ライフサイエンスコーパス: culprit lesion

1 erval [CI]: 1.09 to 1.93 for new vs. initial culprit lesion).

2 t culprits and those without an identifiable culprit lesion.

3 ary artery and unclear identification of the culprit lesion.

4 spitalized after successful treatment of the culprit lesion.

5 e revascularization or treatment of the only culprit lesion.

6 ndings were confirmed in ACS explored at the culprit lesion.

7 ents with AIS and angiographic evidence of a culprit lesion.

8 logy may potentially refine treatment of the culprit lesion.

9 xhibit similar (multiple) plaques beyond the culprit lesion.

10 he epicardial coronary artery containing the culprit lesion.

11 coronary syndrome (ACS) in patients without culprit lesion.

12 in whom coronary angiography does not show a culprit lesion.

13 ruptured plaques in arteries other than the culprit lesion.

14 aring patients with and without identifiable culprit lesions.

15 ites and subsequent coronary events from new culprit lesions.

16 4% [19 of 43 participants]) despite more LAD culprit lesions.

17 , and also the degree of inflammation in the culprit lesions.

18 ng techniques might thus fail to detect such culprit lesions.

19 +CD28null, are preferentially recruited into culprit lesions.

20 Where is the culprit lesion?

21 ntifiable culprit (37%) or multiple apparent culprit lesions (14%).

22 s with AIS were less likely to have coronary culprit lesions (7 of 29 versus 23 of 29; P<0.001) or an

23 cipants as follows: class 1, plaque-mediated culprit lesion (82.5% of women; 94.9% of men); class 2,

24 rlying coronary anatomy and characterize the culprit lesion after non-Q-wave myocardial infarction (N

25 th coronary angiography after Q-wave MI, the culprit lesion after NQWMI has not been well characteriz

26 ularization) is superior to treatment of the culprit lesion alone.

27 eserve (FFR) is superior to treatment of the culprit lesion alone.

28 of coronary artery obstructions, location of culprit lesion and baseline coronary TIMI flow grade.

29 o heparin reduced the thrombus burden of the culprit lesion and improved distal perfusion in patients

30 Although the culprit lesion and infarct-related artery often are easi

31 on model for the presence of an angiographic culprit lesion and internally validated with bootstrappi

32 atients with acute coronary syndrome without culprit lesion and proof of coronary spasm during 3 year

33 ACS patients without culprit lesion and proof of coronary spasm have an excel

34 al stent implantation characteristics at the culprit lesion and residual intrastent plaque/thrombus p

35 A consensus panel identified the culprit lesion and the infarct-related artery using pres

36 decisive link between plaque erosion at the culprit lesion and the manifestation of non-ST-segment e

37 ly attributable to recurrence at the site of culprit lesions and to nonculprit lesions.

38 ion of moderate stenoses, designation of the culprit lesion, and prediction of benefit from revascula

39 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilizati

40 Future culprit lesions are difficult to identify, however, and

41 Coronary culprit lesions are significantly less frequent in AIS p

42 s in acute coronary syndrome, especially for culprit lesions arising from the left coronary artery.

43 irst-time myocardial infarction with a clear culprit lesion at coronary angiography were prospectivel

44 ent than posterior papMI, most likely due to culprit lesions being restricted to a smaller portion of

45 Culprit lesions contained more thrombus (23.7% versus 3.

46 -year-old group (32% vs. 9%, p = 0.009), and culprit lesions contained more thrombus in this group (1

47 the macrophage densities at culprit and non-culprit lesions correlated significantly (r = 0.66, y =

48 An angiographic culprit lesion could not be identified in more than one-

49 e majority of acute coronary events, and the culprit lesions demonstrate distinct histopathologic fea

50 Thirty of 270 patients with culprit lesion died due to a cardiac cause (11.1%) and 1

51 ogressive angina) arising from untreated non-culprit lesions during follow-up.

52 vention (PCI; immediate group) or PCI of the culprit lesion followed by staged multivessel PCI of non

53 ent percutaneous coronary intervention for a culprit lesion, followed by intracoronary multimodality

54 omplications associated with stenting of the culprit lesion following ACS.

55 The ostial circumflex was the culprit lesion for target lesion revascularization in 34

56 A core laboratory examined the culprit lesions for intracoronary thrombus burden (prima

57 nt percutaneous coronary intervention of the culprit lesion, for 52 weeks in addition to high-intensi

58 Culprit lesions from 40 cases of sudden coronary death w

59 Patients with a culprit lesion had a higher mortality and more coronary

60 Six of 18 patients with a yellow culprit lesion had an adverse outcome compared with 1 of

61 Patients without an identifiable culprit lesion had severe coronary disease (obstructive

62 Noninvasive identification of culprit lesions has the potential to improve noninvasive

63 ocardiographic changes or an atherosclerotic culprit lesion identified during angiography.

64 Culprit lesions identified by OCT were classified as def

65 Culprit lesions identified in 200 patients were classifi

66 Events were adjudicated to be related to culprit lesions in 12.9% of patients and to nonculprit l

67 on morphology and plaque composition between culprit lesions in ACS and stable lesions in ACS or stab

68 (Thrombus Aspiration in Thrombus Containing Culprit Lesions in Non-ST-Elevation Myocardial Infarctio

69 Culprit lesions in patients with ACS (n = 14) had signif

70 aque was 71%, 92%, and 85%, respectively, in culprit lesions in patients with ACS and in stable lesio

71 Differences between culprit lesions in patients with ACS and stable lesions

72 receptor blocker, on the characteristics of culprit lesions in patients with unstable angina (UA) or

73 is detected in larger amounts in tissue from culprit lesions in patients with unstable compared to st

74 Characterization of culprit lesions in various coronary syndromes reveals th

75 ll by coronary segment, excluding those with culprit lesions in X-ray angiography.

76 rvention (PCI) is performed routinely on non-culprit lesions (in addition to the culprit lesion) or w

77 at approximately 50% of ACS patients without culprit lesion, in whom intracoronary acetylcholine prov

78 sion) or whether to restrict PCI only to the culprit lesion is a common dilemma.

79 rthermore, mortality was associated with the culprit lesion location (78.6% in left main lesion, 69.7

80 cending coronary artery (LAD) versus non-LAD culprit lesion location (median BNP level 40 vs. 24 pg/m

81 sions in patients with STEMI or NSTEMI after culprit lesion management.

82 ges indicating myocardial ischemia, an acute culprit lesion may be present and patients may benefit f

83 % CI 6.2-10.0) arising from 78 untreated non-culprit lesions (mean baseline angiographic diameter ste

84 coronary syndrome presentations and evolving culprit lesion morphologies and explores how advanced co

85 sus patients <65 years of age with regard to culprit lesion morphology in acute myocardial infarction

86 The analysis focused on patients with a culprit lesion (n = 270) and patients without a culprit

87 prit lesion (n = 270) and patients without a culprit lesion (n = 76) but with acetylcholine provocati

88 ion level and compared between precursors of culprit lesions, nonculprit lesions, and stable coronary

89 itive for glycophorin C, in single slides of culprit lesions obtained from the Athero-Express Biobank

90 ssed the prognostic impact of postprocedural culprit lesion OCT findings in patients with acute coron

91 ng thrombus were observed more frequently in culprit lesions of ACS patients (n=35) compared with non

92 % versus 69+/-10%, P<0.001) were observed in culprit lesions of ACS patients compared with nonculprit

93 Ruptured plaques in culprit lesions of ACS patients have smaller lumens; gre

94 plaque ruptures in 74 patients and compared culprit lesions of ACS patients with nonculprit lesions

95 ibe the pathological and imaging findings in culprit lesions of patients with acute coronary syndrome

96 Culprit lesions of patients, who have had an acute coron

97 e primary end point was presence of coronary culprit lesions on coronary angiograms as analyzed by in

98 rction and Multivessel Disease: Treatment of Culprit Lesion Only or Complete Revascularization), we r

99 In the CULPRIT-SHOCK trial (The Culprit Lesion Only PCI Versus Multivessel PCI in Cardio

100 In a subanalysis of the CULPRIT-SHOCK trial (Culprit Lesion Only PCI versus Multivessel PCI in Cardio

101 tified according to CA in the CULPRIT-SHOCK (Culprit Lesion Only PCI Versus Multivessel PCI in Cardio

102 The CULPRIT-SHOCK trial (Culprit Lesion Only PCI Versus Multivessel PCI in Cardio

103 up for intended nonculprit lesion PCI versus culprit lesion only PCI.

104 The CULPRIT-SHOCK (Culprit Lesion Only Percutaneous Coronary Intervention [

105 ong those who initially underwent PCI of the culprit lesion only than among those who underwent immed

106 ascularization strategies: either PCI of the culprit lesion only, with the option of staged revascula

107 ith complete revascularization compared with culprit-lesion only PCI (HR: 0.77; 95% confidence interv

108 e benefit of complete revascularization over culprit-lesion only PCI was consistent irrespective of t

109 andomized to staged nonculprit-lesion PCI or culprit-lesion only PCI.

110 p compared with 1376 patients (84.3%) in the culprit lesion-only group (absolute difference, 3.2% [95

111 nge, 8.9 [95% CI, 8.0-9.8]; P < .001) in the culprit lesion-only group (between-group difference, 0.9

112 red with 528 (11.5%) of 4577 patients in the culprit lesion-only group (hazard ratio [HR] 0.76 [95% C

113 sation group compared with 209 (4.6%) in the culprit lesion-only group (HR 0.76 [95% CI 0.62-0.93], p

114 oup compared with 370 (8.1%) patients in the culprit lesion-only group (HR 0.85 [95% CI 0.73-0.99], p

115 revascularisation group vs 161 [3.5%] in the culprit lesion-only group; HR 0.98 [95% CI 0.78-1.22], p

116 ced new myocardial infarctions compared with culprit lesion-only PCI (255 [6.0%] vs 357 [7.8%]; HR 0.

117 d a multivessel PCI (MV-PCI) strategy with a culprit lesion-only PCI (CLO-PCI) strategy in patients w

118 Culprit lesion-only PCI is the preferred strategy, both

119 e revascularisation strategy (with PCI) to a culprit lesion-only PCI strategy, and enrolled patients

120 s cardiovascular death alone compared with a culprit lesion-only PCI strategy.

121 In the randomized trial, culprit lesion-only PCI was superior to immediate multiv

122 ed to complete revascularization and 2025 to culprit lesion-only PCI.

123 es major cardiovascular events compared with culprit lesion-only percutaneous coronary intervention (

124 f patients being angina-free compared with a culprit lesion-only strategy.

125 admission time, patients had a benefit from culprit-lesion-only as compared to immediate multivessel

126 ion group and in 159 patients (20.4%) in the culprit-lesion-only group (hazard ratio, 0.93; 95% confi

127 er percutaneous coronary intervention of the culprit-lesion-only or immediate multivessel percutaneou

128 arction, or unplanned revascularization than culprit-lesion-only PCI at 4.8 years.

129 as compared with 339 patients (16.7%) in the culprit-lesion-only PCI group (hazard ratio, 0.51; 95% C

130 with 213 of the 2025 patients (10.5%) in the culprit-lesion-only PCI group (hazard ratio, 0.74; 95% c

131 ed in 158 of the 344 patients (45.9%) in the culprit-lesion-only PCI group and in 189 of the 341 pati

132 The relative risk of death in the culprit-lesion-only PCI group as compared with the multi

133 , complete revascularization was superior to culprit-lesion-only PCI in reducing the risk of cardiova

134 evascularization and 778 assigned to receive culprit-lesion-only PCI.

135 larization at 1 year than those who received culprit-lesion-only PCI.

136 ble nonculprit lesions, versus a strategy of culprit-lesion-only percutaneous coronary intervention (

137 of major cardiovascular events compared with culprit-lesion-only percutaneous coronary intervention i

138 benefit of complete revascularization over a culprit-lesion-only percutaneous coronary intervention s

139 oint occurred in 56% of women treated by the culprit-lesion-only strategy versus 42% men, whereas 55%

140 ology-guided complete revascularization over culprit-lesion-only treatment was sustained at 3 years.

141 nic Shock) demonstrated superior outcome for culprit-lesion-only versus immediate multivessel percuta

142 ent MACEs were adjudicated to either treated culprit lesions or untreated nonculprit lesions.

143 to be related to either originally treated (culprit) lesions or untreated (nonculprit) lesions.

144 ced the intracoronary thrombus burden of the culprit lesions (OR=0.77, P=0.022), improved the perfusi

145 y on non-culprit lesions (in addition to the culprit lesion) or whether to restrict PCI only to the c

146 inically relevant; the identification of the culprit lesion; or whether the plaque (or patient) is at

147 resentation than subsurface infiltration for culprit lesions (p = 0.035) but not for remote lesions (

148 Following PCI of the culprit lesion, patients with STEMI and multivessel CAD

149 f 94) who underwent complete CAG followed by culprit lesion PCI (odds ratio, 4.4 [95% CI, 2.2-9.1]; P

150 r 51.1% of patients (46 of 90) who underwent culprit lesion PCI before CAG and for 19.1% of patients

151 patients (48.9%) were randomized to undergo culprit lesion PCI before CAG, and 94 (51.1%) were rando

152 Patients who underwent culprit lesion PCI before complete CAG had a shorter mea

153 In a subgroup analysis, the effect of culprit lesion PCI before complete CAG on the primary ou

154 randomized in a 1:1 ratio to undergo either culprit lesion PCI before complete CAG or complete CAG f

155 mized clinical trial of patients with STEMI, culprit lesion PCI before complete CAG resulted in short

156 ore complete CAG or complete CAG followed by culprit lesion PCI.

157 artery disease who had undergone successful culprit-lesion PCI to a strategy of either complete reva

158 Following culprit-lesion PCI, 4,041 patients with STEMI and multiv

159 identify the characteristics and outcomes of culprit lesion percutaneous coronary intervention (PCI)

160 udy programme investigates the impact of the culprit lesion phenotype on inflammatory profiles and pr

161 attenuation was significantly higher across culprit lesion precursors compared to nonculprit and sta

162 Culprit lesion precursors had larger total plaque volume

163 ttenuation is significantly increased across culprit lesion precursors in patients with acute coronar

164 Overall, 765 coronary lesions were analyzed (culprit lesion precursors: n=66; nonculprit lesion precu

165 cutaneous coronary intervention (PCI) of the culprit lesion reduces the risk of cardiovascular death

166 The primary end point was culprit lesion-related MACE (CL-MACE), defined as cardia

167 uch lesions were identified had a 4-year non-culprit lesion-related MACE rate of 13.2% (95% CI 9.4-17

168 ge lipid-rich cores by NIRS had a 4-year non-culprit lesion-related MACE rate of 7.0% (95% CI 4.0-10.

169 ed in 1,189 patients, and the 2-year rate of culprit lesion-related MACE was not significantly associ

170 n independent predictor of patient-level non-culprit lesion-related MACEs (adjusted odds ratio 2.27,

171 ts) was also an independent predictor of non-culprit lesion-related MACEs.

172 red in 18.0% of patients, of which 8.3% were culprit lesion-related, 10.7% were nonculprit lesion-rel

173 sed risk of myocardial infarction related to culprit lesion restenosis (4.3% versus 1.1% [OR, 3.78 (9

174 therapy; 158 of 344 patients (45.9%) in the culprit lesion revascularization-only group compared wit

175 Postprocedural OCT assessment of treated culprit lesion revealed at least one of these parameters

176 sible percutaneous coronary intervention of "culprit" lesions should always be used in combination wi

177 ymorphonuclear cells [PMNs]) accumulation in culprit lesion site (CLS) thrombus is a predictor of car

178 disruption, yellow color, or thrombus at the culprit lesion site can identify patients at high risk o

179 ellow color, disruption, and thrombus at the culprit lesion site were associated with an eightfold in

180 d odds ratio 2.27, 95% CI 1.25-4.13) and non-culprit lesion-specific MACEs (7.83, 4.12-14.89).

181 an abundant leukocyte enzyme, is elevated in culprit lesions that have fissured or ruptured in patien

182 Among the culprit lesions, the overall incidence of apoptosis in f

183 In patients without culprit lesion, there was no cardiac death or nonfatal m

184 cutaneous coronary intervention (PCI) of the culprit lesion to receive either FFR-guided complete rev

185 cutaneous coronary intervention (PCI) of the culprit lesion to receive either physiology-guided compl

186 l Flow Reserve Hemodynamic Assessment of Non-Culprit Lesions to Better Predict Adverse Event Outcomes

187 Plaques were dissected, and the culprit lesions used for histology and the measurement o

188 tistical evidence for effect modification by culprit lesion vessel (P=0.8).

189 The culprit lesion was defined by reviewing each patient's a

190 A definite or possible culprit lesion was identified by OCT in 46.2% (67/145) o

191 e obstructive CAD, but a single identifiable culprit lesion was identified in <50% of patients.

192 A single culprit lesion was identified in only 49% of patients un

193 p < 0.001), including 5 patients in whom the culprit lesion was not revascularized owing to coronary

194 Angioscopic characterization of the culprit lesion was performed before PTCA in 32 patients

195 se outcome compared with 1 of 24 in whom the culprit lesion was white (P = .03).

196 mong those with left circumflex or left main culprit lesions was 1.25 (95% CI, 1.02-1.53), for right

197 n this substudy, histological examination of culprit lesions was performed in 600 SCD victims whose d

198 Patients with a single identified culprit lesion were compared with those who had multiple

199 who had successful revascularization of the culprit lesion were enrolled between June 2018 and July

200 en June 10, 2014, and Dec 20, 2017, 3629 non-culprit lesions were characterised in 898 patients (153

201 c total occlusions, and those with uncertain culprit lesions were excluded.

202 Culprit lesions were identified by a combination of ECG,

203 Culprit lesions were longer (17.5+/-10.1, 9.8+/-4.0, and

204 her patients, whereas patients with multiple culprit lesions were more frequently treated with corona

205 Culprit lesions were predominantly hypoechoic (63.2% ver

206 Multiple culprit lesions were seen in 14% of patients.

207 Untreated lesions (also known as non-culprit lesions) were identified by intravascular ultras

208 Associations of the likelihood of being a culprit lesion with both plaque contrast enhancement and

209 e myocardial infarctions develop at sites of culprit lesions without a significant stenosis.