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 Although SVT after SARS-CoV-2 vaccination is rare in absolute ter

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

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

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

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

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

32 with structurally normal hearts affected by SVT and Wolff-Parkinson-White syndrome and determine cau

33 y in which multiple members were affected by SVT or Wolff-Parkinson-White pattern (preexcitation) on

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

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

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

37 eric ischemia, compared with 3% in pre-COVID SVT ( p <0.001).

38 condition, compared to 52% in the pre-COVID SVT cohort ( p =0.01).

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

40 l response factors were also examined during SVT regeneration.

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

42 ts diagnosed at age <=1 year with re-entrant SVT.

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

44 Primary outcome was first SVT recurrence after hospital discharge.

45 as rare, in 72% of cases, no other cause for SVT could be identified following SARS-CoV-2 vaccination

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

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

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

49 cacy and safety of anticoagulant therapy for SVT.

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

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

52 Twenty (69%) had SVT at multiple sites, including 4 (14%) with concomitan

53 onstrate that anticoagulant therapy improves SVT recanalization and reduces the risk of thrombosis pr

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

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

56 SAIGE had inflation in SVT at prevalence 0.1 or lower and the inflation was eli

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

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

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

60 s molecular and genetic tools to investigate SVT regeneration.

61 13 patients continued to have short-lasting SVTs despite 3 ablation procedures during a median follo

62 Group A included simple anomalies with less SVTs.

63 ised predominantly Fontan patients with more SVTs.

64 example, at 30 minutes, there was a 53.7% of SVT conversion in the treatment arm compared to 34.7% in

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

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

67 New cases of SVT were identified from April 2021 to April 2022; follo

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

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

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

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

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

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

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

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

76 973 patients with a first-time diagnosis of SVT between 1980 and 2012.

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

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

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

80 e remained elevated with longer durations of SVT.

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

82 and to produce atrial echoes and episodes of SVT.

83 he onset of numerous spontaneous episodes of SVT.

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

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

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

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

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

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

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

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

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

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

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

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

96 ents receiving anticoagulation, the rates of SVT recanalization, SVT progression, recurrent venous th

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

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

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

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

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

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

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

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

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

106 The effects of phytohormones on SVT regeneration were investigated by applying exogenous

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

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

109 Paroxysmal SVT affects both adult and pediatric populations and is

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

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

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

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

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

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

116 oagulation, the rates of SVT recanalization, SVT progression, recurrent venous thromboembolism (VTE),

117 gene in individuals with familial reentrant SVT, Wolff-Parkinson-White ECG pattern, and structurally

118 revealed an increased incidence of reentrant SVT and bypass tract formation in the setting of preserv

119 electrophysiology studies revealed reentrant SVT in E990G mice.

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

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

122 flecainide and sotalol to control refractory SVT.

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

124 However, how phytohormones regulate SVT regeneration is still unknown.

125 ated these two hormones interact to regulate SVT regeneration.

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

127 ferent from patients with nonvaccine-related SVT, with lower incidence of prothrombotic conditions, h

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

129 SZ or GTSZ where free from supraventricular (SVT) or VT during the 6-month baseline period.

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

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

132 ommon cause of supraventricular tachycardia (SVT) and can lead to sudden cardiac death in otherwise h

133 g infants with supraventricular tachycardia (SVT) are limited.

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

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

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

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

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

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

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

141 -8 years) with supraventricular tachycardia (SVT) underwent catheter ablation.

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

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

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

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

146 , 67 (37%) had supraventricular tachycardia (SVT), and 56 (31%) had nonsustained ventricular tachycar

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

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

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

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

151 esponse during supraventricular tachycardia (SVT).

152 % of pediatric supraventricular tachycardia (SVT).

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

154 patients with supraventricular tachycardias (SVT).

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

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

157 e I error rates in both single variant test (SVT) and gene-based tests, followed by Firth logistic re

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

159 This study highlights that SVT genes, especially SYNJ1, may be promising markers in

160 D (P < 0.05), and PPI analysis revealed that SVT genes PPP2CA, SYNJ1, NSF and PPP3CB were the top fou

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

162 The SVT mapping with the magnetic catheter was successful in

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

164 73.3% to 82.3%) with the GEE method, and the SVT positive predictivity was 100.0% (911 of 911, n=101;

165 ablation is effective in management of these SVTs.

166 Besides CVST, splanchnic vein thromboses (SVT) and other thromboembolic events have been observed.

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

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

169 rst or recurrent splanchnic vein thrombosis (SVT) following a recent SARS-CoV-2 vaccination within th

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

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

172 Treatment of splanchnic vein thrombosis (SVT) is challenging, and evidence to guide therapeutic d

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

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

175 17F screening in splanchnic vein thrombosis (SVT) patients without typical hematologic MPN features i

176 a diagnosis of superficial vein thrombosis (SVT).

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

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

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

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

181 ecular changes of secondary vascular tissue (SVT) regeneration after large-scale bark girdling in tre

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

183 allow dual pathway physiology to progress to SVT.

184 is related to synaptic vesicle trafficking (SVT) dysfunction in PD (P < 0.05), and PPI analysis reve

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

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

187 Taken together, the in vitro SVT regeneration system allows us to make use of various

188 Here, we established a novel in vitro SVT regeneration system in the hybrid aspen (Populus tre

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

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

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

192 ermine incidence and factors associated with SVT recurrence.

193 Twenty-nine patients were identified with SVT occurring with a median of 11 days (range 2-76) afte

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

195 Infants with SVT are most likely to be diagnosed at <=60 days and be

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

197 ata from a pre-COVID cohort of patients with SVT (N=436) were used for comparison of clinical present

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

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

200 % in patients with PeAF, 3% in patients with SVT, and 0% in control patients with AF (p = 0.03).

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

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

203 agnostic work-up in patients presenting with SVT.

204 b resection and scalenectomy presenting with SVT.

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

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

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

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