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1 </=4 mm(2), noncalcified VH-defined thin-cap fibroatheroma).
2 P=0.02) were increased in TCFA versus other fibroatheroma.
3 dvanced coronary plaques, including thin cap fibroatheroma.
4 urbance needed for the formation of thin cap fibroatheroma.
5 r of such lesions is an inflamed thin-capped fibroatheroma.
6 ex (LI), fibrous cap thickness, and thin-cap fibroatheroma.
7 e was the independent predictor for thin-cap fibroatheroma.
8 often on pathological intimal thickening or fibroatheromas.
9 cur mainly among lesions defined as thin-cap fibroatheromas.
10 plaques and in fibrous caps of necrotic core fibroatheromas.
11 aracterizing plaque and identifying thin-cap fibroatheromas.
12 with intraplaque hemorrhage, and in thin-cap fibroatheromas.
13 ed with rupture, now referred to as thin-cap fibroatheromas.
15 1.5 versus 10.2+/-4.7; P<0.001) and thin-cap fibroatheroma (14.0+/-8.9 versus 11.6+/-4.5; P=0.02).
16 microm; P=0.57), the prevalence of thin-cap fibroatheroma (26.5% versus 25.2%; P=0.85), and microcha
19 us 92%), necrotic core (80% versus 65%), and fibroatheroma (80% versus 79%) was comparable with VH-IV
20 02), and in noncalcified VH-defined thin-cap fibroatheroma (9.23 [7.33-11.44] versus 7.65 [6.45-8.62]
25 arc on OCT was an excellent discriminator of fibroatheroma (area under the curve, 0.92; 95% confidenc
28 r and had more plaque volume, more thick-cap fibroatheroma, but fewer nonculprit lesion major adverse
29 s higher in noncalcified VH-defined thin-cap fibroatheroma compared with thick-cap fibroatheromas (me
31 y atherosclerotic plaques, including stable (fibroatheroma [FA]; n = 105), vulnerable (thin-cap fibro
32 cy intravascular ultrasonography as thin-cap fibroatheromas (hazard ratio, 3.35; 95% CI, 1.77 to 6.36
35 s were identified as fibroatheroma, thin-cap fibroatheroma, intraplaque hemorrhage with or without ru
36 eful consideration of OCT features mimicking fibroatheroma lesions and imaging artifacts contributed
37 in-cap fibroatheroma compared with thick-cap fibroatheromas (median [Q1-Q3], 8.44 [6.97-10.64] versus
38 seven regions-of-interest were classified as fibroatheroma on histology, with 22 meeting criteria for
39 Unstable lesions characterized as thin-cap fibroatheromas or plaque rupture were more frequent in B
40 ly angiographically mild, most were thin-cap fibroatheromas or were characterized by a large plaque b
41 istic regression analysis confirmed thin-cap fibroatheroma (OR 29.7, 95% CI 1.4 to 32.1), intrastent
48 ish the vulnerable features such as thin-cap fibroatheroma, suggesting the necessity of complementary
49 d vulnerable lesions, defined as thin-capped fibroatheroma (TCFA) and ruptured plaque, in human coron
52 les the acute plaque rupture is the thin cap fibroatheroma (TCFA), which is characterized by a necrot
53 The decorrelation time constants of thin-cap fibroatheromas (TCFA) (tau=47.5+/-19.2 ms) were signific
54 er, although VH-IVUS could identify thin-cap fibroatheromas (TCFA) with a diagnostic accuracy of betw
55 theroma [FA]; n = 105), vulnerable (thin-cap fibroatheroma [TCFA]; n = 88), and disrupted plaques (pl
56 capped fibroatheroma (VH-TCFA), thick-capped fibroatheroma (ThCFA), fibrotic plaque, and fibrocalcifi
57 classification does not include the thin cap fibroatheroma, the most common form of high-risk, vulner
58 Atherosclerotic plaques were identified as fibroatheroma, thin-cap fibroatheroma, intraplaque hemor
61 alse IVOCT TCFA and caused both thick-capped fibroatheromas to appear as TCFA, and the appearance of
62 atients who had stable angina with thick-cap fibroatheroma treated by DES were selected as controls.
65 hickening (PIT), VH-IVUS-derived thin-capped fibroatheroma (VH-TCFA), thick-capped fibroatheroma (ThC
66 que hemorrhages with or without and thin-cap fibroatheroma (vulnerable plaque), whereas in erosions a
69 ear stress promotes the development of early fibroatheromas, which subsequently follow an individuali
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