ライフサイエンスコーパス: TCFA

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

2 0% of PR and 40% of TCFA; only 5% PR and 10% TCFA were <50% narrowed.

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

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

5 .92; 95% confidence interval, 0.87-0.97) and TCFA (area under the curve, 0.86; 95% confidence interva

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

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

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

9 ment enhances the ability of IVOCT to detect TCFA.

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

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

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

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

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

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

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

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

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

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

20 IVOCT and histological TCFA images were coregistered and compared.

21 >1 quadrant), only 8 were true histological TCFA.

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

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

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

25 </=85 mum over 3 continuous frames improved TCFA identification, with diagnostic accuracy of 89.0%.

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

27 whether combining these modalities improves TCFA identification.

28 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).

29 1.03+/-0.85 mm(2); P=0.02) were increased in TCFA versus other fibroatheroma.

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

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

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

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

34 ight to create the false appearance of IVOCT TCFA.

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

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

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

38 ion of CT prevented direct identification of TCFA.

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

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

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

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

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

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

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

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

47 .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

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

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

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

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

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

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

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

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

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

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

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

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

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

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