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1 of necrosis, or thin-cap fibrous atheromas (vulnerable plaques).
2 ormation of other features characteristic of vulnerable plaque.
3 the treatment of coronary atherosclerosis or vulnerable plaque.
4 s a method for high-resolution assessment of vulnerable plaque.
5 e and may hold promise for identification of vulnerable plaque.
6 0.01 for all), but not with the presence of vulnerable plaque.
7 play an important role in the formation of a vulnerable plaque.
8 ructive nonculprit lesion containing complex vulnerable plaque.
9 of vascular remodeling in the prediction of vulnerable plaque.
10 ctivation in the development of noncalcified vulnerable plaque.
11 as a potential noninvasive method to detect vulnerable plaque.
12 ns with activated complement were found in a vulnerable plaque.
13 atheroma, the most common form of high-risk, vulnerable plaque.
14 plaque imaging may enhance identification of vulnerable plaque.
15 inical as well as pathological evaluation of vulnerable plaques.
16 (1) Rupture-prone plaques are not the only vulnerable plaques.
17 nd rapid progression should be considered as vulnerable plaques.
18 ioscopy may be valuable for the detection of vulnerable plaques.
19 onary syndromes often result from rupture of vulnerable plaques.
20 implicated SLC44A3 in the pathophysiology of vulnerable plaques.
21 tion to include non-flow-limiting, high-risk vulnerable plaques.
22 rongly associated with the presence of focal vulnerable plaques.
23 fied pharmacological and focal treatments of vulnerable plaques.
24 e development of non-flow-limiting high-risk vulnerable plaques.
25 ed the potential of CD163 as a biomarker for vulnerable plaques.
26 nary intervention (PCI) of non-flow-limiting vulnerable plaques.
27 rosclerotic plaques and potentially identify vulnerable plaques.
28 hy is a promising tool for the evaluation of vulnerable plaques.
29 CAD-induced deaths are due to the rupture of vulnerable plaques.
30 g techniques increase diagnostic accuracy of vulnerable plaques.
31 tric mapping of plaques and clearly identify vulnerable plaques.
32 e presence of a lipid core, and therefore of vulnerable plaques.
33 est, especially for the early recognition of vulnerable plaques.
34 IgG can activate macrophages and destabilize vulnerable plaques.
35 ger receptors on macrophages, a biomarker of vulnerable plaques.
36 ne that explicitly evaluate the treatment of vulnerable plaques.
37 es, increased inflammation, and more complex vulnerable plaques.
38 ammatory cells should noninvasively identify vulnerable plaques.
39 therosclerosis, acute coronary syndromes and vulnerable plaques.
40 components that might be useful in targeting vulnerable plaques.
41 between FC accumulation and inflammation in vulnerable plaques.
42 target for drug therapy aimed at stabilizing vulnerable plaques.
43 Is this a vulnerable plaque?
44 dden cardiac death, cardiac arrhythmias, and vulnerable plaque?
45 o two groups: 41 resulting from rupture of a vulnerable plaque (a thin fibrous cap overlying a lipid-
46 strate that macrophages, a characteristic of vulnerable plaques, also assist in expansive remodeling,
47 .7+/-5.1 years), including 1267 (29.2%) with vulnerable plaque and 1474 (34.0%) with plaque progressi
48 tion of at least 50% was rare (25 [3%]), but vulnerable plaque and high Leaman score (ie, >5) were mo
50 sus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable p
51 ng metalloproteinase that is associated with vulnerable plaque and may be a predictor of cardiovascul
52 LMPs favor the neovascularization within the vulnerable plaque and, in the ruptured plaque, they take
53 larly be a valuable imaging tool to identify vulnerable plaques and associated intraplaque inflammati
54 ance imaging techniques may be able to image vulnerable plaques and characterize plaques in terms of
56 er consideration as methods to stabilize the vulnerable plaques and patients that might be detected,
57 tic resonance for the noninvasive imaging of vulnerable plaques and the characterization of plaques i
58 carry contrast agents for early detection of vulnerable plaques and the initiation of preventative th
60 g the ability of such techniques to diagnose vulnerable plaques and to assess the effects of both pha
61 s on the attempted localization of so-called vulnerable plaques and vulnerable, or high-risk patients
62 oronary plaque, noncalcified plaque, CAC >0, vulnerable plaque, and high CAD burden (Leaman score >5)
63 sity related to CAC >0, noncalcified plaque, vulnerable plaque, and Leaman score >5 (all P <= .002).
64 eaturing occlusive coronary atherosclerosis, vulnerable plaque, and premature death and that these ef
65 ion, endothelial dysfunction, development of vulnerable plaque, and ventricular remodeling following
66 real-time the risk posed by plaques, detect vulnerable plaques, and optimize treatment decisions.
67 aques, the prognostic utility of identifying vulnerable plaques, and the future studies needed to exp
69 ility, contributing to the concept that more vulnerable plaques are more likely to have a greater deg
73 acute atherothrombotic vascular occlusion ("vulnerable plaques") are abundant inflammatory mediators
74 cus has been placed on the identification of vulnerable plaques as a means of improving the predictio
75 ries, one of the features that characterizes vulnerable plaques at risk of rupture, can be imaged usi
77 s and radiologists as one of the features of vulnerable plaques, but other characteristics-eg, plaque
79 tively, metalloproteinases could destabilize vulnerable plaques by promoting matrix destruction, angi
80 hanism by which lipid lowering may stabilize vulnerable plaques by reduced expression and activity of
81 odegradable HDL-NP platform for detection of vulnerable plaques by targeting the collapse of mitochon
84 ecause some subtypes of carotid plaques (eg, vulnerable plaques) can predict the occurrence of stroke
85 lprit lesions in patients with ACS have more vulnerable plaque characteristics compared with those wi
87 dverse cardiac events arising from high-risk vulnerable plaques, compared with optimal medical therap
88 eprocedural symptoms in men, and with a more vulnerable plaque composition in both men and women.
90 our transition from focusing on individual "vulnerable plaque," coronary arterial stenosis, and indu
91 y occlusions will lead to future advances in vulnerable plaque detection technology and potentially l
94 hether the prevalence of untreated high-risk vulnerable plaques differs in STEMI and NSTEMI and affec
95 tent diameters suggests that embolization of vulnerable plaque elements may play a pathogenic role.
96 d plaque, coronary artery calcium (CAC), and vulnerable plaque features using multivariable logistic
97 e in the pathogenesis of atherosclerosis and vulnerable plaque formation, and a fundamental function
105 According to the 'response to injury' and 'vulnerable plaque' hypotheses, contractile VSMCs recruit
106 low-limiting (fractional flow reserve >0.80) vulnerable plaques identified via intracoronary imaging.
107 s coronary intervention of non-flow-limiting vulnerable plaques improves clinical outcomes compared w
108 e on the application of AI to the imaging of vulnerable plaque in coronary arteries and provide conse
109 ntial to improve the assessment of images of vulnerable plaque in coronary arteries, but requires rob
111 Advances in the understanding of the role of vulnerable plaque in the causation of coronary events, c
114 ous coronary intervention (PCI) for treating vulnerable plaques in diabetic patients remain unclear.
118 y with percutaneous coronary intervention of vulnerable plaques in reducing adverse cardiac events ar
120 mpowered the clinician to identify suspected vulnerable plaques in vivo and paved the way for the eva
121 ging catheters (to localize and characterize vulnerable plaque) in combination with future genomic an
122 synchronous plaque motion is associated with vulnerable plaque, in this study, synchronisation patter
123 Characteristic histomorphologic features of vulnerable plaques include a high lipid content, increas
125 Unfortunately, the search for the so-called vulnerable plaque is hampered by the lack of both natura
129 that until the natural history of presumed "vulnerable plaques" is known one can never truly identif
130 leading to myocardial infarction (so-called "vulnerable plaques") is an important area of cardiovascu
131 h atherosclerotic coronary plaques (known as vulnerable plaques), many of which are non-flow-limiting
132 stological examinations of brain thrombi and vulnerable plaque material from patients with advanced c
135 plaques that cause severe luminal stenosis, vulnerable plaques may cause relatively minor stenosis,
136 Obstructive lesions more commonly harbored vulnerable plaque morphology than nonobstructive lesions
138 can never truly identify what constitutes a "vulnerable plaque." Much work needs to be done in this a
140 ology- and imaging-based definitions of the "vulnerable plaque," necessitating an improved approach f
144 ion in the extracellular matrix transforming vulnerable plaque phenotypes to more stable coronary les
145 rden index (LCBI), and the presence of focal vulnerable plaques (plaque burden >=70% and maximum LCBI
146 methods can be used in the future to detect vulnerable plaques, potentially to determine patients' p
150 lammatory reaction, the result of which is a vulnerable plaque, prone to rupture and thrombosis.
151 across branch ostia, disruption of adjacent vulnerable plaques, radiation therapy, and extensive pla
153 eatures characteristic of the rupture-prone, vulnerable plaques responsible for acute coronary syndro
154 to enable detection and characterization of vulnerable plaque structure and biology in rabbit abdomi
155 was associated with classical features of a vulnerable plaque, such as a larger lipid core, a higher
157 cept of the vulnerable patient, not just the vulnerable plaque, takes into account the diversity and
159 Early identification and treatment of the vulnerable plaque, that is, a coronary artery lesion wit
160 the biological and compositional features of vulnerable plaques, the non-invasive and invasive diagno
161 vasive diagnostic modalities to characterize vulnerable plaques, the prognostic utility of identifyin
162 potential effect of the focal treatment for vulnerable plaques, these findings support consideration
165 on Stenosis with Functionally Insignificant Vulnerable Plaque) trial was a randomized clinical trial
167 udy, the per-patient prevalence of high-risk vulnerable plaques was comparable in STEMI versus NSTEMI
168 inical, as well as pathologic, evaluation of vulnerable plaques was recently put forward in which fiv
169 cope of recent literature on the concept of "vulnerable plaque" was reviewed by examining 463 abstrac
171 to develop an imaging agent for detection of vulnerable plaques, we evaluated the feasibility of a li
175 with or without and thin-cap fibroatheroma (vulnerable plaque), whereas in erosions and total occlus
176 lesterol - predispose patients to rupture of vulnerable plaques, whereas cigarette smoking predispose
178 dvance particularly in the identification of vulnerable plaques, which are associated with specific p
180 defines histomorphologic characteristics of vulnerable plaques, which may help develop imaging strat
181 o determine whether identifying and treating vulnerable plaques will lead to improved clinical outcom
182 he rate of plaque progression might identify vulnerable plaques with an increased potential for adver
183 ic antibodies allow for in vivo detection of vulnerable plaques with magnetic resonance imaging (MRI)
184 artery plaque but, given to older women with vulnerable plaque, would have a null or even harmful eff