ライフサイエンスコーパス: culprit lesion

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

2 logy may potentially refine treatment of the culprit lesion.

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

4 he epicardial coronary artery containing the culprit lesion.

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

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

7 ruptured plaques in arteries other than the culprit lesion.

8 t culprits and those without an identifiable culprit lesion.

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

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

11 +CD28null, are preferentially recruited into culprit lesions.

12 aring patients with and without identifiable culprit lesions.

13 Where is the culprit lesion?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilizati

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

31 Coronary culprit lesions are significantly less frequent in AIS p

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

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

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

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

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

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

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

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

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

41 Culprit lesions from 40 cases of sudden coronary death w

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

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

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

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

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

47 Culprit lesions identified in 200 patients were classifi

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

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

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

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

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

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

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

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

56 Characterization of culprit lesions in various coronary syndromes reveals th

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

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

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

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

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

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

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

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

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

66 % versus 69+/-10%, P<0.001) were observed in culprit lesions of ACS patients compared with nonculprit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 Culprit lesions were identified by a combination of ECG,

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

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

102 Culprit lesions were predominantly hypoechoic (63.2% ver

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

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

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