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1  the 6th decade was due to sudden death with stable plaque).
2 sion, (ii) intraplaque haemorrhage, or (iii) stable plaque.
3 ad an intraplaque haemorrhage, and 52% had a stable plaque.
4 cin was higher in asymptomatic patients with stable plaque.
5 s and promotes efferocytosis and features of stable plaques.
6 , CXCL9 and SCGF-beta compared to those with stable plaques.
7 ate plaques with a high risk of rupture from stable plaques.
8 with previous descriptions of lymphocytes in stable plaques.
9 erial hemorrhage, which might be due to less stable plaques.
10 ured and eroded unstable plaques, but not in stable plaques.
11 + cells were associated with progressing and stable plaques.
12 reased collagen, which are characteristic of stable plaques.
13 l 147 [60 to 335]) compared to patients with stable plaque (16 [0 to 234] and 55 [36 to 157]; p < 0.0
14  R1 between the 3 and 12 weeks compared with stable plaque (50.80+/-7.2% versus 14.22+/-2.2%; P<0.001
15          Calcification was detected from the stable plaque (540 and 560 nm), whereas TCFA exhibited p
16 ratio [OR] 21), glycoslyated hemoglobin with stable plaque and healed infarct (P = 0.03, OR 41), TC w
17                                   Women with stable plaque and healed infarct had elevated glycosylat
18  a significant association in blacks between stable plaque and left ventricular hypertrophy (risk rat
19                            SLE patients with stable plaque and progressive plaque differed only in ba
20 e of thrombus (acute rupture, acute erosion, stable plaque), and heart weight.
21 icrog/mL in plaque erosion, 2.5 microg/mL in stable plaque, and 1.4 microg/mL in controls.
22 therothrombi, 71 sudden coronary deaths with stable plaque, and 158 control cases (unnatural sudden d
23 ing microparticles compared to patients with stable plaques, and may correlate with serum markers of
24 6 versus 0.47+/-0.02, P= 0.01) compared with stable plaque at 12 weeks.
25 otes repopulation of plaques with a SMC-rich stable plaque cell phenotype while reducing disease prog
26 ase 2, 3, 7, 9, 12, and 13 have more or less stable plaques, consistent with harmful or protective ef
27 t culprit unstable coronary plaques and four stable plaques from eight patients who had died suddenly
28 crimination of histologically vulnerable and stable plaques in this study suggests that NIR spectrosc
29 rosclerotic plaque without acute thrombosis (stable plaque) in 54.
30              The unstable plaque but not the stable plaque is invaded by clonally expanded T cells, s
31 l 78 [56 to 258] compared with patients with stable plaque (n = 14; 20 [0 to 251] and 55 [34 to 102];
32 lism was increased in unstable compared with stable plaque of both Bvra(+/+)Apoe(-/-) and Bvra(-/-)Ap
33 n rupture (P<0.0001), erosion (P=0.005), and stable plaque (P=0.0003) versus controls.
34 ltivariate analysis, atherothrombi (P=0.02), stable plaque (P=0.003), and plaque burden (P=0.03) were
35 ompared with 22 (41 percent) of the men with stable plaques (P<0.001).
36 ssion is associated with histologically more stable plaques (P=0.011).
37 trate that myeloid Acly deficiency induces a stable plaque phenotype characterized by increased colla
38 d atherosclerotic lesions and induced a more stable plaque phenotype, characterized by lower content
39 tion and oxidative stress, indicating a more stable plaque phenotype.
40 is, as well as reduced atherosclerosis and a stable plaque phenotype.
41 gen content was increased, indicating a more stable plaque phenotype.
42 oles, limiting plaque growth and promoting a stable plaque phenotype.
43 phage content in the plaque, indicative of a stable plaque phenotype.
44 lls and collagen, features consistent with a stable plaque phenotype.
45 humoral immunity leads to a smaller but less stable plaque phenotype.
46 compositional characteristics of a potential stable plaque phenotype.
47 feriority trial, adult patients with chronic stable plaque psoriasis (for >/=12 months) who were cand
48 ear stress (ESS) in the transition of early, stable plaques to high-risk atherosclerotic lesions.
49  eroded plaque with acute thrombus (n = 18), stable plaque with healed infarct (n = 18), and stable p
50 ture (P = 0.02, OR 7), and hypertension with stable plaque with healed infarct (P = 0.02, OR 15).
51 d plaques with acute thrombosis (n = 25) and stable plaques with and without healed myocardial infarc
52 ble plaque with healed infarct (n = 18), and stable plaque without infarction (n = 7).