ライフサイエンスコーパス: endoleak

1 formed immediately to identify the suspected endoleak.

2 egardless of the size, pressure, and type of endoleak.

3 t accumulation in the aneurysm sac, denoting endoleak.

4 as positive, negative, or indeterminate for endoleak.

5 two radiologists blinded to the diagnosis of endoleak.

6 esence or absence of immediate postoperative endoleak.

7 and procedure-related complications such as endoleak.

8 re the most sensitive criteria for detecting endoleaks.

9 erage CT data for the presence or absence of endoleaks.

10 -average venous CT data revealed six type II endoleaks.

11 ot be necessary for the routine detection of endoleaks.

12 arterial phase images depicted no additional endoleaks.

13 There were 22 type II and 17 type I or III endoleaks.

14 rred in two patients, each with two separate endoleaks.

15 Duplex US demonstrated six of the seven endoleaks.

16 lay an important role in the pathogenesis of endoleaks.

17 w in the IMA is responsible for many type II endoleaks.

18 (LA), complex LA, and complex IMA-LA type II endoleaks.

19 sociated with the development of IMA type II endoleaks.

20 ic (CT) angiography studies revealed type II endoleaks.

21 measurements in the aorta and the detectable endoleaks.

22 S enabled correct classification of 26 of 33 endoleaks.

23 sac size and in patients with type I or III endoleaks.

24 Imaging is critical for detecting endoleaks.

25 CE US depicted 33 endoleaks.

26 rysms (EVAR) is mainly aimed at detection of endoleaks.

27 Six proximal endoleaks (14.3%) occurred.

28 12 +/- 9), 21 secondary procedures to treat endoleak (20) or to maintain graft limb patency (1) were

29 hes before EVAR than did patients without an endoleak (3.6 +/- 1.7 vs 2.2 +/- 1.4; P < .001).

30 sac rupture 5 (4%), graft migration/ type I endoleak 37 (28%), persistent type II endoleak 40 (38%),

31 type I endoleak 37 (28%), persistent type II endoleak 40 (38%), endotension with sac growth 5 (4%), a

32 systemic inflammatory disease developed more endoleaks (45.1% vs 17.9%; P = .02) and late sac expansi

33 ond +/- 0.83) compared with that for type II endoleaks (9.17 seconds +/- 3.59, P < .0001).

34 e, 60-89 years; mean, 78.5 years) who had an endoleak after endoaortic graft implantation for treatme

35 ment, and outcomes of the different types of endoleaks after endovascular abdominal aortic aneurysm r

36 etrospectively evaluated for the presence of endoleaks after endovascular treatment of AAAs in 33 pat

37 iscusses the different treatment options for endoleaks after EVAR.

38 t predictors of AAA sac enlargement included endoleak, age >/= 80 years, aortic neck diameter >/= 28

39 ct identification of 22 (100%) of 22 type II endoleaks, all of which contained a PTC.

40 CT angiography revealed a total of seven endoleaks, all of which were prospectively classified as

41 bles further characterization of the type of endoleak and facilitates appropriate clinical care.

42 values were significantly different between endoleak and organized or fresh thrombus areas (P < .000

43 Significant endoleak, defined as endoleak and sac diameter increase of 0.5 cm or greater.

44 m sac enlargement are complex IMA-LA type II endoleak and the diameter of the largest feeding and/or

45 NIVE may be able to help characterize endoleak and thrombus organization, regardless of the si

46 guration were compared with the formation of endoleaks and adverse clinical events.

47 Endoleaks and in-stent thrombus of thoracic aorta were d

48 dynamic information differentiates types of endoleaks and shows high diagnostic performance.

49 ment the presence and development of type II endoleaks and the maximal orthogonal aneurysmal sac size

50 rmed every 3-12 months for the evaluation of endoleaks and the maximal sac diameter.

51 aneurysm model containing a stent, simulated endoleaks, and an intraluminal thrombus.

52 ions, perioperative complications and death, endoleaks, and results at 3, 6, and 12 months.

53 ative postoperative scans increases, but new endoleaks are identified as late as 7 years following EA

54 RECENT FINDINGS: Endoleaks are the most frequent complication after EVAR,

55 verall, CT enabled correct identification of endoleaks as type II or type I or III in 37 (95%) of 39

56 Endoleaks associated with minimal aortic volume increase

57 ynamic CT angiography phases (minimum, seven endoleaks at 2 seconds after the bolus-tracking threshol

58 er the bolus-tracking threshold; maximum, 44 endoleaks at 27 seconds after the bolus-tracking thresho

59 The arterial phase images also depicted no endoleaks at these examinations.

60 eter was positively associated with risk for endoleak (B = 0.072, P = 0.04).

61 after EVAR is required to diagnose and treat endoleaks before they result in aneurysm rupture.

62 ded by significant risks of implantation and endoleak, but the patients' acceptance of the technique

63 The majority of endoleaks can be treated with endovascular techniques, a

64 The majority of endoleaks can be treated with endovascular techniques.

65 Endovascular repair for AAA is limited by endoleak caused by inflow or outflow malapposition.

66 CT serves as an adequate screening test for endoleak, causing volumetric increase of more than 2% fr

67 e and negative predictive values for type II endoleak cavities with an ECVDEP of less than 0.5 mL for

68 nt of CE US and CT angiographic findings for endoleak classification.

69 a significantly increased detection rate of endoleaks compared with the detection rates at the time

70 Endoleaks continue to be a challenge and this article di

71 Risk for endoleak declines as the number of negative postoperativ

72 Significant endoleak, defined as endoleak and sac diameter increase

73 l of 52 patients (24%) who underwent EAR had endoleak detected during postoperative follow-up, which

74 l subtraction angiography all have a role in endoleak detection and management.

75 ew will focus on imaging techniques used for endoleak detection and the role imaging surveillance pla

76 e predictive value, and accuracy of CE US in endoleak detection were 97%, 100%, 100%, 98%, and 99%, r

77 ive values, and accuracy were determined for endoleak detection, and Cohen kappa statistic was used t

78 od sensitivity, specificity, and accuracy in endoleak detection, and it might represent a noninvasive

79 dies was negatively associated with risk for endoleak development (B = -3.122, P < 0.001), while incr

80 Endoleak development is a complication of EVAR and repre

81 ssion were used with the end point being new endoleak development.

82 the natural history of and risk factors for endoleak development.

83 s an adjunct to CT angiography in evaluating endoleaks, duplex US provides hemodynamic information th

84 nations performed in 67 patients revealed no endoleak during the venous phase.

85 chieved when the contrast between aortic and endoleak enhancement reached its maximum.

86 lus-tracking threshold, and the highest mean endoleak enhancement was achieved 22 seconds after the b

87 een patency of sac feeders and rate of early endoleak, especially type 2.

88 of patients after EVAR is critical to detect endoleaks for the patient's benefit and to determine the

89 e left subclavian artery), two with type IIo endoleak formation (from other arteries), and three with

90 type Ib endoleak formation, six with type II endoleak formation (from the left subclavian artery), tw

91 f the 64 patients, including 14 with type Ia endoleak formation, one with type Ib endoleak formation,

92 type Ia endoleak formation, one with type Ib endoleak formation, six with type II endoleak formation

93 rom other arteries), and three with type III endoleak formation.

94 One, 6-, 12-, and 24- month endoleak-free survival was 90%, 80%, 77%, and 73%, respe

95 m from aneurysm-related death, type I or III endoleak, graft infection or thrombosis, rupture, or con

96 Patients with an IMA type II endoleak had significantly more patent aortic side branc

97 Ten (62.5%) of the 16 endoleaks have sealed spontaneously during the follow-up

98 in three patients, additional treatment for endoleak in eight patients, and stent-graft collapse or

99 atistically significant predictor of type II endoleak in most patients.

100 cess rate for all indications except type II endoleak in which the initial intervention was successfu

101 Patients without complex IMA-LA type II endoleak in whom the largest feeding and/or draining art

102 m and patients with a complex IMA-LA type II endoleak in whom the largest feeding and/or draining art

103 c, and complete image sets were negative for endoleaks in 100%, 80%, and 100% of patients, respective

104 Sixteen (80%) of the 20 endoleaks in 14 patients were managed with continued obs

105 CT angiography depicted 34 endoleaks in 16 patients (type IA, n=1; type IB, n=1; ty

106 oleak was created in four aneurysms; type II endoleak, in 13 aneurysms; and no endoleak, in one aneur

107 s; type II endoleak, in 13 aneurysms; and no endoleak, in one aneurysm.

108 ong-term follow-up (n = 6) to classify their endoleak into a specific type.

109 Endoleak is a common complication of EAR that can lead t

110 graphy revealed that the peak enhancement of endoleaks is significantly different than that of the ao

111 e used to identify leaks since patients with endoleak may require additional endovascular interventio

112 ly different than that of the aorta and that endoleaks may not be adequately evaluated with conventio

113 r (P < .01) in patients with a type Ia or II endoleak (mean length, 14.3 and 13.9 mm, respectively) t

114 9 mm, respectively) than in patients without endoleaks (mean length, 8.4 mm).

115 The incidence of endoleak, migration, aneurysm enlargement, and graft pat

116 that arterial phase imaging would depict an endoleak missed at venous phase imaging.

117 tion or fabric tear with a subsequent type 3 endoleak (n = 1), and a persistent type 2 endoleak (n =

118 3 endoleak (n = 1), and a persistent type 2 endoleak (n = 13).

119 without occurrence of a clinically relevant endoleak (n = 183).

120 Other late complications included type 1 endoleak (n = 7), aortoduodenal fistula (n = 2), graft t

121 Types I and III high-pressure endoleaks (n = 10) showed a 10.0% (95% CI: 5.0%, 18.2%)

122 Type II low-pressure endoleaks (n = 37) showed a 5.4% (95% CI: 4.6%, 6.2%) in

123 Endoleak occurred in 32.9% of the patients.

124 sac enlargement were complex IMA-LA type II endoleak (odds ratio [OR] = 10.29, P = .004) and the dia

125 as significantly associated with significant endoleak (odds ratio, 5.18; 95% CI, 1.56-17.16; P = .007

126 isceral branches and there was an absence of endoleak on 3-month and 6-month surveillance computed to

127 Endoleaks on contrast material-enhanced images were cons

128 Of 17 type I or III endoleaks, only two (12%) contained a PTC and were miscl

129 e group) and 40 patients without evidence of endoleak or aneurysm enlargement (negative group).

130 ir (EAR) requires long-term surveillance for endoleak or increase in aneurysm diameter.

131 m repair could place the patient at risk for endoleak or sac rupture.

132 No endoleaks or aneurysm enlargement was noted either predi

133 Intervention for other endoleaks or endotension is indicated if the aneurysm sa

134 ratio OR, 6.9; P = 0.004) and device-related endoleak (OR, 16.06; P = 0.009).

135 n devices (OR, 1.2; P < 0.01) and late onset endoleak (OR, 64; P < 0.001).

136 ial strains over consecutive heart cycles in endoleak, organized thrombus, and fresh thrombus areas w

137 with the risk of developing a type Ia or IIa endoleak (P < .01).

138 enal dysfunction, renal artery occlusion, or endoleaks (P > .05).

139 not influence the development of IMA type II endoleaks (P = .51).

140 scular treatment of AAAs in 33 patients with endoleak (positive group) and 40 patients without eviden

141 sed from zero to three to four to six, total endoleak rate increased from 6% (one of 17) to 35% (30 o

142 , the total endoleak rate was 17% and type 2 endoleak rate was 13%, as compared with 60% and 50%, res

143 ith zero to three lumbar arteries, the total endoleak rate was 17% and type 2 endoleak rate was 13%,

144 The initial endoleak rate was 22% versus 20%, based on the first CT

145 Relationships of early endoleak rate with total branch vessel, IMA, and lumbar

146 rom 6% (one of 17) to 35% (30 of 86); type 2 endoleak rate, from 0% to 25%.

147 as significantly associated with total early endoleak rate.

148 significantly higher early total and type 2 endoleak rates after stent-graft repair of AAAs; thus, p

149 d with significantly higher total and type 2 endoleak rates: With zero to three lumbar arteries, the

150 y-two patients had a secondary procedure for endoleak repair of which three were conversions to surgi

151 Endoleaks represent blood flow outside the stent-graft l

152 Type I and III endoleaks require urgent intervention to prevent aneurys

153 isk for postoperative complications, type II endoleak, sac expansion, and additional interventions af

154 was found between strain values and type of endoleak, sac pressure, endoleak size, and aneurysm size

155 ith the uniphasic/unenhanced set, three (9%) endoleaks (seen only on delayed phase images) were misse

156 At CT, endoleak shape (tubular or nontubular) and location (cen

157 expansion should be monitored carefully and endoleak should be suspected.

158 Type I endoleaks showed significantly earlier mean peak contras

159 n values and type of endoleak, sac pressure, endoleak size, and aneurysm size.

160 Areas of endoleak, solid organized thrombus, and fresh thrombus w

161 plications, the most common of which include endoleaks, stenosis or thrombosis at the stagraft and it

162 The 36-month rates of freedom from endoleaks, surgical conversion, and secondary interventi

163 Eight of 50 patients (16%) had type II endoleaks that were attributed to retrograde flow in the

164 ined a PTC and were misclassified as type II endoleaks; the remaining 15 (88%) were correctly classif

165 In 56 (49.5%) of 113 CT studies in type II endoleaks, there was an interval increase in ASV.

166 assess associations between CT findings and endoleak type.

167 An endoleak was classified as type II if it contained a per

168 Type I endoleak was created in four aneurysms; type II endoleak

169 ke and paraplegia occurred each in 8.0%, and endoleak was diagnosed in 18.4% of patients within the f

170 If an endoleak was identified at 30-day postoperative computed

171 With the biphasic set, one (3%) endoleak was interpreted as indeterminate.

172 t enhancement within the stent lumen and the endoleak was measured.

173 No clinically important endoleak was missed at CE US.

174 ase images were evaluated to determine if an endoleak was present.

175 Endoleak was responsible for 66% of EVAR reinterventions

176 independent predictors, risk for IMA type II endoleaks was determined with a sensitivity of 78% (39 o

177 The attenuation of the endoleaks was higher during the 80-kVp acquisition (P <

178 sensitivity and specificity for detection of endoleaks was optimal for centerline diameter (64.3% and

179 The incidence of these endoleaks was significantly higher in patients with grea

180 imaging would contribute to the diagnosis of endoleak were determined.

181 Twenty-five of the 28 endoleaks were also visualized during the arterial phase

182 diagnostic performance for the detection of endoleaks were calculated for time-resolved CT angiograp

183 and/or draining arteries were measured, and endoleaks were classified according to their sources int

184 stent-grafts were successfully deployed, and endoleaks were clearly depicted in the last follow-up el

185 Seventeen of 19 abdominal endoleaks were confirmed with CE US.

186 Twenty-eight type II endoleaks were detected by using combined nonenhanced an

187 Endoleaks were detected in 26 (40%) of the 64 patients,

188 Endoleaks were detected visually in all scan phases; the

189 Endoleaks were detected with helical computed tomographi

190 In total, 44 endoleaks were detected.

191 Within the positive group, endoleaks were diagnosed with the uniphasic/unenhanced,

192 Four (20%) of the 20 endoleaks were embolized secondary to an increasing aneu

193 Four thoracic and 19 abdominal endoleaks were identified by using time-resolved CT angi

194 Twenty type II endoleaks were identified in 16 (19%) of the 83 patients

195 At 3 months, endoleaks were more common in the older age group (P = 0

196 Endoleaks were observed in 80 (50%) of 159 patients (59

197 nd treatment in all patients in whom type II endoleaks were observed.

198 the abdominal aorta and of the region of the endoleaks were obtained.

199 Endoleaks were present in 82 patients (42%) at discharge

200 Three type II endoleaks were seen only during the venous phase.

201 isitions contribute to accurate diagnosis of endoleaks when combined with an arterial phase acquisiti

202 s who were observed for this interval had no endoleaks, whereas one patient (patient 3) showed a smal

203 e 2 patients with growth included a type III endoleak (which resolved after treatment) and pressuriza

204 acquisition enables detection of additional endoleaks, while an unenhanced acquisition helps elimina

205 ; age range, 52-85 years) with early type II endoleak who had undergone EVAR between December 2002 an

206 Type II endoleaks with a stable or decreased aneurysmal sac size

207 hy was performed in patients who had type II endoleaks with an increase in aneurysm sac size and in p

208 The association of IMA type II endoleaks with each variable was analyzed by using univa

209 (P < .001) in type II than in type I or III endoleaks, with a sensitivity, specificity, accuracy, ne

210 Endoleaks without these features were classified as type