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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.
14 s (37.5% versus 20.0%; P=0.019) and thin-cap fibroatheroma (12.5% versus 2.0%; P=0.037).
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
17                           Moreover, thin-cap fibroatheroma (64.7% versus 14.9%, P<0.001), macrophage
18         FD-OCT analysis showed that thin-cap fibroatheroma (76.2% versus 41.4%; P=0.017) prior to PCI
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]
21                         Combining VH-defined fibroatheroma and fibrous cap thickness </=85 mum over 3
22                                     Thin cap fibroatheromas are common in patients with high total ch
23 ency, and precise location of these thin-cap fibroatheromas are further discussed in detail.
24                                     Thin cap fibroatheromas are most frequently observed in patients
25 arc on OCT was an excellent discriminator of fibroatheroma (area under the curve, 0.92; 95% confidenc
26          This review focuses on the thin-cap fibroatheroma, as a specific cause of acute coronary syn
27          In conclusion, presence of thin-cap fibroatheroma at pre-PCI FD-OCT and of intrastent thromb
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
30                    The frequency of thin-cap fibroatheroma (defined by lipid-rich plaque with cap thi
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
33 brous cap, and higher prevalence of thin-cap fibroatheroma in humans.
34                            Although thin-cap fibroatheromas in men clustered within proximal arterial
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
42 ted well with cap thickness in necrotic core fibroatheromas (P>0.05).
43 raplaque hemorrhage (P=0.04) and in thin-cap fibroatheromas (P=0.038).
44                                     Thin-cap fibroatheroma prevalence decreased from 20.0% to 7.1% (p
45  0.001) and in fibrous caps of necrotic core fibroatheromas (r = 0.68, p < 0.001).
46                                     Thin cap fibroatheroma regions demonstrated significantly lower s
47           Fibrous cap thickness and thin-cap fibroatheroma showed no significant difference among the
48 ish the vulnerable features such as thin-cap fibroatheroma, suggesting the necessity of complementary
49                                     Thin-cap fibroatheroma (TCFA) and plaque rupture have been recogn
50 d vulnerable lesions, defined as thin-capped fibroatheroma (TCFA) and ruptured plaque, in human coron
51                                     Thin-cap fibroatheroma (TCFA) are the unstable lesions in coronar
52          We hypothesize that non-thin-capped fibroatheroma (TCFA) causes may scatter light to create
53                                     Thin-cap fibroatheroma (TCFA) is a prominent risk factor for plaq
54 coherence tomography (OCT)-detected thin-cap fibroatheroma (TCFA) on clinical outcomes of diabetes me
55 sessment) or nonobstructive, and as thin-cap fibroatheroma (TCFA) or non-TCFA by optical coherence to
56                 Although rupture of thin-cap fibroatheroma (TCFA) underlies most myocardial infarctio
57 les the acute plaque rupture is the thin cap fibroatheroma (TCFA), which is characterized by a necrot
58 The decorrelation time constants of thin-cap fibroatheromas (TCFA) (tau=47.5+/-19.2 ms) were signific
59 er, although VH-IVUS could identify thin-cap fibroatheromas (TCFA) with a diagnostic accuracy of betw
60 theroma [FA]; n = 105), vulnerable (thin-cap fibroatheroma [TCFA]; n = 88), and disrupted plaques (pl
61 topsy studies have established that thin-cap fibroatheromas (TCFAs) are the most frequent cause of fa
62 almost 5-fold with consistent development of fibroatheromas that were sufficiently large to cause ste
63 accurately differentiate TCFA from thick-cap fibroatheroma (ThCFA) and not lipid rich plaque (non-LRP
64 capped fibroatheroma (VH-TCFA), thick-capped fibroatheroma (ThCFA), fibrotic plaque, and fibrocalcifi
65 classification does not include the thin cap fibroatheroma, the most common form of high-risk, vulner
66   Atherosclerotic plaques were identified as fibroatheroma, thin-cap fibroatheroma, intraplaque hemor
67 he technique to identify lipid-rich thin-cap fibroatheromas through blood.
68 ansive remodeling, which transforms an early fibroatheroma to a high-risk plaque.
69 alse IVOCT TCFA and caused both thick-capped fibroatheromas to appear as TCFA, and the appearance of
70 atients who had stable angina with thick-cap fibroatheroma treated by DES were selected as controls.
71 s, in which any lipid signal originates from fibroatheroma under the stent.
72 osis, as the lipid signal may originate from fibroatheroma underlying the stent.
73 hickening (PIT), VH-IVUS-derived thin-capped fibroatheroma (VH-TCFA), thick-capped fibroatheroma (ThC
74 que hemorrhages with or without and thin-cap fibroatheroma (vulnerable plaque), whereas in erosions a
75                                     Thin-cap fibroatheroma was more frequently observed in patients w
76  within proximal arterial segments, thin-cap fibroatheromas were evenly distributed in women.
77 ear stress promotes the development of early fibroatheromas, which subsequently follow an individuali
78 ge atherosclerotic plaques compared to early fibroatheroma with thick and protective fibrous caps in
79                                 In contrast, fibroatheromas with cores in a late stage of necrosis or