ライフサイエンスコーパス: carotid

1 smooth muscle differentiation markers in the carotids.

2 cases into the VQI registry, including 8,155 carotid, 21,428 lower extremity, and 5,800 aortic aneury

3 a regression of pre-existing plaques in the carotids (-24%, p < 0.001).

4 d vascular compartment and controlled by (2) carotid and (3) femoral samples obtained under physiolog

5 so found in human atherosclerotic plaques of carotid and coronary arteries.

6 Carotid and femoral 3-dimensional vascular ultrasound an

7 ine a plaque number score; 3DVUS to quantify carotid and femoral plaque volume; and coronary artery c

8 in SMC-conditional Prkcd knockout mice, and carotid angioplasty was conducted in rats receiving tran

9 ient disease and indications for undertaking carotid [aOR:1.04 (0.84-1.28)], lower extremity [aOR:1.0

10 mpted from an ostial position or an external carotid approach to minimize the risk of potentially vis

11 coil filter directly placed into both common carotid arteries (CCAs) was designed to capture emboli >

12 es (CSE activity high) and plaque-containing carotid arteries (CSE activity low); (2) cultured human

13 Blood flow (Q) in the internal and external carotid arteries (ICA and ECA, respectively) and vertebr

14 light-sheet microscopy were applied to image carotid arteries and brachiocephalic arteries, allowing

15 alizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the

16 of the intima-media thickness of both common carotid arteries blinded from the randomization arm.

17 er RNA and protein levels in plaque-invested carotid arteries compared with control arteries.

18 Microarrays of carotid arteries from Pcsk6(-/-) versus control mice rev

19 sion of Abeta-activated platelets to injured carotid arteries in mice.

20 Here we show that vascular injury in rodent carotid arteries induces YY1 expression along with reduc

21 ition and between-group comparison of common carotid arteries intima-media thickness change.

22 The change in common carotid arteries intima-media thickness was -2.69 um (95

23 Significant differences were detected in the carotid arteries of normal patients and those with aneur

24 nderwent high-resolution MR imaging of their carotid arteries on a 1.5 T MR system.

25 ligible if they included bilaterally scanned carotid arteries using ultrasonography and defined incre

26 te stiffening of the aorta compared with the carotid arteries, reducing protective impedance mismatch

27 ing, coronary CT angiography, and MRI of the carotid arteries.

28 th young mice in both ligated and un-ligated carotid arteries.

29 an important role in the remodelling of the carotid arteries.

30 order of 100 mm Hg at the cranial end of the carotid arteries.

31 in adults: intima-media thickness of common carotid artery ([Formula: see text]), carotid plaque (CP

32 eudo-occlusion (PO) of the cervical internal carotid artery (cICA) can be caused by distal ICA occlus

33 >18 years with vasospasm>50% of the internal carotid artery (ICA), anterior cerebral artery (ACA), an

34 s and the extracircular part of the internal carotid artery (p < 0.05).

35 scently-labeled solutes injected through the carotid artery after tDCS.

36 ine solution was used to inject the external carotid artery and a collagen sponge was positioned over

37 with stenotic, aneurysmal, dissection of the carotid artery and its branches?

38 ifferent geometries were observed within the carotid artery and scored by volumetric analysis.

39 Brain uptake of (89)Zr-BVDFO on carotid artery and tail vein infusion with an intact BBB

40 nching of the internal intracranial internal carotid artery and the basilar artery.

41 he proximal and distal portion of the common carotid artery and the mean value was taken.

42 th burst incidence was less sensitive as the carotid artery became stiffer in older men and women, wh

43 ed with burst area was more sensitive as the carotid artery became stiffer in older women but not in

44 n end-tidal PCO2 and blood pressure External carotid artery blood flow increased by ~43% during both

45 sive heat stress, with no change in internal carotid artery blood flow Neurovascular coupling (i.e. t

46 Intracranial carotid artery calcifications (ICACs) are one type of ca

47 delivery to the cortex from the ipsilateral carotid artery can be improved by temporarily occluding

48 on of endovascular therapy as a component of carotid artery care.

49 Moyamoya disease, characterised by internal carotid artery dilatation, terminal segment stenosis and

50 ntly, advances in percutaneous therapies for carotid artery disease have been reported and provide a

51 Ten patients with carotid artery disease underwent high-resolution MR imag

52 tal (10 symptomatic and 10 with asymptomatic carotid artery disease) had ferumoxytol-enhanced MR imag

53 in the care of the patient with asymptomatic carotid artery disease.

54 the detection of structural deterioration in carotid artery diseases.

55 ss, telomere elongation, genome instability, carotid artery distension and increased intima-media thi

56 We assessed carotid artery EDD and aPWV across the lifespan in mice

57 erformed the tail-vein bleeding test and the carotid artery ferric chloride-induced thrombosis model.

58 BackgroundStenosis of the internal carotid artery has a higher risk for stroke.

59 randomized, first-in-human clinical CAPTURE (Carotid Artery Implant for Trapping Upstream Emboli for

60 Using 3 complementary mouse models of carotid artery injury, we demonstrated that both tamoxif

61 ponse is necessary for EC regeneration after carotid artery injury.

62 Mean common carotid artery intima-media thickness (IMT) and pulse-wa

63 l (3D) profiling of the vascular response to carotid artery ligation and induction of atherosclerosis

64 Five ex vivo porcine carotid artery models (n = 6 each) were compared-native,

65 term experimental permanent bilateral common carotid artery occlusion (BCCAO).

66 ation and brain infarct injury in the middle carotid artery occlusion ischemia/reperfusion model.

67 diet and modeled VCID via unilateral common carotid artery occlusion.

68 before and after ischemia induced by middle carotid artery occlusion.

69 was restricted to the territory of a single carotid artery on brain magnetic resonance imaging (MRI)

70 In 24 patients with terminal internal carotid artery or the proximal middle cerebral artery oc

71 Internal carotid artery patency was 100%, while the overall final

72 Internal carotid artery peak systolic velocity was used by all ce

73 art Association-lesion type VI) nonstenosing carotid artery plaques (CAPs) in cryptogenic stroke (CS)

74 features of both T cells and macrophages in carotid artery plaques of patients with clinically sympt

75 pulse pressure, systolic blood pressure, and carotid artery procedures, implicating modulation of the

76 Our aim was to examine whether carotid artery reactivity (CAR; a novel, simple procedur

77 e short-term, outcomes of patients following carotid artery revascularization.

78 hyroid due to its proximity to the pulsating carotid artery significantly impacts the visualization o

79 es and Canada who underwent TCAR and CEA for carotid artery stenosis (2016- 2019) were included.

80 Here we used a bilateral common carotid artery stenosis (BCAS) mouse model of VaD to inv

81 to reduce the stroke impact of asymptomatic carotid artery stenosis has proved difficult over the la

82 arotid endarterectomy for severe symptomatic carotid artery stenosis.

83 epresentative 30-day readmissions data after carotid artery stenting (CAS) and carotid endarterectomy

84 gnificantly lower stroke rates compared with carotid artery stenting via the transfemoral approach.

85 platelet therapy, carotid endarterectomy and carotid artery stenting.

86 Older women had greater carotid artery stiffness compared with older men, while

87 burst occurrence in older women with greater carotid artery stiffness to regulate BP similar to that

88 ive adventitial plexus after ligation of the carotid artery that evolved and matured over time.

89 In vivo, reperfusion of carotid artery thrombotic occlusion was also enhanced.

90 were quantified in 3,392 participants using carotid artery ultrasound imaging acquired over a mean o

91 ic plaque on carotid bifurcation or internal carotid artery using the Mannheim consensus definition a

92 ; P < 0.05), catheterization route (internal carotid artery vs. external carotid or posterior communi

93 otion associated with the thyroid due to the carotid artery was primarily in the lateral direction, w

94 the lumen of the proximal cervical internal carotid artery without evidence of calcification.

95 els, vessel grade, and vessel type (internal carotid artery, vertebral artery) with BCVI-associated s

96 the rigid trachea, thyroid and the pulsating carotid artery, we hypothesize that imaging of thyroid m

97 (control) starting 7 days before end-to-side carotid artery-jugular vein fistula creation and for up

98 differential gene expression profiles in the carotid artery.

99 M1-/proximal M2-segment or terminal internal carotid artery.

100 mm) wide neck aneurysm of the right internal carotid artery.

101 d by temporarily occluding the contralateral carotid artery.

102 s and maturation of a plexus surrounding the carotid artery.

103 hest prevalence in the intracranial internal carotid artery.

104 assess feasibility of ferumoxytol in imaging carotid atheroma (with histological assessment); and the

105 ces allows assessment of inflammation within carotid atheroma in symptomatic and asymptomatic patient

106 The optimum MR imaging time for carotid atheroma is 48 hrs after its administration.

107 de (NaF) uptake in culprit versus nonculprit carotid atheroma, (2) spatial distributions of uptake, a

108 Asynchronous movement of the carotid atheromatous plaque from B-mode ultrasound has b

109 gh-quality epidemiological investigations on carotid atherosclerosis are needed to better address the

110 eeded to better address the global burden of carotid atherosclerosis at finer levels.

111 -based studies that quantified prevalence of carotid atherosclerosis by means of increased carotid in

112 Estimation of the epidemiological burden of carotid atherosclerosis can serve as a basis for prevent

113 The impact on carotid atherosclerosis evolution is not known.

114 A substantial global burden of carotid atherosclerosis exists.

115 eview and meta-analysis of the prevalence of carotid atherosclerosis in China.

116 lence, number of cases, and risk factors for carotid atherosclerosis in the general population global

117 produced significantly greater regression of carotid atherosclerosis than an LDL-C target of 90 to 11

118 ded for primary prevention and management of carotid atherosclerosis.

119 or the clinical assessment and management of carotid atherosclerosis.

120 RNA and single-cell ATAC sequencing on human carotid atherosclerotic plaques to define the cells at p

121 A+ cells and upregulated after 5 days in rat carotid balloon injury model, with positive correlation

122 ue to occlusion of the intracranial internal carotid, \basilar, or middle cerebral artery were includ

123 assessed with burst area after adjusting for carotid beta-stiffness (-116.1 +/- 135.0 vs. -185.9 +/-

124 negatively (more sensitive) correlated with carotid beta-stiffness in older women (r = -0.53, P = 0.

125 Carotid beta-stiffness was greater in older women than m

126 Carotid beta-stiffness was measured with B-mode ultrason

127 arterial chemoreceptor organ located in the carotid bifurcation and has a well-recognized role in ca

128 ticular, 3D imaging was used to identify the carotid bifurcation for targeting the CBs.

129 re newly diagnosed atherosclerotic plaque on carotid bifurcation or internal carotid artery using the

130 NaF uptake was concentrated at carotid bifurcations, while FDG was distributed evenly t

131 tal hypoxia, or changes in fetal heart rate, carotid blood flow or carotid oxygen delivery.

132 Carotid bodies (CBs) are chemoreceptors that monitor and

133 We show that the carotid bodies are also sensitive to asthma-associated p

134 Stimulation of the carotid bodies by these asthmakines involves a PKCepsilo

135 We also show that the carotid bodies contribute predominantly to hypoxia-induc

136 As the carotid bodies' oxygen sensitivity is independent of PKC

137 primary autonomic oxygen chemoreceptors, the carotid bodies, in parasympathetic-mediated asthmatic ai

138 rototypical Th2 cytokines also stimulate the carotid bodies.

139 The carotid body (CB) is an arterial chemoreceptor organ loc

140 ptin receptor, LepR(b) , was detected in the carotid body (CB), a key peripheral hypoxia sensor.

141 imulatory factors and cellular mechanisms of carotid body activation are unknown.

142 pendent, oxygen-independent function for the carotid body and suggest that targeting PKCepsilon provi

143 ogating both ventilatory acclimatization and carotid body cell proliferative responses to sustained h

144 ed oxygen sensitivity of glomus cells in the carotid body has long puzzled physiologists.

145 This novel sensing role for the carotid body is mediated by a PKCepsilon-dependent stimu

146 Importantly, carotid body oxygen sensing was unaffected by blocking e

147 We have previously shown that carotid body stimulation by lysophosphatidic acid elicit

148 odest expansion of TH(+) glomus cells in the carotid body upon SDHC loss, PPGL is not observed in suc

149 on of atypical mitochondrial subunits in the carotid body, and genetic deletion of Cox4i2 mimicked th

150 prototypical acute O(2)-sensing organ is the carotid body, which contains glomus cells expressing K(+

151 ine the intracellular signalling involved in carotid body-mediated sensing of asthmatic blood-borne i

152 as measured with B-mode ultrasonic image and carotid BP.

153 l decline in contrast above the level of the carotid bulb.

154 ransverse foramina of the atlas and the left carotid canal in StW 573 further suggests there may have

155 xia as a reliable, sensitive, measure of the carotid chemoreceptor contribution to tonic sympathetic

156 Hypersensitivity of the carotid chemoreceptor leading to sympathetic nervous sys

157 The carotid chemoreceptor mediates the ventilatory and muscl

158 Eighty-two PAD patients demonstrated carotid constriction and 90 patients demonstrated dilati

159 onal hazard models showed that patients with carotid constriction continued to show higher risk for c

160 , acute coronary syndrome, valvular disease, carotid disease, hyperlipidemia, hypertension, retinal v

161 e changes differ in patients with normal and carotid disease?

162 received the diagnosis of carotid stenosis, carotid dissection, and extra or intracranial aneurysm w

163 ween IVSR and VSF-trained surgeons following carotid endarterectomy (8%-IVSR vs. 7%-VSF), lower extre

164 data after carotid artery stenting (CAS) and carotid endarterectomy (CEA) are lacking.

165 for management include antiplatelet therapy, carotid endarterectomy and carotid artery stenting.

166 ars of age, and at standard or high risk for carotid endarterectomy are eligible for enrollment.

167 anticoagulation for atrial fibrillation and carotid endarterectomy for severe symptomatic carotid ar

168 The risk of stroke or death associated with carotid endarterectomy for symptomatic carotid stenosis

169 single-cell RNA sequencing of advanced human carotid endarterectomy samples and compared these with s

170 (>=2 mm, NASCET [North American Symptomatic Carotid Endarterectomy Trial] <70%).

171 m of stroke to target interventions, such as carotid endarterectomy, anticoagulation for atrial fibri

172 SMCs and atherosclerotic plaques obtained at carotid endarterectomy.

173 msR4M-L1 binds to MIF in plaques from human carotid-endarterectomy specimens.

174 Carotid femoral pulse-wave velocity (cfPWV) measured art

175 Central (carotid-femoral artery PWV, PWV(CF) ) and peripheral (ca

176 s (2007-2009 and 2012-2013) by measuring the carotid-femoral pulse wave velocity (cf-PWV).

177 was the adjusted between-group difference in carotid-femoral pulse wave velocity at 12 months.

178 We analyzed the primary outcome, carotid-femoral pulse wave velocity, using a linear mixe

179 of atherosclerosis as assessed by bilateral carotid/femoral vascular ultrasound.

180 ferential baroreceptor feedback (i.e. aortic-carotid g-gradient).

181 cular ultrasound (2DVUS) of abdominal aorta, carotid, iliac, and femoral territories to determine a p

182 fidence interval {CI}: 1.6, 2.4]; P < .001), carotid injuries versus vertebral artery injuries (49 of

183 irment of reendothelialization in the murine carotid-injury model.

184 e largest share of global cases of increased carotid intima-media thickness (317.62 million [33.36%]

185 had the smallest share of cases of increased carotid intima-media thickness (59.08 million [6.21%]) a

186 n = 672) and women (n = 713), with vascular (carotid intima-media thickness (cIMT), pulse wave veloci

187 onal numbers of people living with increased carotid intima-media thickness and carotid plaque in 201

188 nsion were common risk factors for increased carotid intima-media thickness and carotid plaque.

189 ss the effects of risk factors for increased carotid intima-media thickness and carotid plaque.

190 using ultrasonography and defined increased carotid intima-media thickness as a thickness of 1.0 mm

191 in 2020, the global prevalence of increased carotid intima-media thickness is estimated to be 27.6%

192 of 1.0 mm or more, carotid plaque as a focal carotid intima-media thickness of 1.5 mm or more encroac

193 CSK6 variant rs1531817 with maximum internal carotid intima-media thickness progression in high-cardi

194 0.5 mm or 50% compared with the surrounding carotid intima-media thickness values, and carotid steno

195 ence intervals) on outcomes were as follows: carotid intima-media thickness, 0.01 mm (-0.01 to 0.03),

196 rachial index, test result <25th percentile (carotid intima-media thickness, apolipoprotein B, galect

197 The prevalence of increased carotid intima-media thickness, carotid plaque, and caro

198 arotid atherosclerosis by means of increased carotid intima-media thickness, carotid plaque, and caro

199 ic and sex-specific prevalences of increased carotid intima-media thickness, carotid plaque, and caro

200 Ankle brachial pressure index and carotid intima-medial thickness alone did not predict (c

201 pectively), total ICA diameters (p = 0.000), carotid left O diameters (p = 0.026), right and left tot

202 ed reduced intimal hyperplasia response upon carotid ligation in vivo, accompanied by decreased MMP14

203 crophage recruitment to the vessel wall in a carotid ligation model in ApoE-/- mice.

204 rovider-specific clinical outcomes following carotid, lower extremity, and aortic aneurysm repair pro

205 3.4 [6.(2)-18.9] ms; p = 0.001) was found on carotid MR imaging at 48 hrs following the ferumoxytol i

206 69 carotid MR imaging studies were completed.

207 tively by high-resolution, contrast-enhanced carotid MRI at 3T using dedicated surface coils.

208 S/SVS (n = 79), or LAS (n = 19) and complete carotid MRI data.

209 al arterial thrombosis, as tested in vivo by carotid occlusion assays.

210 estar rats underwent bilateral or unilateral carotid occlusion of 28-45%.

211 inical or animal studies have evaluated mild carotid occlusion, and few examined unilateral occlusion

212 radical output, and thrombus formation, and carotid occlusion, while tail hemostasis was unaffected.

213 route (internal carotid artery vs. external carotid or posterior communicating artery; P < 0.001), a

214 s in fetal heart rate, carotid blood flow or carotid oxygen delivery.

215 .36%] of 952.13 million affected people) and carotid plaque (240.77 million [33.20%] of 725.25 millio

216 common carotid artery ([Formula: see text]), carotid plaque (CP) burden, and coronary artery calcific

217 thickness as a thickness of 1.0 mm or more, carotid plaque as a focal carotid intima-media thickness

218 diterranean region had the smallest share of carotid plaque cases (44.59 million [6.15%]).

219 ith CAC = 0, CAC <=10, low galectin-3, or no carotid plaque had remarkable low cardiovascular risk, c

220 (Carotid Plaque Imaging in Acute Stroke [CAPIAS]; NCT0128

221 CAPIAS (Carotid Plaque Imaging in Acute Stroke) is an observatio

222 ng prospective studies who underwent ASL and carotid plaque imaging with use of 3-T MRI in the same s

223 g contrast material-enhanced MR angiography, carotid plaque imaging, and arterial spin labeling (ASL)

224 increased carotid intima-media thickness and carotid plaque in 2015 using a risk factors-based model

225 a percentage change of 57.46% from 2000; of carotid plaque is estimated to be 21.1% (13.2-31.5), equ

226 reviously observed that CEPT1 is elevated in carotid plaque of patients with diabetes, we evaluated t

227 inflammation-are promising as biomarkers of carotid plaque vulnerability.

228 of increased carotid intima-media thickness, carotid plaque, and carotid stenosis increased consisten

229 of increased carotid intima-media thickness, carotid plaque, and carotid stenosis.

230 of increased carotid intima-media thickness, carotid plaque, and carotid stenosis.

231 onary artery calcium (CAC) = 0, CAC <=10, no carotid plaque, no family history, normal ankle-brachial

232 increased carotid intima-media thickness and carotid plaque.

233 increased carotid intima-media thickness and carotid plaque.

234 p had a similar incidence of newly diagnosed carotid plaque: 46/201 (5-year rate, 26.1%) versus 45/21

235 f stroke are needed because some subtypes of carotid plaques (eg, vulnerable plaques) can predict the

236 taT(2)* and DeltaT(2)) was identified in all carotid plaques (symptomatic and asymptomatic).

237 Carotid plaques and intima media thickness (IMT) were me

238 mmol/L) did not reduce the incidence of new carotid plaques but produced significantly greater regre

239 In total, 27 carotid plaques from 20 patients were scanned by ultraso

240 PFKFB3 were also found to be upregulated in carotid plaques of patients with elevated levels of Lp(a

241 Carotid plaques revealed no significant association with

242 demonstrate the ability to detect vulnerable carotid plaques using combined SWE, with group velocity

243 Ferumoxytol uptake by carotid plaques was assessed by histopathological analys

244 Carotid plaques were associated with vascular dementia w

245 wave elastography (SWE) to detect vulnerable carotid plaques, evaluating group velocity and frequency

246 red in ruptured versus stable areas of human carotid plaques, including many of the same functional c

247 reased uptake of both FDG and NaF in culprit carotid plaques, with discrete distributions of pathophy

248 and stable areas of freshly harvested human carotid plaques.

249 hat motion encountered by the thyroid due to carotid pulsations can be effectively tracked and correc

250 patibility studies and a preliminary in vivo carotid rabbit model.

251 emoral artery PWV, PWV(CF) ) and peripheral (carotid-radial artery PWV, PWV(CR) ) arterial stiffness

252 nted intimal hyperplasia in a mouse model of carotid restenosis without modifying vital cardiovascula

253 is a novel minimally invasive procedure for carotid revascularization in high-risk patients that is

254 patients are readmitted within 30 days of a carotid revascularization procedure.

255 efined as myocardial infarction, coronary or carotid revascularization, transient ischemic attack, or

256 ative feedback reflex mediated by aortic and carotid sinus baroreceptors when systemic arterial press

257 receptors in the wall of the aortic arch and carotid sinus initiates autonomic reflexes to change hea

258 We found that leptin enhanced carotid sinus nerve activity at baseline and in response

259 ur hypothesis that gradual formation of mild carotid stenosis along the life course leads to progress

260 g carotid intima-media thickness values, and carotid stenosis as 50% or more stenosis.

261 alues that warranted the diagnosis of severe carotid stenosis at centers in the 5th percentile, but n

262 with carotid endarterectomy for symptomatic carotid stenosis decreased over an 8-year period, indepe

263 Individuals with carotid stenosis enter surveillance or are considered fo

264 nosis.Materials and MethodsParticipants with carotid stenosis from two ongoing prospective studies wh

265 ients who underwent surgery for asymptomatic carotid stenosis in the Vascular Quality Initiative regi

266 intima-media thickness, carotid plaque, and carotid stenosis increased consistently with age and was

267 a percentage change of 58.97% from 2000; and carotid stenosis is estimated to be 1.5% (1.1-2.1), equi

268 with acute ischemic stroke with ipsilateral carotid stenosis of >=50% underwent FDG-positron-emissio

269 In humans, carotid stenosis of 70% and above might be the cause of

270 orts (n=12 781), all with either symptomatic carotid stenosis or major acute stroke.

271 reshold would assign a diagnosis of moderate carotid stenosis to twice as many individuals as the 95t

272 The diagnostic threshold for carotid stenosis varies considerably.

273 th >=70% and symptomatic patients with >=50% carotid stenosis, <=80 years of age, and at standard or

274 for any reason and received the diagnosis of carotid stenosis, carotid dissection, and extra or intra

275 We found that mild carotid stenosis, even in a unilateral occlusion, create

276 intima-media thickness, carotid plaque, and carotid stenosis.

277 ecent ischemic symptoms in participants with carotid stenosis.

278 intima-media thickness, carotid plaque, and carotid stenosis.

279 ymptomatic and symptomatic participants with carotid stenosis.Materials and MethodsParticipants with

280 This supports the hypothesis that carotid stiffness may contribute to the development of l

281 burst occurrence in older women with greater carotid stiffness.

282 ntion of ischemic stroke includes additional carotid surgery or stenting in selected symptomatic pati

283 the ages 9-17 years and arterial stiffness (carotid to femoral pulse wave velocity [PWV]) measured a

284 ical Technologies database directly from the carotid ultrasound device.

285 To describe the variation in carotid ultrasound diagnostic thresholds, we examined te

286 Ultrasonographers were certified and carotid ultrasound examinations were performed using M'A

287 raindicated, and by transcranial Doppler and carotid ultrasound if CT angiography was contraindicated

288 ation, we applied the range of thresholds to carotid ultrasound parameters from 2 groups: a populatio

289 maging, dual-energy X-ray absorptiometry and carotid ultrasound.

290 Carotid ultrasounds were conducted post-procedure, pre-d

291 defined using validated diagnosis codes for carotid/vertebral artery dissection.

292 re high RF status was associated with higher carotid wall thickness (0.99+/-0.11 mm) and lipid-rich n

293 aseline RF status was associated with higher carotid wall thickness (beta-coefficient, 0.015; 95% CI,

294 here were weak correlations between risk and carotid wall volume (Kendall tau = 0.29), noncalcified p

295 ed for noncalcified plaque, CAC, and average carotid wall volume and were compared with ACC/AHA risk

296 d plaque extent compared with measurement by carotid wall volume, CAC, and noncalcified plaque in 22.

297 The carotid web is a proposed stroke mechanism that may unde

298 e not likely to capture the possibility of a carotid web.

299 hough they can be readily visualised on CTA, carotid webs may be missed or misinterpreted because the

300 Carotid webs should be suspected in a young patient pres