ライフサイエンスコーパス: vasospasm

1 uch as thrombus formation, inflammation, and vasospasm.

2 nding on the presence or absence of clinical vasospasm.

3 sion, it was stronger among patients without vasospasm.

4 usceptibility to ergonovine-induced coronary vasospasm.

5 and severity of sequelae, including cerebral vasospasm.

6 e management of post-subarachnoid hemorrhage vasospasm.

7 , rebleeding, and cerebral infarction due to vasospasm.

8 llent accuracy for angiographic detection of vasospasm.

9 lar filling defects consistent with arterial vasospasm.

10 , vascular permeability, arteriogenesis, and vasospasm.

11 heart failure, atherosclerosis, and coronary vasospasm.

12 been written about the treatment of cerebral vasospasm.

13 apparent before the presence of symptomatic vasospasm.

14 ACH test, 33% for CMD and 26% for epicardial vasospasm.

15 und data of 199 patients; 55 had symptomatic vasospasm.

16 erebral angiography at detecting symptomatic vasospasm.

17 eatment studies of patients with symptomatic vasospasm.

18 r monoamines, particularly dopamine, mediate vasospasm.

19 by pathological vasoconstriction or cerebral vasospasm.

20 dvantageous for reduction of coronary artery vasospasm.

21 tandard test for determining the presence of vasospasm.

22 correlated to clinical and SPECT evidence of vasospasm.

23 vascular dysregulation, sometimes including vasospasm.

24 ty and specificity of SPECT for diagnosis of vasospasm.

25 sultant endothelin-mediated renal arteriolar vasospasm.

26 thout clinical or arteriographic evidence of vasospasm.

27 y play an important role in prevention of RA vasospasm.

28 resence of clinical findings consistent with vasospasm.

29 st for corroboration of clinical findings of vasospasm.

30 vascular and endothelial function, promoting vasospasm.

31 ation of cells and matrix, with thrombus and vasospasm.

32 e plus estradiol failed to protect, allowing vasospasm.

33 progesterone increases the risk of coronary vasospasm.

34 y artery, PFA routinely provokes subclinical vasospasm.

35 reas both Q and R were unrelated to coronary vasospasm.

36 mplications, and lower MinG (p = 0.015) with vasospasm.

37 m MCA CBFv >= 120 cm/s was the threshold for vasospasm.

38 y, accelerated atherosclerosis, and coronary vasospasm.

39 rasound was performed to identify and follow vasospasm.

40 n without vasospasm and in 15% of those with vasospasm.

41 y without vasospasm and in 40% of those with vasospasm.

42 emic drug administration in the treatment of vasospasm.

43 ong the proposed pathomechanisms is coronary vasospasm.

44 logical situations, such as hypertension and vasospasm.

45 interventional procedures performed to treat vasospasm.

46 semiquantitatively assessed in patients with vasospasm.

47 Post-SAH r-OPN treatment also prevented vasospasm.

48 an effective therapy to ameliorate cerebral vasospasm.

49 ested for neuroprotection and attenuation of vasospasm.

50 for the prevention and treatment of cerebral vasospasm.

51 dal vessels predisposes them particularly to vasospasms.

52 or hypersensitivity to catecholamine-induced vasospasms.

53 were 0.93 and 0.95, and in diagnosis of mild vasospasm, 0.90 and 0.91.

54 vs 19%, SCAD 11% vs 0.7%, embolism 2% vs 2%, vasospasm 3% vs 1%, MINOCA-U 3% vs 2%).

55 al toxic effects, which can present as acute vasospasm, acute thrombosis and accelerated atherosclero

56 synthase, have been used to prevent cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

57 tors of outcome in patients with symptomatic vasospasm after SAH.

58 to identify patients at risk for developing vasospasm after SAH.

59 e-dependent integrin receptors and prevented vasospasm after SAH.

60 combinant OPN (r-OPN) could prevent cerebral vasospasm after subarachnoid hemorrhage (SAH) in rats.

61 Symptomatic vasospasm after subarachnoid hemorrhage (SAH) is associa

62 y have a critical role in the development of vasospasm after subarachnoid hemorrhage is accumulating.

63 schemia and infarction and for evaluation of vasospasm after subarachnoid hemorrhage.

64 Symptomatic vasospasm also was associated with thickness of clot on

65 ents had 14 episodes of clinical evidence of vasospasm and 14 SPECT studies were performed in these 1

66 esponsive as a result of clinically presumed vasospasm and 4 of 5 of these patients had diffuse or he

67 Verapamil treatment eliminated evidence of vasospasm and ameliorated histological and functional ev

68 reduced volume of ischemia in patients with vasospasm and an uncomplicated coiling procedure.

69 in CSF may contribute to the development of vasospasm and cerebral ischemia.

70 ntial post-hemorrhagic complications such as vasospasm and delayed cerebral ischemia.

71 Vasospasm and embolism are possible mechanisms of ischem

72 play a major role in the intense intrarenal vasospasm and hypertension provoked by cyclosporine.

73 me was seen in 29% of those children without vasospasm and in 15% of those with vasospasm.

74 with moderate traumatic brain injury without vasospasm and in 40% of those with vasospasm.

75 on is important since heme may contribute to vasospasm and increase oxidative stress in cells.

76 ng increased intracranial pressure, cerebral vasospasm and ischemia, glutamate excitotoxicity, and ne

77 n the increased incidence of coronary artery vasospasm and ischemic heart disease in postmenopausal w

78 Vasospasm and ischemic organ injury are important in the

79 es should establish the relationship between vasospasm and long-term functional outcomes and should a

80 r variables, detecting and treating cerebral vasospasm and managing systemic complications.

81 orrhage who are at high risk for symptomatic vasospasm and may be helpful at following success of end

82 he susceptibility of RA to the perioperative vasospasm and may have an impact on the long-term graft

83 ide that has been closely linked to cerebral vasospasm and more recently to oxidative stress after tr

84 Pre-SAH administration of r-OPN prevented vasospasm and neurological impairments at 24-72 hours po

85 consumption may exacerbate ischemia-mediated vasospasm and nitrate tolerance.

86 irubin are involved in complications such as vasospasm and or pathological vasoconstriction associate

87 he CSF inhibited hemoglobin-induced cerebral vasospasm and preserved vascular NO signaling.

88 onsecutive cases performed to treat clinical vasospasm and quantified the changes in perfusion metric

89 We conclude that spontaneous coronary vasospasm and sudden death in SUR2 null mice arises from

90 ated dopamine release on neurons involved in vasospasm and the control of cortical circulation.

91 zing the detection and treatment of cerebral vasospasm and the management of systemic complications.

92 dothelial function could contribute to focal vasospasm and thrombosis and predispose to premature ath

93 patient suffering from spontaneous coronary vasospasm and was puzzled by these dramatic alterations

94 ibute to increased arterial tone, leading to vasospasm and, ultimately, to arterial occlusion.

95 rwent MRI within 0-3 days of ictus (prior to vasospasm) and a repeat MRI (median 7 days).

96 endarterectomy at the site of injury-induced vasospasm) and matured for 30 minutes before rTPA was st

97 ions occurred in 83 (38.2%), 124 (57.1%) had vasospasm, and 41 (18.9%) died.

98 oronary microcirculatory disorders, coronary vasospasm, and bridging in the absence of obstructive ep

99 remain poor, with high rates of rebleeding, vasospasm, and cerebral ischaemia.

100 ases, such as systemic hypertension, cancer, vasospasm, and fibrogenic diseases.

101 ing for endothelial dysfunction and coronary vasospasm, and intravascular imaging for identification

102 gical findings, aneurysm treatment, clinical vasospasm, and ischemic lesion.

103 rding hyperthermia, cerebral edema, cerebral vasospasm, and lethal interactions with commonly used me

104 o microvascular dysfunction and large vessel vasospasm, and medical complications such as stunned myo

105 l was approved for the treatment of cerebral vasospasm, and more recently, ripasudil was approved for

106 Morbidity and mortality rates for vasospasm are high despite improvements in management.

107 an cause hypertension, tachycardia, coronary vasospasm, arrhythmias, and increased core temperature.

108 he severity and the ischemic consequences of vasospasm as assessed on computed tomography.

109 has been implicated in SAH-induced cerebral vasospasm as it causes cerebral artery constriction and

110 recent studies argue against a pure focus on vasospasm as the cause of delayed ischaemic complication

111 Severity of vasospasm, as assessed on the most severe angiogram, was

112 tion, respiratory failure, hydrocephalus and vasospasm, as well as repeated measured Glasgow Coma Sca

113 rcise = reduced coronary flow reserve and/or vasospasm at rest) might also represent a plausible expl

114 at risk of delayed ischemic deficits due to vasospasm, autoregulatory failure, and intravascular vol

115 of moderate to severe cerebral angiographic vasospasm (aVS) between days 7 and 9 after aneurysm rupt

116 R = 3.14; 95% CI 1.20-8.22) in patients with vasospasm, but not in counterparts without vasospasm (p

117 tial brain imaging and investigated cerebral vasospasm by angiography or time-of-flight magnetic reso

118 Estradiol at low doses may protect against vasospasm by stimulating endothelium-derived NO release

119 ggests that structure-independent epicardial vasospasm can be an important element in serious cardiac

120 st that outcome in patients with symptomatic vasospasm can be effectively predicted by routinely avai

121 Patients at high risk for symptomatic vasospasm can be identified early in the course of SAH u

122 variectomized monkeys revealed that coronary vasospasm can be stimulated without preexisting vascular

123 mal cerebral blood flow, such as in cerebral vasospasm, can induce neurological deficits.

124 nding immunohistochemical examination of non-vasospasm components of secondary brain injury, and is a

125 These data indicate that secondary vasospasm contributes to the development of cardiomyopat

126 Vasospasm contributes to the pulmonary hypertension comp

127 lassical contributors like proximal cerebral vasospasm, CSD clusters may reduce O(2) supply and incre

128 Cerebral vasospasm (CV) and the resulting delayed cerebral ischem

129 on, blood pressure (BP) management, cerebral vasospasm (CV) prophylaxis and the need for digital subt

130 he role of intestinal microbiome in cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage

131 Cerebral vasospasm (CVS) is an important contributor to delayed c

132 in animal models and may attenuate cerebral vasospasm (cVSP) in human aneurysmal subarachnoid haemor

133 cs have a higher risk of developing cerebral vasospasms (CVSP) after subarachnoid hemorrhagic stroke

134 Thus, in this model, coronary artery vasospasm derives from a vascular smooth muscle-cell ext

135 Children in whom vasospasm developed were more likely to have been involv

136 Children in whom vasospasm developed were more likely to have been involv

137 Additional criteria required for vasospasm diagnosis in the middle cerebral artery was a

138 lower Glasgow Coma scores than in those whom vasospasm did not develop.

139 gs that marked reduction in the incidence of vasospasm does not translate to a reduction in DCI, or b

140 one of the segmental arteries resulting from vasospasm due to the placement of the guiding wire neces

141 Brain injury and cerebral vasospasm during the 14 days after the subarachnoid hemo

142 These cases may be caused by vasospasm, embolism, dissection, or branch occlusion.

143 ntifiable mechanism (spontaneous dissection, vasospasm, embolism; 1.5% women, 0.2% men); and class 5,

144 Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (

145 es that show gap junction inhibitors reverse vasospasm following experimental SAH, they failed to imp

146 re treated with vasopressors for symptomatic vasospasm for a mean duration of 5 days (range, 8 hrs to

147 rillation, adjacent left circumflex arterial vasospasm frequently occurred with PFA and not RFA but w

148 d samples were obtained during or outside of vasospasm from aSAH patients whose maximal vasospasm was

149 We included patients aged >18 years with vasospasm >50% of the internal carotid artery (ICA), ant

150 We included patients aged>18 years with vasospasm>50% of the internal carotid artery (ICA), ante

151 zem, which is used empirically to prevent RA vasospasm, had little effect on human RA contractions (r

152 ational change of each arterial layer during vasospasm has not been studied in detail.

153 Cerebral vasospasm has traditionally been regarded as an importan

154 n of ROCK can ameliorate conditions, such as vasospasm, hypertension, and inflammation.

155 in the pathologies of cerebral and coronary vasospasm, hypertension, cancer, and arteriosclerosis.

156 necessary to attenuate neuronal cell death, vasospasm, impaired cognitive function, and clearance of

157 Transcranial Doppler ultrasound signs of vasospasm improved after endovascular treatment in 30 pa

158 ebral-vessel perforation in 7, and transient vasospasm in 11.

159 id isthmus ablation provoked severe subtotal vasospasm in 5 of 5 (100%) consecutive patients, and thi

160 id hemorrhage (SAH), SAH is not required for vasospasm in bTBI, which suggests that the unique mechan

161 The prevalence of basilar artery vasospasm in children with moderate traumatic brain inju

162 The prevalence of middle cerebral artery vasospasm in children with moderate traumatic brain inju

163 In addition to vasospasm in large diameter arteries, enhanced constrict

164 factors, which increase the risk of coronary vasospasm in older people.

165 , and the occurrence of symptomatic cerebral vasospasm in patients with aneurysmal subarachnoid haemo

166 s an established role in diagnosing cerebral vasospasm in patients with aneurysmal subarachnoid hemor

167 Coronary vasospasm in response to pathophysiological stimulation

168 Susceptibility to drug-induced coronary vasospasm in rhesus monkeys increases after removal of t

169 nsient, repeated episodes of coronary artery vasospasm in Sur2(-/-) mice.

170 Mean duration of vasospasm in the middle cerebral artery was 2 days (+/-

171 tial preventative or therapeutic options for vasospasm in these children.

172 mmend aggressive screening for posttraumatic vasospasm in these patients.

173 otentiates vascular remodeling, and cerebral vasospasm, in bTBI patients.

174 s prophylactic adjuvant therapies to prevent vasospasm, including magnesium, phosphodiesterase 3 inhi

175 rotective against the lipid peroxidation and vasospasm induced by hemoglobin, by increasing heme clea

176 hese drug-induced vasospasms were similar to vasospasms induced by mechanical injury followed by sero

177 and angiograms were compared with those from vasospasms induced in human patients.

178 determine whether statin therapy diminished vasospasm-induced ischemia as assessed using daily measu

179 rcontractility and remodeling, indicative of vasospasm initiation.

180 tions such as cerebral and coronary arterial vasospasm, intimal hyperplasia, and hypertension.

181 Delayed cerebral ischemia (DCI) secondary to vasospasm is a determinate of outcomes following non-tra

182 Cerebral vasospasm is a dreaded sequelae of aneurysmal subarachno

183 Cerebral vasospasm is a frequent complication after subarachnoid

184 Cerebral vasospasm is a recognised but poorly understood complica

185 eatment of cerebral aneurysms and associated vasospasm is gaining credibility.

186 ptions developed from the understanding that vasospasm is primarily caused by endothelial dysfunction

187 ainty as to whether proximal cerebral artery vasospasm is the only cause of DIND, other processes sho

188 Though vasospasm is usually associated with the presence of sub

189 in-1 (ET-1) is induced resulting in cerebral vasospasm, ischemia, reperfusion and the activation of v

190 Cerebral vasospasm largely contributes to a devastating outcome a

191 According to the institutional standards of vasospasm management, the mean 14 days MAP >= 95 mmHg wa

192 noid hemorrhage patients who are at risk for vasospasm may benefit from an increase in cerebral blood

193 artery dissection, coronary artery embolism, vasospasm, myocardial bridging and stress-induced cardio

194 coronary artery dissection (SCAD), embolism, vasospasm, myocardial infarction with nonobstructed coro

195 butions were identified, as was angiographic vasospasm (n = 35).

196 the basis for a functional etiology of those vasospasms not explained on a structural basis.

197 constricted 2- to 4-fold more intensely, and vasospasm occurred in some vessels.

198 Vasospasm occurred more often in patients who received I

199 sence of vascular pathology, coronary artery vasospasm occurs as a result of local regions of vascula

200 Vasospasm occurs in a sizeable number of children with m

201 Cerebral vasospasm occurs more frequently, and with earlier onset

202 emale-male odds ratio for CMD and epicardial vasospasm of 4.2 (95% confidence interval: 3.1 to 5.5; p

203 nism of cocaine-induced cerebral ischemia is vasospasm of large cranial arteries or within the cortic

204 Reproducible vasospasm of primate coronary arteries in response to th

205 cerebral blood flow, SAH grade, and cerebral vasospasm of SAH mice.

206 tates, high vasopressor requirements causing vasospasm of the artery of Adamkiewicz, occlusion of ret

207 Vasospasm of the cerebrovasculature is a common manifest

208 ud's phenomenon is characterised by episodic vasospasm of the fingers and toes typically precipitated

209 IC catheter, synergistically caused coronary vasospasm on the second or third challenge in five of se

210 e mechanics of blast injury could potentiate vasospasm onset, accounting for the increased incidence.

211 edural events and is considered to be due to vasospasm or coronary artery stretch.

212 naries and ACH test performed for epicardial vasospasm or coronary microvascular dysfunction (CMD) du

213 It may be caused by vasospasm or direct compression of cerebral vessels by t

214 es did not allow the differentiation between vasospasm or retinal emboli, the OCTA imaging might help

215 inG 90 mg/dL had nearly 2x increased odds of vasospasm (OR = 1.8; 95% CI 1.01-3.21; p = 0.0422).

216 P<0.001), and delayed cerebral ischemia from vasospasm (OR, 1.3 per quintile; 95% CI, 1.07 to 1.7; P=

217 -FU may have the potential to cause arterial vasospasm outside the cardiac vasculature, resulting in

218 ced in cases of middle cerebral artery (MCA) vasospasm (p < 0.05).

219 enus Acidaminococcus was associated with MCA vasospasm (p = 0.00013).

220 h vasospasm, but not in counterparts without vasospasm (p = 0.113/p = 0.086).

221 in the cerebrospinal fluid (CSF) of cerebral vasospasm patients has been made.

222 fying patients who would develop symptomatic vasospasm (percentage of area under receiver operating c

223 latin casting for the assessment of cerebral vasospasm, permits outstanding immunohistochemical exami

224 It is increasingly clear that although vasospasm plays a role, PH is an obstructive lung panvas

225 and transcranial Doppler ultrasound signs of vasospasm presentation were 6.4 +/- 2 and 6.1 +/- 3 days

226 epict the onset of the accompanying cerebral vasospasm, preventive and therapeutic options are limite

227 us on inpatient treatment including cerebral vasospasm prophylaxis and follow-up imaging for perimese

228 In case 1 and case 2 neither cerebral vasospasm prophylaxis nor transcranial doppler sonograph

229 or responses to intracoronary acetylcholine (vasospasm provocation) was performed in 151 INOCA subjec

230 here is emerging evidence of coronary artery vasospasm provoked by PFA.

231 d endothelium, E-selectin, could inhibit the vasospasm provoked by subarachnoid blood in a rat subara

232 We found that SAH-induced vasospasm, reduced RBC deformability, and augmented endo

233 flow velocities in patients with symptomatic vasospasm related to middle cerebral and internal caroti

234 ngioplasty with a retrievable stent to treat vasospasm related to SAH due to an aneurysm in four neur

235 was paralleled by a lower clinical need for vasospasm rescue therapy in the implant group (2 of 20 p

236 terial papaverine were used in patients with vasospasm resistant to standard treatment.

237 for diagnosis of mild and moderate-to-severe vasospasm, respectively.

238 inhibitor used clinically to treat cerebral vasospasm, restored platelet counts in adult mice that w

239 s curve +/- SEM) was higher with symptomatic vasospasm risk index (68%+/-8%) compared with thickness

240 We developed a scoring system (symptomatic vasospasm risk index) based on a combination of these pr

241 SAH, lower MinG is associated with increased vasospasm risk.

242 tent is a safe and efficacious treatment for vasospasm secondary to SAH due to an aneurysm, improving

243 The intermittent coronary artery vasospasm seen in Sur2(-/-) mice provides a model for th

244 t disease such as endothelial dysfunction or vasospasm should be discussed instead.

245 therapy for arterial spasm is now available, vasospasm still occurs in at least 5% to 10% of RA graft

246 ed number of false-negative findings in both vasospasm subgroups.

247 Arterial grafts are prone to vasospasm subsequent to surgical manipulation, and appli

248 be precipitating stimuli in the etiology of vasospasm, suggests that structure-independent epicardia

249 In aSAH individuals with cerebral vasospasm, sustained increase of blood pressure exceedin

250 c events, particularly the focal, persistent vasospasms that occur without plaques or injury.

251 s (endothelial activation, inflammation, and vasospasm) that occur in approximately 10% to 20% of pre

252 Although no agent alone caused vasospasm, the combination of pathophysiologic concentra

253 In patients without symptomatic vasospasm, the mean time for mean cerebral blood flow ve

254 l microRNAs (miRNAs) have been implicated in vasospasm, the underlying mechanisms for CVS remain poor

255 e four independent predictors of symptomatic vasospasm: thickness of subarachnoid clot on computed to

256 er used to treat postsubarachnoid hemorrhage vasospasm, to mice presenting CM markedly increased surv

257 cerebral ischemia in patients with cerebral vasospasm.Trial registration number: German clinical tri

258 s led to the hypothesis that coronary artery vasospasm underlies cardiomyopathy in this disorder.

259 ped a novel technique for assessing cerebral vasospasm using cerebrovascular perfusion with ROX, SE (

260 tified independent predictors of symptomatic vasospasm using stepwise logistic regression analysis fr

261 Cerebral vasospasm (VSP) is a common phenomenon after aneurysmal

262 Mean time to onset of vasospasm was 4 days (+/- 2 d) in the middle cerebral ar

263 ior circulation in patients with symptomatic vasospasm was 73% with a specificity of 80%.

264 ncy and severity of left circumflex arterial vasospasm was assessed and monitored, as were time to re

265 Vasospasm was defined as the new onset of neurological s

266 nd computed tomography angiography (CTA) for vasospasm was determined.

267 re dichotomized based on whether symptomatic vasospasm was diagnosed.

268 Vasospasm was graded as mild (< or =25% reduction in ves

269 f vasospasm from aSAH patients whose maximal vasospasm was moderate or severe.

270 Coronary vasospasm was not provoked during PFA at locations remot

271 In the overall population, cerebral vasospasm was significantly less common in the statin-tr

272 Clinical diagnosis of symptomatic vasospasm was used as the standard to determine sensitiv

273 ne A2 implicated in the etiology of cerebral vasospasm, we observed significant increases in contract

274 To reduce this secondary vasospasm, we treated gamma-sarcoglycan-deficient mice w

275 erapy from the standpoint of coronary artery vasospasm, we treated ovariectomized rhesus monkeys with

276 arameters in diagnosis of moderate-to-severe vasospasm were 0.93 and 0.95, and in diagnosis of mild v

277 sed (IMAP) and the patients with and without vasospasm were analyzed separately.

278 Arteries with moderate or severe vasospasm were combined in one group.

279 ial hemorrhage, emboli to new territory, and vasospasm were compared.

280 These drug-induced vasospasms were similar to vasospasms induced by mechani

281 ary endpoints (mortality, complications, and vasospasm) were assessed using multivariate logistic reg

282 s was stronger among patients diagnosed with vasospasm, whereas for transfusion, it was stronger amon

283 ain and coronary angiography showed coronary vasospasm, which led to the diagnosis of variant angina.

284 nimodipine), 93 (33%) developed symptomatic vasospasm within 14 days after SAH.