ライフサイエンスコーパス: vasospasm

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

2 e management of post-subarachnoid hemorrhage vasospasm.

3 , rebleeding, and cerebral infarction due to vasospasm.

4 llent accuracy for angiographic detection of vasospasm.

5 lar filling defects consistent with arterial vasospasm.

6 , vascular permeability, arteriogenesis, and vasospasm.

7 heart failure, atherosclerosis, and coronary vasospasm.

8 been written about the treatment of cerebral vasospasm.

9 apparent before the presence of symptomatic vasospasm.

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

11 erebral angiography at detecting symptomatic vasospasm.

12 eatment studies of patients with symptomatic vasospasm.

13 r monoamines, particularly dopamine, mediate vasospasm.

14 by pathological vasoconstriction or cerebral vasospasm.

15 dvantageous for reduction of coronary artery vasospasm.

16 tandard test for determining the presence of vasospasm.

17 correlated to clinical and SPECT evidence of vasospasm.

18 ty and specificity of SPECT for diagnosis of vasospasm.

19 sultant endothelin-mediated renal arteriolar vasospasm.

20 thout clinical or arteriographic evidence of vasospasm.

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

22 resence of clinical findings consistent with vasospasm.

23 st for corroboration of clinical findings of vasospasm.

24 vascular and endothelial function, promoting vasospasm.

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

26 e plus estradiol failed to protect, allowing vasospasm.

27 progesterone increases the risk of coronary vasospasm.

28 rasound was performed to identify and follow vasospasm.

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

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

31 vascular dysregulation, sometimes including vasospasm.

32 emic drug administration in the treatment of vasospasm.

33 ong the proposed pathomechanisms is coronary vasospasm.

34 logical situations, such as hypertension and vasospasm.

35 semiquantitatively assessed in patients with vasospasm.

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

37 an effective therapy to ameliorate cerebral vasospasm.

38 ested for neuroprotection and attenuation of vasospasm.

39 for the prevention and treatment of cerebral vasospasm.

40 uch as thrombus formation, inflammation, and vasospasm.

41 nding on the presence or absence of clinical vasospasm.

42 sion, it was stronger among patients without vasospasm.

43 usceptibility to ergonovine-induced coronary vasospasm.

44 and severity of sequelae, including cerebral vasospasm.

45 dal vessels predisposes them particularly to vasospasms.

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

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

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

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

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

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

52 Symptomatic vasospasm after subarachnoid hemorrhage (SAH) is associa

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

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

55 Symptomatic vasospasm also was associated with thickness of clot on

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

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

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

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

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

61 Vasospasm and embolism are possible mechanisms of ischem

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

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

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

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

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

67 Vasospasm and ischemic organ injury are important in the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 Vasospasm contributes to the pulmonary hypertension comp

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

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

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

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

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

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

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

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

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

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

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

117 Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (

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

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

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

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

122 Cerebral vasospasm has traditionally been regarded as an importan

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

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

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

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

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

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

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

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

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

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

133 Coronary vasospasm in response to pathophysiological stimulation

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

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

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

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

138 mmend aggressive screening for posttraumatic vasospasm in these patients.

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

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

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

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

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

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

145 rcontractility and remodeling, indicative of vasospasm initiation.

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

147 Cerebral vasospasm is a frequent complication after subarachnoid

148 Cerebral vasospasm is a recognised but poorly understood complica

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

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

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

152 Though vasospasm is usually associated with the presence of sub

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

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

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

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

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

158 Vasospasm occurred more often in patients who received I

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

160 Vasospasm occurs in a sizeable number of children with m

161 Cerebral vasospasm occurs more frequently, and with earlier onset

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

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

164 Reproducible vasospasm of primate coronary arteries in response to th

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

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

167 Vasospasm of the cerebrovasculature is a common manifest

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

202 Vasospasm was defined as the new onset of neurological s

203 re dichotomized based on whether symptomatic vasospasm was diagnosed.

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

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

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

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

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

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

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

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

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

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

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

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

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