1:1 SVT and VT if the arrhythmia persists.

10 ng sequences suitable for analysis (1381 1:1 SVT episodes in 32 patients and 26 1:1 VT episodes in 6

11 Antitachycardia pacing terminated 66 of 1381 SVT (5%; generalized estimating equations adjusted, 23.8

12 minated or correctly classified 1379 of 1381 SVT sequences for an overall specificity of 99.9% (gener

13 ralized estimating equation adjusted, 70.2%) SVT episodes.

14 Nineteen patients with 20 SVTs (atypical atrioventricular nodal reentrant tachycar

15 dred fifty-four SVT ablation procedures (228 SVTs) using a 3D-electroanatomic mapping system in 116 a

16 rent between groups (none [3.8%], AE [4.3%], SVT [3.7%], AF [0%], p = 0.43).

17 rent between groups (none [5.7%], AE [8.3%], SVT [0%], AF [9.0%], p = 0.005).

18 layed (4/8 [50%]), or terminated (5/8 [63%]) SVT in all accessory pathway patients.

19 ar between groups (none [22.7%], AE [27.8%], SVT [17.7%], AF [25.7%], p = 0.10).

20 PGE2 was increased after SVT (1465+/-234 pg/ml) compared with PVSal (597+/-99; P<

21 ly, with the highest risk also shortly after SVT.

22 s; 95% confidence interval, 3.03-35.0) or AH(SVT)<AH(NSR) (normal sinus rhythm) His-refractory ventri

23 The AH criteria, or paradoxically AH(SVT)<AH(NSR), differentiates NF reentrant tachycardia/at

24 atio [HR] = 1.30; 95% CI, 1.18 to 1.43), all SVT (HR = 1.28; 95% CI, 1.19 to 1.38), and stroke (HR =

25 The risk for all SVT increased 7% for each increase of five bisphosphonat

26 d as VT (n=740), FVT (n=350), VF (n=77), and SVT (n=396).

27 ensitivity, VT/VF positive predictivity, and SVT positive predictivity along with corrections for mul

28 e of acute myocardial infarctions (AMIs) and SVTs, and an increase in bradycardia and hypotension.

29 Simian virus 40 (SV40) large T antigen (SVT) interferes with normal cell regulation and thus has

30 ived a diagnosis of atrial fibrillation, any SVT, or stroke; or died.

31 lar nodal pathways in the donor heart caused SVT in 3 patients.

32 Thus, symptomatic extensions are common SVT complications and, whether or not reaching the SFJ,

33 clinical presentation as well as the common SVTs causing heart failure, pathophysiology of SVT causi

34 patients developed AE, 185 (3.4%) developed SVT, and 43 (0.8%) developed AF.

35 the reflex changes in autonomic tone during SVT remain poorly understood.

36 terns of initiation and termination of fetal SVT are more diverse than is generally believed and that

37 Contributory risk factors for SVT are the same for VTE.

38 ghest separate risk estimates were found for SVT with surgery (42.5; 95% CI, 10.2-177.6), hospitaliza

39 ith first rib resection and scalenectomy for SVT as those without hypercoagulability.

40 One hundred fifty-four SVT ablation procedures (228 SVTs) using a 3D-electroana

41 Furthermore, SVT-expressing cells contain higher levels of acetylated

42 There was no difference in SVT recurrence in infants treated with digoxin versus pr

43 es H3K56 and H4K12 are markedly increased in SVT-expressing cells.

44 e a high prevalence of MPNs and JAK2V617F in SVT patients and show differences in underlying etiology

45 e inducible SVTs than group B, and all index SVTs were located in the remainder of the morphological

46 Group A patients had more inducible SVTs than group B, and all index SVTs were located in th

47 13 patients continued to have short-lasting SVTs despite 3 ablation procedures during a median follo

48 Group A included simple anomalies with less SVTs.

49 ised predominantly Fontan patients with more SVTs.

50 The MGS was used for successful ablation of SVT in seven of seven patients.

51 The electrophysiologic behavior of SVT in these patients strongly suggests that the mechani

52 and confluence fell by >25% after 7 days of SVT and were accompanied by an 80% increase in LV myocar

53 Specifically, 21 days of SVT resulted in a >50% increase in LV dimension, a 56% f

54 e in LV and myocyte function with 21 days of SVT was accompanied by signs and symptoms of CHF.

55 After 7 days of SVT, LV end-diastolic dimension and myocyte length both

56 After 14 days of SVT, total LV myocardial collagen content was reduced by

57 rcent shortening fell by 16% after 7 days of SVT, with no change in the steady-state velocity of shor

58 ased by approximately 2-fold after 7 days of SVT.

59 The rate of inappropriate detection of SVT was 39.5% in the single-chamber detection arm compar

60 973 patients with a first-time diagnosis of SVT between 1980 and 2012.

61 apy of patients with a clinical diagnosis of SVT obviates extensive imaging and laboratory workup and

62 d most patients with a clinical diagnosis of SVT the same as those with VTEs.

63 Longer durations of SVT caused progressive LV dilation, LV pump failure, and

64 e remained elevated with longer durations of SVT.

65 APDs introduced during sustained episodes of SVT either altered its behavior or terminated it.

66 and to produce atrial echoes and episodes of SVT.

67 he onset of numerous spontaneous episodes of SVT.

68 nd now report that the ectopic expression of SVT in several cell types in vivo and in vitro results i

69 years, 55% female, and 60% had a history of SVT.

70 t SVT, and assessed the prognostic impact of SVT on cancer survival by applying the Kaplan-Meier meth

71 e data indicate the prognostic importance of SVT and may form the basis for clinical decision-making

72 inux was associated with lower incidences of SVT extension to </= 3 cm (0.3%; 5/1502; P < .001) and >

73 heart failure, evaluation and management of SVT causing heart failure, and prognosis of SVT causing

74 er rate control have improved the outcome of SVT management and subsequently improved the heart failu

75 Ts causing heart failure, pathophysiology of SVT causing heart failure, evaluation and management of

76 SVT causing heart failure, and prognosis of SVT causing heart failure.

77 edications for antiarrhythmic prophylaxis of SVT in infants: digoxin and propranolol.

78 The primary end point was the proportion of SVT episodes inappropriately detected from the time of p

79 eal-world clinical practice, a proportion of SVT patients are left untreated because the risks associ

80 The primary end point was recurrence of SVT requiring medical intervention.

81 han rare nonsustained episodes or slowing of SVT to a clinically tolerable rate.

82 Efficacy was defined as suppression of SVT to no more than rare nonsustained episodes or slowin

83 vement and the initiation and termination of SVT, suggesting that autonomic influences play a key rol

84 ve bleeding is not infrequent at the time of SVT diagnosis, and major risk factors for bleeding, such

85 ion of JAK2V617F in the diagnostic workup of SVT patients.

86 n allowed safe and successful elimination of SVTs, using an exclusively retrograde approach, resultin

87 The majority of SVTs in stable OHT patients can be attributed to macro-r

88 ncidence, clinical course, and management of SVTs in a cohort of 729 adult patients who underwent OHT

89 ) compared with PVSal (6.3+/-0.3; P<0.01) or SVT (6.3+/-0.3; P<0.04).

90 ited value to identify the location of AT or SVT mechanisms.

91 Other persistent or paroxysmal SVTs were seen in 47 stable OHT patients (7%).

92 Treatment of patients' SVT with parenteral anticoagulants appears to be both ef

93 Individuals with previous SVT alone had a 5.5-fold (95% confidence interval [CI],

94 nous thrombosis in individuals with previous SVT and a mild thrombotic risk factor (smoking or overwe

95 kedly increased in individuals with previous SVT who have an acquired thrombotic risk factor.

96 rs into Lewis recipients at the time of PVT, SVT, PVSal, or PVT + indomethacin (COX1/2 inhibitor).

97 n contrast to the expectation that reentrant SVT is initiated by spontaneous premature atrial contrac

98 an safely and effectively control refractory SVT and may obviate the need for RFA in children <1 year

99 flecainide and sotalol to control refractory SVT.

100 A) is the definitive treatment of refractory SVT; however, interventional therapy poses a high risk o

101 ces in their ability to confirm VT or reject SVT.

102 gorithm for discriminating supraventricular (SVT) and ventricular (VT) tachycardias with 1:1 atrioven

103 With placebo (n = 1500), symptomatic SVT extension to </= 3 cm or > 3 cm from the SFJ occurre

104 We reviewed supraventricular tachycardia (SVT) ablation in adult patients with congenital heart di

105 Supraventricular tachycardia (SVT) causing heart failure is an important cause of tach

106 r ablation, of supraventricular tachycardia (SVT) in a large series of patients after orthotopic hear

107 of refractory supraventricular tachycardia (SVT) in children <1 year of age.

108 pacing-induced supraventricular tachycardia (SVT) in pigs.

109 Supraventricular tachycardia (SVT) is one of the most common conditions requiring emer

110 recruited for supraventricular tachycardia (SVT) mapping, and seven of these underwent ablation.

111 isdetection of supraventricular tachycardia (SVT) remains a substantial complication of implanted car

112 -8 years) with supraventricular tachycardia (SVT) underwent catheter ablation.

113 of paroxysmal supraventricular tachycardia (SVT) were analyzed to determine the mechanism by which t

114 therapies for supraventricular tachycardia (SVT) were compared among 582 patients (primary preventio

115 g ablation for supraventricular tachycardia (SVT) were compared with a matched nonoperative control g

116 s: 9 reentrant supraventricular tachycardia (SVT), 2 ventricular tachycardia (VT), 2 sinus tachycardi

117 , 67 (37%) had supraventricular tachycardia (SVT), and 56 (31%) had nonsustained ventricular tachycar

118 sifications of supraventricular tachycardia (SVT), and stroke among older patients with cancer.

119 trial flutter, supraventricular tachycardia (SVT), or AE.

120 eentrant fetal supraventricular tachycardia (SVT), the most common form of life-threatening fetal arr

121 s (n=149) were supraventricular tachycardia (SVT).

122 esponse during supraventricular tachycardia (SVT).

123 % of pediatric supraventricular tachycardia (SVT).

124 duced and sustained ventricular tachycardia (SVT) or prevent induction of ventricular tachycardia.

125 patients with supraventricular tachycardias (SVT).

126 incidence of supraventricular tachycardias (SVTs) and ventricular arrhythmias.

127 ndent long RP supraventricular tachycardias (SVTs) can be challenging.

128 ts for a median of 1.6 years, and found that SVT was a marker of occult cancer.

129 We have previously shown that SVT-mediated transformation requires interaction with th

130 The SVT mapping with the magnetic catheter was successful in

131 g to 5.1 (95% CI 4.6-5.5), 5 years after the SVT.

132 73.3% to 82.3%) with the GEE method, and the SVT positive predictivity was 100.0% (911 of 911, n=101;

133 ablation is effective in management of these SVTs.

134 the relevance of splanchnic vein thrombosis (SVT) as a marker of occult malignant disease.

135 e apparent that superficial vein thrombosis (SVT) can have serious complications.

136 Superficial vein thrombosis (SVT) increases the risk of venous thrombosis fourfold to

137 tic treatment of splanchnic vein thrombosis (SVT) is a clinical challenge.

138 tic, lower-limb superficial-vein thrombosis (SVT) is debated.

139 Subclavian vein thrombosis (SVT) is usually caused by vigorous activity or extensive

140 17F screening in splanchnic vein thrombosis (SVT) patients without typical hematologic MPN features i

141 a diagnosis of superficial vein thrombosis (SVT).

142 diagnosis of superficial venous thrombosis (SVT) are thoroughly evaluated, the degree and extent of

143 is unknown if splanchnic venous thrombosis (SVT) is a marker of occult cancer and a prognostic facto

144 Thus, SVT causes time-dependent changes in LV geometry and fun

145 study including all patients with first-time SVT (n = 1191) between 1994 and 2011.

146 episodes in the dual-chamber arm were due to SVT.

147 allow dual pathway physiology to progress to SVT.

148 of Wistar-Furth blood, systemic transfusion (SVT), or saline via portal vein (PVSal).

149 This unusual SVT requires separate maneuvers to delineate its upper a

150 d Kupffer cell PGE2 (5370+/-533; P<0.001 vs. SVT and vs. PVSal) even more substantially.

151 The main study outcome was SVT extension by day 77, whether to </= 3 cm or > 3 cm f

152 opulation-based setting during a period when SVT was not treated routinely with anticoagulants.

153 As most individuals with SVT do not develop venous thrombosis, additional risk fa

154 multicenter study of infants <4 months with SVT (atrioventricular reciprocating tachycardia or atrio

155 ee and extent of thrombosis in patients with SVT are characteristically underestimated ( approximatel

156 in patients with PeAF, 13% in patients with SVT, and 0% in control patients with AF (p = 0.007).

157 % in patients with PeAF, 3% in patients with SVT, and 0% in control patients with AF (p = 0.03).

158 range] age, 32 [16-71] years) presented with SVT, of whom 55 patients (43 females and 12 males; mean

159 icoagulant drugs in patients presenting with SVT, including symptomatic as well as incidentally detec

160 b resection and scalenectomy presenting with SVT.

161 agnostic work-up in patients presenting with SVT.

162 our findings, we believe younger women with SVT should undergo hypercoagulable testing to identify t

163 nosine was administered to 229 patients with SVTs during EP study: atrioventricular (AV) reentry (AVR

164 Two distinct regions within SVT, one located in the amino terminus and one in the ca

165 comparison cohort of cancer patients without SVT, and assessed the prognostic impact of SVT on cancer