ライフサイエンスコーパス: vascular event

1 ammatory event (major surgery, infection, or vascular event).

2 n for angina, heart failure, or a peripheral vascular event).

3 table angina, heart failure, or a peripheral vascular event.

4 itional 15% reduction in the risk of a major vascular event.

5 nts with less than 1% annual risk of a major vascular event.

6 nit of analysis was the patient and not each vascular event.

7 42 patients (19.6%) had at least 1 recurrent vascular event.

8 approach for prevention of atherothrombotic vascular events.

9 esion and thrombus formation during ischemic vascular events.

10 edictive values for incident major occlusive vascular events.

11 arotid plaque are associated with subsequent vascular events.

12 ials in secondary prevention from thrombotic vascular events.

13 independent risk factor for stroke and other vascular events.

14 re in the arterial system and to the risk of vascular events.

15 nal risk stratification in predicting future vascular events.

16 , which affect the risk of both bleeding and vascular events.

17 is study, we examined an MeDi in relation to vascular events.

18 n MeDi was associated with decreased risk of vascular events.

19 zumab does not increase the risk of systemic vascular events.

20 isk of cerebral, but not coronary, ischaemic vascular events.

21 influenza by vaccination reduces the risk of vascular events.

22 us control done originally for prevention of vascular events.

23 ed with a transient increase in the risk for vascular events.

24 did not result in a significant reduction in vascular events.

25 higher incidence of major strokes and major vascular events.

26 ations between incidental carotid plaque and vascular events.

27 pertension is associated with a high risk of vascular events.

28 hether such a reduction will result in fewer vascular events.

29 been recently used in the settings of acute vascular events.

30 the risk, manifestation, and progression of vascular events.

31 average, and higher relative risk for future vascular events.

32 eighed by a long-term reduction in recurrent vascular events.

33 opment for the treatment of atherothrombotic vascular events.

34 effective than aspirin in preventing serious vascular events.

35 tiplatelet agent for preventing and treating vascular events.

36 ma progression was associated with recurrent vascular events.

37 emic optic neuropathy as well as for retinal vascular events.

38 risk factors to determine and reduce risk of vascular events.

39 pecific physiology, may increase the risk of vascular events.

40 f statin therapy for the prevention of major vascular events.

41 ation in estimated 10-year risk of recurrent vascular events.

42 lthough it did not have an adverse effect on vascular events.

43 and aspirin prevents reinfarction and other vascular events.

44 py (ERT) is associated with adverse arterial vascular events.

45 vaccination increase the short-term risk of vascular events.

46 lerosis is associated with increased risk of vascular events.

47 aditional (disease-related) risk factors for vascular events.

48 produce a detectable increase in the risk of vascular events.

49 rstanding of the morning peak in cardiac and vascular events.

50 congestive heart failure, stroke, and other vascular events.

51 d with progressive atherosclerosis and acute vascular events.

52 ted with a transient increase in the risk of vascular events.

53 tes plaque instability, a precursor of acute vascular events.

54 IMT have all relevant with the occurrence of vascular events.

55 m underwent therapeutic procedures for these vascular events.

56 ponse rate, RBC transfusions, and thrombotic vascular events.

57 ng disease and/or unrelated arteriosclerotic vascular events.

58 ication of patients at higher risk for acute vascular events.

59 consider absence of disease progression and vascular events.

60 y aspirin versus no aspirin in prevention of vascular events.

61 -15% reduction of annual incidence rates for vascular events.

62 lded a 12% proportional reduction in serious vascular events (0.51% aspirin vs 0.57% control per year

63 70-0.92; p < 0.01) and a lower risk of major vascular events (0.91; 0.86-0.96; p < 0.001).

64 nterval [CI]: 0.68 to 0.85) for any ischemic vascular event, 0.74 (95% CI: 0.65 to 0.85) for ischemic

65 no significant effect on the rates of major vascular events (1034 patients [16.5%] vs. 1017 patients

66 P=0.03), as was the rate of the first major vascular event (11.0 vs. 12.8; hazard ratio, 0.86; 95% C

67 Vascular events (13 cardiovascular, 18 cerebrovascular,

68 significant effect on the incidence of major vascular events (13.2% and 13.7% of participants with an

69 d vascular death (2.38 [1.50-3.78]), and all vascular events (2.48 [1.57-3.91]), after adjusting for

70 ns in stroke (27%) and separately, all major vascular events (21%).

71 For important vascular events (241 cases), excluding revascularization

72 lded a greater absolute reduction in serious vascular events (6.7%vs 8.2% per year, p<0.0001), with a

73 Of 3096 acute cerebral or peripheral vascular events, 748 (24.2%) were AF-related.

74 Aspirin reduced major vascular events (8.7%/yr versus 5.7%/yr; HR, 0.66; 95% C

75 The relative risk (RR) of major vascular events (a composite of cardiovascular death, ac

76 Over a mean follow-up of 9 y, 518 vascular events accrued (171 ischemic strokes, 133 MIs,

77 y-four patients (6.2%) developed one or more vascular event after time 0.

78 f SBP maintained at such levels with risk of vascular events after a recent ischemic stroke is unclea

79 opidogrel plus aspirin, to prevent secondary vascular events after stroke or TIA.

80 Long-term data on recurrent vascular events after young stroke are limited.

81 s to examine the long-term risk of recurrent vascular events after young stroke.

82 oses are more effective for preventing major vascular events, albeit with evidence of increased toxic

83 tity of sleep may be independently linked to vascular events although prospective and multiethnic stu

84 cate that CRP and IL-6 independently predict vascular events among apparently healthy postmenopausal

85 oven benefit, the absolute risk of recurrent vascular events among patients taking aspirin remains re

86 carotid plaque, plaque characteristics, and vascular events among PLWHIV is unclear.

87 n I and BNP were associated with the risk of vascular events and all-cause mortality.

88 Associations between vascular events and baseline concentrations of cholester

89 are effective in the secondary prevention of vascular events and death after acute myocardial infarct

90 tinin is associated with increased renal and vascular events and death compared to its alternatives.

91 edication adherence and rates of first major vascular events and decreased patient spending without i

92 count for all blood-pressure-related risk of vascular events and for the benefits of antihypertensive

93 ressure variability in prediction of risk of vascular events and in accounting for benefits of antihy

94 d not significantly reduce the risk of major vascular events and increased the risk of serious advers

95 These factors are intimately associated with vascular events and induce VEGF expression by binding to

96 life threatening or treatable causes such as vascular events and malignant diseases, and patients sho

97 hat calcification is causal in precipitating vascular events and mediating chronic cardiovascular dam

98 thereafter followed up for the occurrence of vascular events and mortality within the Three-City Stud

99 e Trial, UK-TIA Aspirin Trial) prevention of vascular events and one trial of different doses of aspi

100 l as premature mortality related to cerebral vascular events and peripheral thrombosis.

101 jor vascular procedures (p < 0.001), and all vascular events and procedures (p < 0.0001).

102 ated LOOH levels were predictive of nonfatal vascular events and procedures in patients with stable C

103 23 (95% CI 1.44 to 3.44; p = 0.0003) for all vascular events and procedures.

104 All patients are alive and well with no new vascular events and resolution of hematological and immu

105 le of C-reactive protein (CRP) in predicting vascular events and response to statin therapy remains u

106 t reported in SLE, emerged as a predictor of vascular events and should be strongly discouraged.

107 EDS is independently associated with future vascular events and stroke in particular in healthy comm

108 isorders remains largely based on preventing vascular events and symptomatic control, with allogeneic

109 n an individual's absolute risk of occlusive vascular events and the absolute reduction in LDL choles

110 Treatment of HDL to Reduce the Incidence of Vascular Events and The Atherothrombosis Intervention in

111 The predictive value of N-BNP for occlusive vascular events and the effects of statins in people wit

112 age risk, 660,000 person-years, 3554 serious vascular events) and 16 secondary prevention trials (17,

113 events or revascularization, the first major vascular event, and health expenditures.

114 nfarction, 149 hospitalizations for nonfatal vascular events, and 139 patients underwent a major vasc

115 ssociated with higher risk for stroke, major vascular events, and composite after full adjustment amo

116 ial infarction, heart failure, stroke, other vascular events, and hospitalization for unstable angina

117 course of effects on incident cancer, major vascular events, and major extracranial bleeds, with str

118 th lower rates of all-cause mortality, major vascular events, and revascularizations compared with pl

119 5% CI 2.55 to 6.60; p < 0.0001) for nonfatal vascular events, and RR of 3.84 (95% CI 2.56 to 5.76; p

120 d kidney function decline with stroke, major vascular events, and the composite of stroke, death, maj

121 renal involvement, damage accrual, arterial vascular events, and venous thrombosis.

122 ention of recurrent stroke and other serious vascular events are all improving rapidly.

123 Such vascular events are insufficiently appreciated complicat

124 Clinical features, presenting symptoms, and vascular events are reviewed for the first 447 patients

125 The mechanisms by which hypertension causes vascular events are unclear.

126 ischemic attack, vascular deaths, and major vascular events as defined by the Antiplatelet Trialists

127 s such as myocardial infarction and cerebral vascular events as well as in normal physiologic conditi

128 ies of PCSK9 Inhibition and the Reduction of Vascular Events), assessing evolocumab and bococizumab,

129 ible for myeloproliferation (and potentially vascular events) associated with myeloproliferative diso

130 rization is associated with fewer peripheral vascular events at 6 months.

131 ween influenza vaccination and major adverse vascular events because the association remains uncertai

132 t baseline, and 185 had come up to the final vascular events (brain infarction, intracerebral hemorrh

133 d not significantly reduce the risk of major vascular events but did increase the risk of serious adv

134 ifen, especially gynaecological problems and vascular events, but arthralgia and fractures were incre

135 steinemia confers a high risk for thrombotic vascular events, but homocysteine-lowering therapies hav

136 tion of rivaroxaban to aspirin lowered major vascular events, but increased major bleeding.

137 01) partly accounted for the reduced risk of vascular events, but reduced visit-to-visit variability

138 Lowering of LDL cholesterol reduces major vascular events, but whether more intensive therapy safe

139 tion reducing the annual rate of these major vascular events by just over a fifth.

140 sion, but rather the prevention of recurrent vascular events by more powerful platelet inhibition or

141 ents, the modest benefit in reducing serious vascular events can be offset by the increased risk of b

142 twice the excess risk of fatal and nonfatal vascular events, compared with men with type 1 diabetes.

143 A vascular event comprising the secondary end point occurr

144 11-18; p<0.0001) further reduction in major vascular events, consisting of separately significant re

145 riate analysis, the risk of mortality and of vascular events decreased across the categories of ideal

146 wo secondary end points were (1) all initial vascular events defined as a composite of a primary end

147 The primary endpoint was major vascular events, defined as coronary death, myocardial i

148 disease are at increased risk for subsequent vascular events despite effective use of statins to lowe

149 d trial of simvastatin versus placebo (>5000 vascular events during 5.3 years of follow-up among 20 0

150 e debris) aortic atherosclerotic plaques and vascular events during follow-up in a random sample of 5

151 ssociated with reduced risk of major adverse vascular events during influenza seasons when the influe

152 rong relationship with the new occurrence of vascular events, especially the brain infarction (HR: 2.

153 less than 1.8 mmol/L had a 55% reduction in vascular events (event rate 1.11 vs 0.51 per 100 person-

154 roke remain at substantial risk of recurrent vascular events for decades, suggesting that the underly

155 essed whether rimonabant would improve major vascular event-free survival.

156 0 000 patients would typically prevent major vascular events from occurring in about 1000 patients (i

157 dverse impact of these side-effects on major vascular events has already been taken into account in t

158 An association between infections and vascular events has been observed, but the specific effe

159 Prevention of vascular events has been so far the main objective of th

160 te coronary, cerebrovascular, and peripheral vascular events have common underlying arterial patholog

161 dverse effects of calcium supplementation on vascular events have raised widespread concern.

162 ma progression was associated with composite vascular events (hazard ratio 5.8, 95% confidence interv

163 as associated with a 5% reduced risk for all vascular events (hazard ratio [HR]: 0.95; 95% confidence

164 -Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE), but its net effects on he

165 46), HDL-C was not associated with recurrent vascular events (HR: 1.02; 95% CI: 0.98 to 1.07) irrespe

166 hat statin therapy reduces the risk of major vascular events (ie, coronary deaths or myocardial infar

167 ional phenotypes that subsequently influence vascular events important for adaptive remodeling.

168 the IMT and IMT-Progression as Predictors of Vascular Events (IMPROVE) cohort, to identify the functi

169 This suggests that the vascular event in AMI patients is determined by local pr

170 623 (73%) coronary, and 147 (78%) peripheral vascular events in 12 886 (14%) individuals aged 65 year

171 of patients with stroke and other peripheral vascular events in a consecutive group of patients with

172 s [IMT] and IMT-Progression as Predictors of Vascular Events in a High Risk European Population) stud

173 lerosis is associated with increased risk of vascular events in a non-selected population.

174 ution of estimated 10-year risk of recurrent vascular events in a secondary prevention population.

175 tatin regimens reduces the risk of occlusive vascular events in a wide range of individuals.

176 Statin therapy safely reduces the risk of vascular events in a wide range of patients.

177 eepiness and the risk of ischemic stroke and vascular events in an elderly, multiethnic prospective c

178 UPITER trial found that rosuvastatin reduces vascular events in apparently healthy subjects with elev

179 -type natriuretic peptide (N-BNP) to predict vascular events in high-risk people and to test whether

180 therapy) safely reduces mortality and major vascular events in hospital, and should be considered ro

181 pared with what is known about predictors of vascular events in middle-aged persons, less is known ab

182 Ethnicity was not associated with vascular events in our patients.

183 alues <0.15), we recorded a 65% reduction in vascular events in participants allocated to rosuvastati

184 factors have been linked to these recurrent vascular events in patients prescribed aspirin, includin

185 s were used to evaluate the risk of HDL-C on vascular events in patients using no, usual dose, or int

186 aortic arch (AA) atheroma is associated with vascular events in patients with stroke or transient isc

187 than aspirin alone in preventing subsequent vascular events in patients with unstable angina, the co

188 calculate adjusted relative risks for first vascular events in relation to physical activity.

189 he possible therapeutic utility of targeting vascular events in sepsis with cysteinyl-LT blockade.

190 ntiplatelet regimens in preventing secondary vascular events in stroke and TIA patients.

191 Of 3096 acute cerebral or peripheral vascular events in the 92 728 study population, 383 inci

192 rocesses in Cox-2-/- mice is the deregulated vascular events in the absence of COX-2.

193 is may not be an independent risk factor for vascular events in the general population.

194 daily) versus control for the prevention of vascular events in the UK.

195 dependent predictor of damage accrual and of vascular events in women with lupus.

196 e of hematologic malignancy, infections, and vascular events in younger patients.

197 so poor clinical outcomes, such as recurrent vascular events, in patients treated with aspirin.

198 h bleomycin and vinca alkaloids, can lead to vascular events including acute coronary thrombosis and

199 ndex stroke/TIA (range 0.5 to 4.5 years) for vascular events including stroke, TIA, myocardial infarc

200 a prime mediator of the pathogenesis of many vascular events, including angiogenesis.

201 ferative neoplasm that may be complicated by vascular events, including both thrombosis and bleeding.

202 line N-BNP was strongly predictive of future vascular events independently of other characteristics.

203 people living with HIV (PLWHIV), the risk of vascular events is increased; however, whether incidenta

204 fest vascular disease, the risk of recurrent vascular events is likely to vary.

205 nslate into a short-lived increased risk for vascular events is not known.

206 mation, but which of these are predictive of vascular events is not known.

207 The prevention of secondary vascular events is of paramount importance in patients w

208 k factor, how it causes end-organ damage and vascular events is poorly understood.

209 of AF-related stroke and peripheral embolic vascular events is uncertain.

210 rticipants, with the risks of incident major vascular events, major coronary events, revascularizatio

211 n of FMD patients may present with a serious vascular event, many present with nonspecific symptoms a

212 udies (8,021 incident, 7,513 prevalent major vascular events [MVE] in 74,683 individuals) and 10 acut

213 pg/ml had adjusted relative risks for major vascular events (MVEs) (i.e., major coronary events [MCE

214 We undertook meta-analyses of serious vascular events (myocardial infarction, stroke, or vascu

215 New vascular events (myocardial infarction, stroke, or vascu

216 [CI] 1.86 to 5.65; p = 0.0001) for nonfatal vascular events (n = 149), 1.80 (95% CI 1.13 to 2.88; p

217 were infections after discharge (n = 10) and vascular events (n = 6).

218 The primary outcome was the first major vascular event (nonfatal myocardial infarction, death fr

219 Major vascular events occurred in 1477 (24.5%) participants al

220 2024 acute vascular events occurred in 1657 individuals: 918 (45%)

221 irect evidence for the importance of ECAS in vascular events occurrence.

222 sed all individuals presenting with an acute vascular event of any type in any arterial territory irr

223 uclear estrogen receptor signaling regulates vascular events of physiological relevance and suggest t

224 jor adverse cardiovascular events, and major vascular events of the arm at 60 days.

225 The reduced risk of major vascular events on aspirin was initially offset by an in

226 ermine the effect of secondary prevention of vascular events on cognitive function after stroke.

227 et the patients at highest risk of recurrent vascular events on medical therapy.

228 let treatment is recommended after ischaemic vascular events, on the basis of trials done mainly in p

229 The primary outcome was the first major vascular event or revascularization.

230 hout aura did not have increased risk of any vascular events or angina.

231 ion, treated brain metastases, and no recent vascular events or bleeding diatheses were eligible.

232 e with diabetes risk factors, a total of 134 vascular events or deaths were avoided for every 54 new

233 For such individuals, a total of 86 vascular events or deaths were avoided with no new cases

234 nsignificant reductions in the rate of major vascular events or revascularization for patients treate

235 The rates of total major vascular events or revascularization were significantly

236 e rates of medication adherence, total major vascular events or revascularization, the first major va

237 ated with an increase in fatal and non-fatal vascular events (OR 2.58, 95% CI 2.05-3.24, p<0.0001).

238 poB, and a corresponding lower risk of major vascular events (OR, 0.946 [95% CI, 0.921-0.972]) that w

239 s, and the composite of stroke, death, major vascular events, or myocardial infarction using multivar

240 nostic value for subsequent clinical course, vascular events, or survival.

241 The high rates of acute vascular events outside the coronary arterial territory

242 51 (6%) patients experienced stroke or other vascular events over 7 +/- 7 years, including 44 patient

243 al cardiac events, and nonfatal extracardiac vascular events over a mean period of 7.8 years +/- 1.5

244 evels had a 3.8-fold increase in risk of any vascular event (P<0.001).

245 major vascular events (p = 0.0149), nonfatal vascular events (p < 0.0001), major vascular procedures

246 owed an independent effect of TBARS on major vascular events (p = 0.0149), nonfatal vascular events (

247 The Periodontitis and Vascular Events (PAVE) pilot study was conducted to inve

248 In the Periodontitis and Vascular Events (PAVE) pilot study, periodontal therapy

249 The RR for major vascular events per 1-mmol/L (38.7-mg/dL) reduction in L

250 0.77 (95% CI, 0.75-0.79, P < .001) for major vascular events per 1-mmol/L reduction in LDL-C level.

251 ed, similar proportional reductions in major vascular events per 1.0 mmol/L LDL cholesterol reduction

252 R 0.75, 95% CI 0.70-0.80) reduction in major vascular events per 1.0 mmol/l reduction in low-density

253 uld be expected to prevent at least 37 major vascular events per 1000 such people treated for 4 years

254 -C were associated with similar RRs of major vascular events per change in LDL-C.

255 are at increased risk but have not yet had a vascular event (primary prevention).

256 associated with lower combined bleeding and vascular event rate (27% vs. 46%; p = 0.05), shorter med

257 ER participants with moderate CKD had higher vascular event rates (hazard ratio [HR]: 1.54, 95% confi

258 ts that may optimize this process and reduce vascular event rates beyond currently available LDL lowe

259 whether reducing inflammation will decrease vascular event rates.

260 pirin versus placebo on recurrent VTE, major vascular events (recurrent VTE, myocardial infarction, s

261 hree times the risk of death associated with vascular events (relative risk, 2.54; 95 percent confide

262 ct of pneumococcal polysaccharide vaccine on vascular events remains controversial.

263 is highly beneficial regarding mortality and vascular event risks.

264 rval [CI] 1.47 to 7.42; p = 0.038) for major vascular events, RR of 4.10 (95% CI 2.55 to 6.60; p < 0.

265 l reductions in the aggregate of all serious vascular events seemed similar for men and women.

266 fety profile without obvious accumulation of vascular events, several types of vascular adverse event

267 andomised trials of aspirin in prevention of vascular events showed that daily aspirin reduced the in

268 lity and increased CIMT have associated with vascular events significantly (P < 0.05).

269 The rate of vascular events significantly increased in the first 4 w

270 ound no reduction in incidence of AF-related vascular events since publication of the BAFTA trial.

271 ng the three-year study, there were 51 major vascular events such as fatal/nonfatal myocardial infarc

272 ough presence of metabolic syndrome predicts vascular events, such prediction is inferior and does no

273 gnificantly higher in patients who developed vascular events than in those who did not (7.1 versus 5.

274 rage risk, 43,000 person-years, 3306 serious vascular events) that compared long-term aspirin versus

275 grel Trial With Irbesartan for Prevention of Vascular Events, there was no evidence of interaction be

276 es the incidence of coronary and other major vascular events to a similar extent, irrespective of KIF

277 Clinical events comprised death, vascular events, tricuspid regurgitation requiring surge

278 ed an independent effect of LOOH on nonfatal vascular events, vascular procedures, and all events or

279 se, median 10-year risk of a recurrent major vascular event was 17% (interquartile range, 11%-28%), v

280 Cumulative 20-year risk of any vascular event was 27.7% (95% CI = 18.5-37.0) after TIA

281 or nonfatal myocardial infarction, and major vascular event was pre-defined as major coronary event p

282 History of vascular events was analyzed using logistic regression,

283 , the risk (hazard ratio [HR]) of developing vascular events was assessed in patients with and withou

284 An increased risk for arterial and venous vascular events was seen in patients with CML treated wi

285 5.8% versus 11.4% (P < .001), and thrombotic vascular events were 2.8% versus 1.4% (P = .038), respec

286 ease-activated receptor-1 antagonism on limb vascular events were accompanied by an increased risk of

287 A past or presenting history of vascular events were common: 19.2% of patients had a tra

288 Variables at time 0 and vascular events were examined by univariable and multiva

289 all known risk factors for the occurrence of vascular events were included in the model.

290 22.3 mg/dL]) from 49 trials with 39645 major vascular events were included.

291 Independent predictors of vascular events were older age, current smoking status,

292 ant reductions of about one-quarter in major vascular events were seen both overall and in different

293 idence rate of acute thrombosis, and develop vascular events when additional thrombosis risk factors

294 The 6% (SE 3.5%) reduction in major vascular events with a further 0.35 mmol/L reduction in

295 rapy significantly reduced the risk of major vascular events with greater potential for absolute bene

296 dered for primary or secondary prevention of vascular events with regard to the 2 independent risk fa

297 Proportional reductions in the risk of major vascular events with statin therapy were similar (intera

298 nt, especially in terms of the likelihood of vascular events, with 5' mutations most detrimental.

299 a significant reduction in the rate of major vascular events, with improved net clinical benefit.

300 of $100,000/QALY, the annual risk of serious vascular events would have to be >/=2.5 times higher wit