ライフサイエンスコーパス: cerebrovascular event

1 iffer in women who have experienced a recent cerebrovascular event.

2 s, respectively, had been hospitalized for a cerebrovascular event.

3 for acute coronary syndromes after a recent cerebrovascular event.

4 articularly at risk of hospitalization for a cerebrovascular event.

5 r risk for an acute major adverse cardiac or cerebrovascular event.

6 sociated with an increased risk of recurrent cerebrovascular events.

7 ocardial infarction are at increased risk of cerebrovascular events.

8 se and increased risk for cardiovascular and cerebrovascular events.

9 Major adverse cardiovascular or cerebrovascular events.

10 ined by magnetic resonance imaging (MRI) for cerebrovascular events.

11 sis (PCI arm), and major adverse cardiac and cerebrovascular events.

12 ficant benefit on rates of cardiovascular or cerebrovascular events.

13 in asymptomatic group experienced recurrent cerebrovascular events.

14 s thrombosis are less common causes of acute cerebrovascular events.

15 are associated with increased risk of future cerebrovascular events.

16 t studies have raised concerns about adverse cerebrovascular events.

17 , venous thromboembolic events, and ischemic cerebrovascular events.

18 Presence of IPH on MRI strongly predicts cerebrovascular events.

19 dentifies high-risk features associated with cerebrovascular events.

20 quent increases in the rates of coronary and cerebrovascular events.

21 oramen ovale (PFO) are at risk for recurrent cerebrovascular events.

22 and an increased risk of cardiovascular and cerebrovascular events.

23 carotid restenosis on the risk of recurrent cerebrovascular events.

24 AD) are at risk of major adverse cardiac and cerebrovascular events.

25 atherosclerosis, they are poor predictors of cerebrovascular events.

26 es that were likely to affect NfL, including cerebrovascular events.

27 laque hemorrhage as a predictor of recurrent cerebrovascular events.

28 ) were all predictive of subsequent maternal cerebrovascular events.

29 has been associated with potentially serious cerebrovascular events.

30 es are not associated with future cardiac or cerebrovascular events.

31 ependently associated with either cardiac or cerebrovascular events.

32 h has been implicated in atherosclerosis and cerebrovascular events.

33 investigate the association between CED and cerebrovascular events.

34 ndently associated with an increased risk of cerebrovascular events.

35 ssive surveillance, 802 were validated to be cerebrovascular events.

36 tification of high-risk plaques that lead to cerebrovascular events.

37 fficacy, drug cost, and rates of cardiac and cerebrovascular events.

38 ngenital heart disease are at risk of having cerebrovascular events.

39 likely to develop major adverse cardiac and cerebrovascular events.

40 in terms of major adverse cardiovascular and cerebrovascular events.

41 be a marker of increased risk for recurrent cerebrovascular events.

42 thrombosis (0.44%; range, 0.28%-0.68%), and cerebrovascular events (0.32%; range, 0.18%-0.53%) were

43 Twenty-two patients (13.6%) had 29 cerebrovascular events (1/100 patient-years).

44 0.9-1.6%, I(2) = 87%) were hospitalized for cerebrovascular events, 1.1% (95% CI = 0.8-1.3%, I(2) =

45 of cell therapy on major adverse cardiac and cerebrovascular events (14.0% versus 16.3%; hazard ratio

46 al, 1.32-1.90) and major adverse cardiac and cerebrovascular events (2.62; 2.28-3.01; all P<0.001).

47 , there were 36 deaths (2.2%) and 48 adverse cerebrovascular events (2.9%) in the postoperative hospi

48 The commonest of these were first cerebrovascular events, 205 (CI: 183, 230); shingles, 14

49 patients were more likely to have had prior cerebrovascular events (22% versus 15%; P=0.0003) and me

50 elated to the incidence of both coronary and cerebrovascular events, 24-hour ambulatory diastolic blo

51 ardial infarction (35 523 individuals), 6 on cerebrovascular events (27 689 individuals), and 5 on al

52 <0.001) and major adverse cardiovascular and cerebrovascular events (4.3% vs. 5.9%; hazard ratio, 0.7

53 , P=0.003), major adverse cardiovascular and cerebrovascular events (4.6% versus 5.7%, P=0.007), and

54 0.034), and major adverse cardiovascular or cerebrovascular events (40.2% vs. 47.9%, respectively; p

55 782 cancer survivors were hospitalized for a cerebrovascular event-40% higher than expected (SHR=1.4,

56 r events end point, including death, MI, and cerebrovascular event (5.0% versus 2.6% in men; 5.1% ver

57 was associated with a higher rate of 30-day cerebrovascular events (7.1% versus 0.4%; P=0.030).

58 Those with CM-associated cerebrovascular events (8%) may benefit from short-term

59 y; p < 0.001), and major adverse cardiac and cerebrovascular events (8.7% vs. 23.9%, respectively; p

60 -year freedom from major adverse cardiac and cerebrovascular events (89.4% versus 71.2%; 81.9% versus

61 roups in the number of combined coronary and cerebrovascular events: 96 (3.7%) with placebo, 82 (3.2%

62 ombosis and major adverse cardiovascular and cerebrovascular events (a composite of death, myocardial

63 rel in High-Risk Patients With Non-disabling Cerebrovascular Events), a similar trial treating with c

64 Coronary or cerebrovascular events (adjusted for age, gender, tradit

65 the rate of major adverse cardiovascular and cerebrovascular events after a median follow-up of 3.8 y

66 boembolic events; HR 1.5, 95% CI 0.7-3.2 for cerebrovascular events) after adjusting for age, sex, bo

67 vestigate the risks of hospitalization for a cerebrovascular event among 5-year survivors of cancer d

68 evaluate the risks of hospitalization for a cerebrovascular event among long-term survivors of teena

69 The risk of a cerebrovascular event among subjects with ASA was nearly

70 nt for the secondary prevention of recurrent cerebrovascular events among patients with PFO-related t

71 Prior cerebrovascular events and a low glomerular filtration r

72 tion of long-term risk of cardiovascular and cerebrovascular events and death.

73 eduction in major adverse cardiovascular and cerebrovascular events and increased bleeding.

74 may be responsible for the increased risk of cerebrovascular events and neurodegenerative disorders i

75 the rate of major adverse cardiovascular and cerebrovascular events and no increase in the risk of st

76 The incidence of cerebrovascular events and peripheral vascular disease e

77 alysis was used to estimate CVE (cardiac and cerebrovascular events) and all-cause mortality hazard r

78 nary heart disease event, 17,822 had a first cerebrovascular event, and 14,550 had a first venous thr

79 ndrome (ACS), cardiac dysrhythmia, CV death, cerebrovascular event, and venous thromboembolism (secon

80 d their components of cardiovascular events, cerebrovascular events, and 30-day mortality.

81 here were 44 (11%) cardiac events, 18 (4.5%) cerebrovascular events, and 41 deaths (10.3%).

82 of TAVR candidates, led to a higher rate of cerebrovascular events, and accounted for a third of arr

83 infarction, major adverse cardiovascular and cerebrovascular events, and Global Utilization of Strept

84 ower rates of new-onset atrial fibrillation, cerebrovascular events, and readmissions.

85 The cumulative incidence of cerebrovascular events, and rehospitalization due to car

86 cidence rates of peripheral arterial events, cerebrovascular events, and venous thromboembolic events

87 Cerebrovascular events are a serious complication of cya

88 However, bleeding and cerebrovascular events are common; these may be modifiab

89 Fatal cerebrovascular events are often caused by rupture of at

90 g profiles of antipsychotics and the risk of cerebrovascular events are unclear.

91 increased risk of major adverse cardiac and cerebrovascular events as compared with SAVR (42.5% vers

92 the rate of early major adverse cardiac and cerebrovascular events as well as long-term survival.

93 a include an increased risk of mortality and cerebrovascular events, as well as metabolic effects, ex

94 ere excluded, there was an increased risk of cerebrovascular events associated with microcytosis (p <

95 the occurrence of major adverse cardiac and cerebrovascular event at 6 months.

96 patients in the CHAMPION trials with a prior cerebrovascular event at least 1 year before the percuta

97 yocardial infarction, revascularization, and cerebrovascular events at 12 months.

98 e early events and major adverse cardiac and cerebrovascular events at 3 years.

99 bined incidence of major adverse cardiac and cerebrovascular events at 30 days after intervention, in

100 to compare major adverse cardiovascular and cerebrovascular events at 30 days and 1 year between pat

101 omposite of major adverse cardiovascular and cerebrovascular events at 30 days.

102 from any cause and major adverse cardiac and cerebrovascular events at 5 years.

103 er rates of major adverse cardiovascular and cerebrovascular events at 7 years.

104 n the subgroup of patients with a history of cerebrovascular events at least 1 year prior to randomiz

105 dent predictors of major adverse cardiac and cerebrovascular events at long-term follow-up.

106 mptomatic, 41 urgent, and 24 patients with a cerebrovascular event between 5 and 180 days of the caro

107 group, there was no difference in recurrent cerebrovascular events between DWI+ and DWI- patients.

108 xhibited a positive linear relationship with cerebrovascular events but a curvilinear relationship wi

109 CIP-BB measure was associated with increased cerebrovascular events but not improved cardiovascular e

110 ombosis and major adverse cardiovascular and cerebrovascular events but was associated with an increa

111 eenage and young adult cancer are at risk of cerebrovascular events, but the magnitude of and extent

112 hibitors and the hazard of cardiovascular or cerebrovascular events, but the use of antiretroviral dr

113 mg/day atorvastatin reduces both stroke and cerebrovascular events by an additional 20% to 25% compa

114 cardial infarction [major adverse cardiac or cerebrovascular event] by day 30 plus ipsilateral stroke

115 During a median follow-up of 5.1 years, cerebrovascular events (cerebrovascular disease-related

116 y, only patient age (P=0.012), but not prior cerebrovascular events, cognitive status, direct TAVI, c

117 ll events together or for cardiovascular and cerebrovascular events combined.

118 l/L) had an adjusted 2.6-fold higher risk of cerebrovascular events compared to those in the highest

119 Relative incidence of cerebrovascular events compared with coronary events was

120 wer rate of major adverse cardiovascular and cerebrovascular events compared with FFR-guided PCI, dri

121 Presentation of cerebrovascular event complicated with out-of-hospital c

122 We evaluated incidence of cerebrovascular events consistent with stroke or transie

123 Recurrent cerebrovascular events constitute an estimated 200,000 o

124 nt (nonfatal myocardial infarction, nonfatal cerebrovascular event, coronary revascularization, or ca

125 ts (nonfatal myocardial infarction, nonfatal cerebrovascular event, coronary revascularization, or ca

126 replacement (TAVR) patients at high risk for cerebrovascular events (CVE) is of major clinical releva

127 hard, patient-centered outcomes of death and cerebrovascular events (CVEs) after heart rhythm disorde

128 predictive factors, and prognostic value of cerebrovascular events (CVEs) after transcatheter aortic

129 Cerebrovascular events (CVEs) are devastating complicati

130 aterals influenced the risk of recurrence of cerebrovascular events (CVEs: stroke or transient ischem

131 roup differences in major adverse cardiac or cerebrovascular events, deaths, readmissions, functional

132 d point was major adverse cardiovascular and cerebrovascular events, defined as all-cause death, myoc

133 tissue plasminogen activator (tPA) following cerebrovascular events demonstrates that tPA also plays

134 By principal management strategy, cerebrovascular events developed in 2.0%, 14.9%, and 1.9

135 -cause mortality, cardiovascular disease and cerebrovascular events, diabetes, cognitive impairment,

136 death, dialysis, myocardial infarction, and cerebrovascular events did not differ significantly at 3

137 nt mortality and nonfatal cardiovascular and cerebrovascular events for those with ST-segment-elevati

138 High-risk patients with Acute Non-disabling Cerebrovascular Events), for efficacy and safety outcome

139 Low homoarginine is strongly associated with cerebrovascular events, graft loss and progression of ki

140 domized patients, 1270 patients (5.1%) had a cerebrovascular event >1 year old, including 650 assigne

141 Patients who had a cerebrovascular event had a significantly increased tend

142 All patients who had a cerebrovascular event had developed > or = 1 risk factor

143 in the 80-mg arm experienced a reduction in cerebrovascular events (hazard ratio 0.77, 95% CI 0.64 t

144 P=0.036) and major adverse cardiovascular or cerebrovascular events (hazard ratio, 1.97 [95% CI, 1.08

145 all-cause mortality, coronary artery events, cerebrovascular events, heart failure, nephropathy, and

146 all-cause mortality, coronary artery events, cerebrovascular events, heart failure, nephropathy, and

147 Secondary outcomes were arrhythmia, cerebrovascular events, hemorrhagic stroke, ischemic str

148 at risk of future major adverse cardiac and cerebrovascular events, highlighting the great potential

149 e was no association of SW with the risk for cerebrovascular events (HR 1.76, 95% CI 0.45-7.01).

150 nd points included major adverse cardiac and cerebrovascular events (ie, death from any cause, stroke

151 High-Risk Patients with Acute Non-disabling Cerebrovascular Events II) trial.

152 in improved major adverse cardiovascular and cerebrovascular event in patients with 2- and 3-vessel c

153 difference between those with and without a cerebrovascular event in terms of age, smoking history,

154 zard ratio, 0.32; 95% CI, 0.20 to 0.54), and cerebrovascular events in 0 and 4 patients (0 vs. 0.7%).

155 ambient air pollution and risk for ischemic cerebrovascular events in a US community.

156 ht to determine the frequency of spontaneous cerebrovascular events in adult patients with cyanotic c

157 occurrence and/or outcomes of patients with cerebrovascular events in association with their SARS-Co

158 , but MBL-deficient genotypes were not, with cerebrovascular events in Caucasians being the exception

159 id stenting has an increased risk of adverse cerebrovascular events in elderly patients but mortality

160 fficacy in reducing the rate of coronary and cerebrovascular events in patients 75 years of age or yo

161 The CENTER (Cerebrovascular EveNts in patients undergoing Transcathe

162 that HMG-CoA reductase inhibition may reduce cerebrovascular events in patients with prevalent corona

163 e incidence, predictors, and implications of cerebrovascular events in patients with ST-segment-eleva

164 There was a nonsignificant greater rate of cerebrovascular events in PD patients.

165 is not an independent risk factor for future cerebrovascular events in the general population.

166 There were no major adverse cardiac and cerebrovascular events in the hospital or at 3-month fol

167 umber of myocardial infarctions and ischemic cerebrovascular events in the rofecoxib group.

168 We describe an analysis of cerebrovascular events in the Treating to New Targets st

169 We evaluated the risk of coronary and cerebrovascular events in the Women's Health Initiative

170 een shown to predict both cardiovascular and cerebrovascular events in various patient populations, i

171 Older age, previous cerebrovascular event, in-hospital coronary artery bypas

172 e of a composite of major adverse cardiac or cerebrovascular events, in functional status, or in qual

173 edom from combined major adverse cardiac and cerebrovascular events (including all-cause death, AMI r

174 nsion, alcoholic cardiomyopathy, cancer, and cerebrovascular events, including cerebrovascular hemorr

175 identify all women aged 12 to 55 years with cerebrovascular events, including transient ischemic att

176 l infarction, coronary revascularization, or cerebrovascular events) independently of each other, wit

177 ed death, especially with cardiovascular and cerebrovascular events, independently of other prognosti

178 f gender difference and estrogen in ischemic cerebrovascular events is controversial.

179 symptomatic OSA to reduce cardiovascular and cerebrovascular events is not currently supported by hig

180 n coronary endothelial dysfunction (CED) and cerebrovascular events is unknown.

181 associated with coronary artery disease) and cerebrovascular events (ischemic fatal and non-fatal str

182 The 30-day major adverse cardiac and cerebrovascular event (MACCE) rate for CABG and PCI was

183 ary endpoint was a major adverse cardiac and cerebrovascular event (MACCE), which was defined as comp

184 rimary outcome was major adverse cardiac and cerebrovascular events (MACCE) (i.e., death, stroke, myo

185 the risk of major adverse cardiovascular and cerebrovascular events (MACCE) among those with AF.

186 tin use and major adverse cardiovascular and cerebrovascular events (MACCE) and amputation-free survi

187 e of perioperative major adverse cardiac and cerebrovascular events (MACCE) and bleeding and its rela

188 Major adverse cardiovascular and cerebrovascular events (MACCE) are a significant source

189 from any cause and major adverse cardiac and cerebrovascular events (MACCE) at 1 year.

190 activity, and risk of major adverse cardiac/cerebrovascular events (MACCE) at 1 year: myocardial inf

191 point consisted of major adverse cardiac and cerebrovascular events (MACCE) at 30 days, and the prima

192 composite of major adverse cardiovascular or cerebrovascular events (MACCE) including all-cause death

193 rimary endpoint was major adverse cardiac or cerebrovascular events (MACCE), a composite of all-cause

194 rimary endpoint was major adverse cardiac or cerebrovascular events (MACCE), a composite of all-cause

195 including any CVD, major adverse cardiac and cerebrovascular events (MACCE), myocardial infarction (M

196 ombosis and major adverse cardiovascular and cerebrovascular events (MACCE).

197 ing, or death), and major adverse cardiac or cerebrovascular events (MACCE).

198 Mortality and major adverse cardiac and cerebrovascular events (MACCE, defined as all-cause mort

199 rimary endpoint was major adverse cardiac or cerebrovascular events ([MACCE] the composite of all-cau

200 e and the primary (major adverse cardiac and cerebrovascular event [MACCE] or all-cause mortality) an

201 e primary endpoint (major adverse cardiac or cerebrovascular events [MACCE]) was a composite of all-c

202 cardiac endpoint (major adverse cardiac and cerebrovascular events [MACCE]), and quality of life (QO

203 outcomes of major adverse cardiovascular or cerebrovascular events (MACCEs) and their components of

204 status, or major adverse cardiovascular and cerebrovascular events (MACCEs) in older adults undergoi

205 e, or death (termed major cardiovascular and cerebrovascular events [MACCEs]) were compared between t

206 posite end point of major adverse cardiac or cerebrovascular events (major adverse cardiac event or i

207 ne cells in plaques that are associated with cerebrovascular events may enable the design of more pre

208 We recorded cardiac and cerebrovascular events, mortality, and clinical progress

209 The cumulative incidence of cerebrovascular events, myocardial infarction, and coron

210 jor adverse cardiovascular events (n = 103), cerebrovascular events (n = 53), graft failure or doubli

211 ian follow-up of 19.6 months, a total of 108 cerebrovascular events occurred (15.7% event rate).

212 No cerebrovascular events occurred in the GSNO group.

213 Major adverse cardiovascular and cerebrovascular events occurred most frequently in patie

214 No in-hospital major adverse cardiac and cerebrovascular events occurred.

215 From January 2000 to December 2002, 2,350 cerebrovascular events occurred.

216 l end points and was effective in preventing cerebrovascular events (odds ratio [OR], 0.61; 95% confi

217 ctors of stroke at 30 days were a history of cerebrovascular events (odds ratio, 2.2; 95% CI, 1.4-3.6

218 in terms of major adverse cardiovascular and cerebrovascular events of 2 different complete coronary

219 We sought to assess the effects on cerebrovascular events of treating patients with stable

220 Complex plaques were associated with cerebrovascular events only univariately.

221 to first clinical event (renal, cardiac, or cerebrovascular event or death).

222 peri-procedural or major adverse cardiac or cerebrovascular event or need for cardiac surgical inter

223 ny increase in the rate of cardiovascular or cerebrovascular events or related mortality.

224 ta-blocker therapy only reduced the odds for cerebrovascular events (OR, 0.75; 95% CI, 0.57-0.98) but

225 .84-1.29; P=0.73), major adverse cardiac and cerebrovascular events (OR, 1.05; 95% CI, 0.80-1.38; P=0

226 BB measure was not associated with increased cerebrovascular events (OR, 1.22; 95% CI, 0.62-2.38).

227 0.66-1.54) but was associated with increased cerebrovascular events (OR, 3.01; 95% CI, 1.00-10.07).

228 the single strongest factor associated with cerebrovascular events (OR, 4.32; 95% CI, 1.26 to 14.83)

229 fined as death, acute myocardial infarction, cerebrovascular event, or further revascularization at h

230 erebrovascular death, myocardial infarction, cerebrovascular event, or revascularization.

231 y safety end point was a composite of death, cerebrovascular events, or serious treatment-related adv

232 und that 342 of the 119,668 mothers suffered cerebrovascular events over 14-19 years' follow-up.

233 ids had a significant reduction in secondary cerebrovascular events (P = .0049).

234 iated with a 0.6% relative risk reduction in cerebrovascular events (p = 0.002) and a 0.5% relative r

235 ted that LA fibrosis independently predicted cerebrovascular events (p = 0.002) and significantly inc

236 event (a composite of any coronary event, a cerebrovascular event, peripheral vascular disease, or h

237 D events, comprising coronary heart disease, cerebrovascular events, peripheral artery disease, and c

238 1994 and 2000, 308 consecutive patients with cerebrovascular events presumably related to PFO underwe

239 One-year mortality, cerebrovascular events, Q-wave myocardial infarction, ta

240 st that the 1-year major adverse cardiac and cerebrovascular event rate is higher among diabetic pati

241 th CED had a significantly higher cumulative cerebrovascular event rate than those without (P=0.04).

242 The overall 1-year major adverse cardiac and cerebrovascular event rate was higher among diabetic pat

243 unadjusted major adverse cardiovascular and cerebrovascular event rate was reduced with CABG for pat

244 uld be detected on major adverse cardiac and cerebrovascular event rates after BMMNC infusion after a

245 nt in crude major adverse cardiovascular and cerebrovascular event rates at 30 days and 1 year betwee

246 Major adverse cardiac and cerebrovascular event rates at 5 years was 36.9% in PCI

247 mple in which age- and sex-specific ischemic cerebrovascular event rates were determined and in a sam

248 Major adverse cardiovascular and cerebrovascular event rates were not statistically diffe

249 infarct size, and major adverse cardiac and cerebrovascular event rates.

250 ower mortality and major adverse cardiac and cerebrovascular events rates than transfemoral TAVR perf

251 HIV-associated cerebrovascular events remain highly prevalent even in t

252 year mortality and major adverse cardiac and cerebrovascular events remained consistent in the TO-tre

253 population), whereas the pathophysiology of cerebrovascular events remains largely unknown.

254 has been broadly studied, little is known on cerebrovascular events revealed by out-of-hospital cardi

255 hmia (RR=0.99; 95% CI, 0.85-1.16; P=0.92) or cerebrovascular events (RR=1.03; 95% CI, 0.92-1.16; P=0.

256 55%; 86% of the heterozygotes had recurrent cerebrovascular event(s) and 40% died.

257 New coronary and/or cerebrovascular events served as outcome variables over

258 3602 patients (2.0%) experienced at least 1 cerebrovascular event (stroke: 63 patients; transient is

259 onal hazards regression, we compared risk of cerebrovascular events (stroke, carotid revascularizatio

260 ) and have found a stronger association with cerebrovascular events than global stiffness measures.

261 the perinatal and neonatal period, including cerebrovascular events that are diagnosed during the per

262 spectively evaluated for any well documented cerebrovascular events that occurred at > or = 18 years

263 The methods involved ascertaining cerebrovascular events that occurred in Nueces County, T

264 cular disease and ensuing cardiovascular and cerebrovascular events, the leading causes of death worl

265 nd points included major adverse cardiac and cerebrovascular events, transient ischemic attack, and d

266 Prediction of major cardiovascular and cerebrovascular events using conventional risk factor mo

267 Ten-year incidence of cerebrovascular events was 34% in patients treated with

268 ereas freedom from major adverse cardiac and cerebrovascular events was 80.9% after SAVR and 67.3% af

269 ow-up, the rate of major adverse cardiac and cerebrovascular events was 9.9% per patient-year, and th

270 The risk of cerebrovascular events was also associated with increase

271 ference in overall major adverse cardiac and cerebrovascular events was found between treatment group

272 ncidence of major adverse cardiovascular and cerebrovascular events was higher in the FFR-guided PCI

273 uding those with a history of cardiovascular/cerebrovascular events, was 1.75 (95% confidence interva

274 As endothelial activation is a hallmark of cerebrovascular events, we postulated that this may also

275 o, rates of major adverse cardiovascular and cerebrovascular events were 4.2% versus 5.0% among patie

276 arction, and major adverse cardiovascular or cerebrovascular events were 43.0%, 4.1%, 15.2%, and 52.6

277 ilar results were obtained when coronary and cerebrovascular events were analyzed separately.

278 Cerebrovascular events were associated with significantl

279 d composite major adverse cardiovascular and cerebrovascular events were compared between the CABG an

280 served numbers of first hospitalizations for cerebrovascular events were compared with that expected

281 However, when only the cerebrovascular events were considered, the difference b

282 Major adverse cardiac and cerebrovascular events were defined as the composite of

283 Risk estimates of the presence of IPH for cerebrovascular events were derived in random effects re

284 Among the study population, a total of 25 cerebrovascular events were documented, 22 in patients w

285 Cerebrovascular events were independently predicted by o

286 All cerebrovascular events were less frequent after PCI than

287 l and freedom from major adverse cardiac and cerebrovascular events were observed after SAVR compared

288 Cerebrovascular events were often disabling and were str

289 and overall major adverse cardiovascular or cerebrovascular events were recorded.

290 Early major adverse cardiac and cerebrovascular events were reported in 18 (15%) patient

291 Major adverse cardiac and cerebrovascular events were similar between arms in pati

292 Rates of postoperative cerebrovascular events were similar between groups (2.7%

293 ncidence of major adverse cardiovascular and cerebrovascular events, which were defined as cardiac de

294 equivalent major adverse cardiovascular and cerebrovascular event with PCI for 2-vessel (hazard rati

295 d increased major adverse cardiovascular and cerebrovascular event with PCI for patients with 2-vesse

296 d go on to develop major adverse cardiac and cerebrovascular events with an area under the curve of 0

297 absolute hazard of major adverse cardiac or cerebrovascular events with PCI compared with CABG rose

298 Emerging data indicate an increased risk of cerebrovascular events with severe acute respiratory syn

299 tely symptomatic patients ([urgent] ischemic cerebrovascular event within the previous 5 days) underg

300 In HORIZONS-AMI, cerebrovascular events within 3 years after ST-segment-e