ライフサイエンスコーパス: TCFA

1 TCFA was defined as a lesion with mean fibrous cap thick

2 nal stenosis (area under the curve: FA, 1.0; TCFA, 0.89; PR, 0.90).

3 Among LRP patients, 98 (34.5%) had >=1 TCFA.

4 groups based on the presence or absence of 1 TCFA lesion.

5 0% of PR and 40% of TCFA; only 5% PR and 10% TCFA were <50% narrowed.

6 On a lesion level, there were 58 TCFAs among 150 obstructive nonculprit lesions compared

7 tructive nonculprit lesions compared with 74 TCFAs among 275 nonculprit lesions (adjusted TCFA preval

8 laque types (area under the curve: FA, 0.82; TCFA, 0.58; PR, 0.72).

9 eath are believed to arise from rupture of a TCFA followed by thrombosis.

10 TCFAs among 275 nonculprit lesions (adjusted TCFA prevalence: 35.4% versus 23.2%, P=0.022).

11 .92; 95% confidence interval, 0.87-0.97) and TCFA (area under the curve, 0.86; 95% confidence interva

12 oth thick-capped fibroatheromas to appear as TCFA, and the appearance of TCFAs when no lipid core was

13 hy other plaque components can masquerade as TCFA and cause low positive predictive value of IVOCT fo

14 reserve-negative lesions, patients carrying TCFA lesions represent only one-third of LRP patients an

15 Vessels demonstrating TCFA do not usually show severe narrowing but show posit

16 ment enhances the ability of IVOCT to detect TCFA.

17 studied the natural history of OCT-detected TCFA, ThCFA, and non-LRP in patients enrolled in the pro

18 cient resolution to accurately differentiate TCFA from thick-cap fibroatheroma (ThCFA) and not lipid

19 Thin-cap fibroatheroma (TCFA) and plaque rupture have been recognized as the mos

20 Thin-cap fibroatheroma (TCFA) are the unstable lesions in coronary artery diseas

21 Thin-cap fibroatheroma (TCFA) is a prominent risk factor for plaque rupture.

22 raphy (OCT)-detected thin-cap fibroatheroma (TCFA) on clinical outcomes of diabetes mellitus (DM) pat

23 nobstructive, and as thin-cap fibroatheroma (TCFA) or non-TCFA by optical coherence tomography criter

24 Although rupture of thin-cap fibroatheroma (TCFA) underlies most myocardial infarctions, reliable TC

25 laque rupture is the thin cap fibroatheroma (TCFA), which is characterized by a necrotic core with an

26 sions, defined as thin-capped fibroatheroma (TCFA) and ruptured plaque, in human coronary artery auto

27 othesize that non-thin-capped fibroatheroma (TCFA) causes may scatter light to create the false appea

28 = 105), vulnerable (thin-cap fibroatheroma [TCFA]; n = 88), and disrupted plaques (plaque rupture [P

29 n time constants of thin-cap fibroatheromas (TCFA) (tau=47.5+/-19.2 ms) were significantly lower than

30 IVUS could identify thin-cap fibroatheromas (TCFA) with a diagnostic accuracy of between 74% and 82%

31 ve established that thin-cap fibroatheromas (TCFAs) are the most frequent cause of fatal coronary eve

32 ty, specificity, and diagnostic accuracy for TCFA identification was 63.6%, 78.1%, and 76.5% for VH-I

33 a on histology, with 22 meeting criteria for TCFA.

34 e low positive predictive value of IVOCT for TCFA detection (47% for obtuse lipid arcs).

35 IVOCT and histological TCFA images were coregistered and compared.

36 >1 quadrant), only 8 were true histological TCFA.

37 Multivariable analyses identified TCFA as the strongest independent predictor of primary e

38 regression multivariable analysis identified TCFA as the strongest predictor of major adverse clinica

39 d not reliably classify plaques and identify TCFA, such that high-risk plaques may be misclassified o

40 al coherence tomography (IVOCT) can identify TCFA and assess cap thickness, which provides an opportu

41 Both VH-IVUS and OCT can reliably identify TCFA, although OCT accuracy may be improved using lipid

42 ificity of the LSI technique for identifying TCFAs were >90%.

43 </=85 mum over 3 continuous frames improved TCFA identification, with diagnostic accuracy of 89.0%.

44 mbined VH-IVUS/OCT imaging markedly improved TCFA identification.

45 whether combining these modalities improves TCFA identification.

46 f the primary endpoint was 13.3% and 3.1% in TCFA-positive vs. TCFA-negative groups, respectively (ha

47 ibrous cap thickness </=85 mum was higher in TCFA (6.5 [1.75-11.0] versus 2.0 [0.0-7.0]; P=0.03).

48 1.03+/-0.85 mm(2); P=0.02) were increased in TCFA versus other fibroatheroma.

49 In TCFAs the necrotic core length is approximately 2 to 17

50 ation was responsible for 70% of false IVOCT TCFA and caused both thick-capped fibroatheromas to appe

51 Other false IVOCT TCFA causes included smooth muscle cell-rich fibrous tis

52 As were identified, and sensitivity of IVOCT TCFA detection increased from 63% to 87%, and specificit

53 ight to create the false appearance of IVOCT TCFA.

54 Of 21 IVOCT TCFAs (fibrous cap <65 mum, lipid arc >1 quadrant), only

55 (obtuse) criterion was disregarded, 45 IVOCT TCFAs were identified, and sensitivity of IVOCT TCFA det

56 ong DM patients with 1 FFR-negative lesions, TCFA-positive patients represented 25% of this populatio

57 For nonobstructive lesions, TCFA lesions had similar lesion length (16.7 versus 14.6

58 ive TCFA-positive patients with FFR-negative TCFA-negative patients for a composite of cardiac mortal

59 The primary endpoint compared FFR-negative TCFA-positive patients with FFR-negative TCFA-negative p

60 and as thin-cap fibroatheroma (TCFA) or non-TCFA by optical coherence tomography criteria.

61 us 84.2 degrees , P<0.001) compared with non-TCFA.

62 Compared with obstructive non-TCFAs, obstructive TCFAs had similar lesion length (23.1

63 On a patient level, at least one obstructive TCFA was observed in 44/93 (47%) of patients.

64 ared with obstructive non-TCFAs, obstructive TCFAs had similar lesion length (23.1 versus 20.8 mm, P=

65 ea stenosis was seen in 70% of PR and 40% of TCFA; only 5% PR and 10% TCFA were <50% narrowed.

66 ystem may enhance the clinical evaluation of TCFA, as well as expand our understanding of coronary ar

67 ion of CT prevented direct identification of TCFA.

68 The majority of TCFA and ruptured plaque localized in the proximal third

69 Although the majority of TCFA were found in the 54- to 84-mum thickness group, th

70 mas to appear as TCFA, and the appearance of TCFAs when no lipid core was present.

71 repeatable, and comprehensive evaluations of TCFAs.

72 However, within LRP patients, TCFA patients had a much higher risk for primary end poi

73 id arcs (both obtuse and acute, <1 quadrant) TCFA, and we also propose new mechanisms involving light

74 erlies most myocardial infarctions, reliable TCFA identification remains challenging.

75 acy of between 74% and 82% (depending on the TCFA definition used), the spatial resolution of CT prev

76 Twenty-three TCFA and 19 ruptured plaques were found (mean +/- SD: 0.

77 H-IVUS-derived thin-capped fibroatheroma (VH-TCFA), thick-capped fibroatheroma (ThCFA), fibrotic plaq

78 .0 mm(2) [6.5 to 12.0 mm(2)], p < 0.001), VH-TCFAs (8.6 mm(2) [7.3 to 9.9 mm(2)] to 9.5 mm(2) [7.8 to

79 As, 2 became fibrotic plaque, and 5 (25%) VH-TCFAs remained unchanged.

80 were VH-TCFAs; during follow-up, 15 (75%) VH-TCFAs "healed," 13 became ThCFAs, 2 became fibrotic plaq

81 t differ between VH-TCFAs that healed and VH-TCFAs that remained VH-TCFAs.

82 plaque composition did not differ between VH-TCFAs that healed and VH-TCFAs that remained VH-TCFAs.

83 new VH-TCFAs developed; 6 late-developing VH-TCFAs were PITs, and 6 were ThCFAs at baseline.

84 Compared with VH-TCFAs that healed, VH-TCFAs that remained VH-TCFAs located more proximally (va

85 Most VH-TCFAs healed during 12-month follow-up, whereas new VH-T

86 ed during 12-month follow-up, whereas new VH-TCFAs also developed.

87 Conversely, 12 new VH-TCFAs developed; 6 late-developing VH-TCFAs were PITs, a

88 PITs, VH-TCFAs, and ThCFAs showed significant plaque progression

89 TCFAs that healed, VH-TCFAs that remained VH-TCFAs located more proximally (values are median [interq

90 As that healed and VH-TCFAs that remained VH-TCFAs.

91 At baseline, 20 lesions were VH-TCFAs; during follow-up, 15 (75%) VH-TCFAs "healed," 13

92 Compared with VH-TCFAs that healed, VH-TCFAs that remained VH-TCFAs locat

93 oint was 13.3% and 3.1% in TCFA-positive vs. TCFA-negative groups, respectively (hazard ratio 4.65; 9

94 Among FFR-negative patients, 98 (25%) were TCFA positive and 292 (75%) were TCFA negative.

95 (25%) were TCFA positive and 292 (75%) were TCFA negative.

96 the stable plaque (540 and 560 nm), whereas TCFA exhibited phospholipids/cholesterol (1040 nm, 1210

97 of low attenuation filled with lipids within TCFA.