ライフサイエンスコーパス: ischemia

1 plications, and the functional evaluation of ischemia.

2 o 92%) for exclusion of inducible myocardial ischemia.

3 users to safely exclude inducible myocardial ischemia.

4 increase was associated with the duration of ischemia.

5 cocaine users for mechanisms independent of ischemia.

6 s response implicated in cell survival after ischemia.

7 G-CSFR 24 h prior to 22-min unilateral renal ischemia.

8 schemic heart disease and moderate or severe ischemia.

9 did not prevent capillary closure or retinal ischemia.

10 determining neuronal activity signatures of ischemia.

11 s detected a cTn increase after only 30 s of ischemia.

12 siologic pathways undergoing during cerebral ischemia.

13 cognitive dysfunction after global cerebral ischemia.

14 tivity for exclusion of inducible myocardial ischemia.

15 the Alzheimer's disease brain and following ischemia.

16 ternans (n=7), in the presence of myocardial ischemia.

17 D11c(+)F4/80(+) renal macrophages after cold ischemia.

18 focusing on Parkinson's disease and cerebral ischemia.

19 nociception, fear memory, mood disorders and ischemia.

20 , are biomarkers of kidney injury after warm ischemia.

21 and/or MI, independently of the presence of ischemia.

22 al survival and cognitive recovery following ischemia.

23 urvival and growth in models of experimental ischemia.

24 as the A2 reactive astrocyte phenotype after ischemia.

25 sisted of 4 x 5 min cycles of left hind limb ischemia.

26 ered as an optimal therapy following cardiac ischemia.

27 autophagy following transient focal cerebral ischemia.

28 sed in human kidneys following extended cold ischemia.

29 nd determine its roles after global cerebral ischemia.

30 e CGRP receptor antagonists, worsen cerebral ischemia.

31 art preparations before and during simulated ischemia.

32 vs. 3.0%) and hospitalization for acute limb ischemia (1.6% vs. 1.7%) were not different by sex.

33 hether patients had chronic limb-threatening ischemia (1480 patients) or intermittent claudication (8

34 mplications (23%), including prolapse (26%), ischemia (16%), and parastomal hernia (19%).

35 Following hypoxia-ischemia, 20 newborn piglets were randomized to: (i) Coo

36 defined as modified thrombolysis in cerebral ischemia 2b to 3.

37 among patients with chronic limb-threatening ischemia (33.4% [249 patients] in the drug-coated-device

38 mice impaired recovery from chronic hindlimb ischemia, a model of peripheral artery disease.

39 al revascularization strategy for acute limb ischemia (ALI) remains unclear, and contemporary compara

40 sitive proteins and myocardial damage due to ischemia alone.

41 minitis, ileus, Ogilvie syndrome, mesenteric ischemia) among critically ill patients with coronavirus

42 synergistic or overlapping mechanism between ischemia and Abeta toxicity are lacking.

43 distinct anatomical units in the brain after ischemia and Abeta toxicity will help in the design of e

44 an enable the reduction or avoidance of cold ischemia and allows for pretransplant measurement of fun

45 enuated superoxide production in response to ischemia and excitotoxicity in vitro and ex vivo Last, d

46 of a coronary stenosis to induce myocardial ischemia and guide decisions for percutaneous coronary i

47 ted stress cardiac MRI who were negative for ischemia and had no signs of structural heart disease.

48 Myocardial ischemia and infarction, both in the acute and chronic p

49 es from Lewis rat livers as a result of cold ischemia and machine perfusion.

50 ction, can cause chronic or acute myocardial ischemia and may lead to development of heart failure.

51 0 kg pigs were exposed to 30 minutes of warm ischemia and randomized to receive 22-hour HMP with eith

52 rly under states of oxidative stress such as ischemia and reperfusion (I/R), remains unexplored.

53 y promoting renal tubular inflammation after ischemia and reperfusion (IR).

54 nd then tested the effect of LV unloading on ischemia and reperfusion injury, cardiac metabolism, and

55 Myocardial infarction, following heart ischemia and reperfusion, is associated with profound ch

56 repair some of harmful consequences of heart ischemia and reperfusion, re-establishing myocardial fun

57 under baseline conditions, as well as during ischemia and reperfusion.

58 se-7 in endothelial cells promotes capillary ischemia and retinal neurodegeneration.

59 al for EC function and tissue recovery after ischemia and that fenofibrate rescues CEPT1-mediated act

60 e kidneys were exposed to 30 minutes of warm ischemia and then reimplanted following either 16 hours

61 elated complication that often leads to limb ischemia and thromboembolism, is proposed.

62 a, limb revascularization, or amputation for ischemia) and VTE (deep vein thrombosis or pulmonary emb

63 lemic pigs underwent MI induction (90 min of ischemia) and were kept for 42 days.

64 ed conditions associated with heart failure, ischemia, and atrial fibrillation, enhance Na(+) influx,

65 omplications like significant bleeding, limb ischemia, and cannula site bleeding were 15.4% (95% CI,

66 al and fungal), multiple sclerosis, cerebral ischemia, and cerebral malaria.

67 ving transplant outcome by early reversal of ischemia, and decreasing the risk of unintentional surgi

68 mitochondrial fate determination in cerebral ischemia, and in improving neurological deficit after st

69 nous RvD1 enhances perfusion recovery during ischemia, and mice deficient in Alx/Fpr2 have an endogen

70 hologies, including endothelial dysfunction, ischemia, and stroke.

71 HLA mismatch, number of veins/arteries, cold ischemia, and travel times.

72 Patients with ischemia (any segment with MPRI < 2) were more likely to

73 een case reports of patients with myocardial ischemia, arrhythmia, and sudden cardiac death.

74 ADC mapping showed evidence of ischemia as early as 27 min and follow-up T2w scans conf

75 characterized by intestinal inflammation and ischemia, as well derangements in intestinal microcircul

76 We hypothesized that myocardial ischemia assessed by CMR is associated with myocardial f

77 l Cdkl5 inhibition mitigates nephrotoxic and ischemia-associated AKI.

78 orkup in cases of suspected acute mesenteric ischemia because it can rule out other causes of acute a

79 g kidneys underwent 0, 30, or 60 min of warm ischemia, before hypothermic machine perfusion.

80 identify patients admitted for critical limb ischemia between 2005 and 2014.

81 Increasing ischemia burden (number of segments with MPRI < 2) was a

82 truction remained a significant predictor of ischemia burden (P = 0.03).

83 re procured after 30 minutes of warm in situ ischemia by cross-clamping the renal arteries.

84 ety of diseases, including neuronal death in ischemia, cancer, cardiac atrial fibrillation, malaria i

85 (2) donor kidneys subjected to ex vivo cold ischemia (CI); (3) donor kidneys subjected to kidney tra

86 RTEC-specific Vgf gene ablation exacerbates ischemia-, cisplatin-, and rhabdomyolysis-associated AKI

87 transcriptional stress response in RTECs to ischemia-, cisplatin-, and rhabdomyolysis-associated ren

88 ial cohort of patients without critical limb ischemia (CLI) have not been described.

89 Critical limb ischemia (CLI) is the most advanced stage of peripheral

90 oidal ischemia, defined as any new choroidal ischemia clinically diagnosed within 35 days after an IA

91 s in patients with critical limb threatening ischemia(CLTI) or diabetic foot infection(DFI).

92 stic pathways of kidney CD4(+) T cells after ischemia compared with normal mouse kidney.

93 After transient focal ischemia, Cxcr4 deficiency reduces monocyte infiltration

94 l advances have been made in elucidating how ischemia damages the brain.

95 performance for predicting delayed cerebral ischemia (DCI) (area under curve (AUC) > 0.750), and had

96 Acute choroidal ischemia, defined as any new choroidal ischemia clinical

97 Acute choroidal ischemia developed in 35 of 206 included eyes after a me

98 s but with supporting evidence of myocardial ischemia, different after PCI and CABG.

99 stering ACSL4 inhibitor rosiglitazone before ischemia diminished the ferroptotic damage in IR-injured

100 ) myocardial infarction, ischemic stroke, or ischemia-driven coronary revascularization.

101 d co-primary outcome of CV death, new MI, or ischemia-driven revascularization was determined.

102 of cardiac death, myocardial infarction, or ischemia-driven target lesion revascularization) were as

103 Tailoring hypothermia duration to ischemia duration may improve outcome from out-of-hospit

104 post Abeta toxicity and endothelin-1 induced ischemia (ET1) in rats.

105 nd determine its roles after global cerebral ischemia (GCI) in male and female mice.

106 udy the crucial role of astrocytes in edema, ischemia, glioma progression, stroke, and epilepsy.

107 es, 1 (11%), 0, and 0 patients from the 60-s ischemia group and 5 (63%), 2 (25%), and 1 (11%) from th

108 5 (63%), 2 (25%), and 1 (11%) from the 90-s ischemia group, respectively, fulfilled criteria for a b

109 mic effects in the acute phase of myocardial ischemia has not been investigated so far.

110 In response to TAE-induced ischemia, HCC cells adapt their growth program to effect

111 injury (especially birth asphyxia or hypoxia ischemia [HI]) is unclear.

112 Ischemia (hypoxia) and/or reperfusion (reoxygenation) in

113 8.4%) versus 45 (17.9%), access site-related ischemia in 55 (21.6%) versus 31 (12.3%), abdominal comp

114 rst hours after experimental balloon-induced ischemia in humans.

115 edures with no incidence of anterior segment ischemia in our cases.

116 he prediction of underlying acute myocardial ischemia in patients with chest pain.

117 d to exercise pathophysiology and myocardial ischemia in patients with coronary microvascular dysfunc

118 ally ameliorated liver injury and sinusoidal ischemia in SCD mice.

119 o develop endovascular approach for inducing ischemia in swine.

120 Stress cardiac MRI was positive for ischemia in two heart transplant patients; these finding

121 with intraportal MMP inhibitor, given after ischemia, in the 5-week HFHF rat reduced ALT by 71% and

122 ved mechanisms to tolerate severe hypoxia or ischemia, including the hibernation-capable Arctic groun

123 Here we found that hindlimb ischemia increases levels of resolvin D1 (RvD1), an infl

124 data suggest that FAD mutants may attenuate ischemia-induced brain angiogenesis.

125 Systemically administered ZT-1a reduces ischemia-induced CCC phosphorylation, attenuates cerebra

126 ng tool in protecting distant organs against ischemia-induced damage.

127 ated internalization of Cx43 and exacerbated ischemia-induced lateralization of Cx43 in isolated adul

128 tive LPSx4 provides complete protection from ischemia-induced neuron loss and hindlimb paralysis.

129 ves of ML385, an NRF2 inhibitor, showed that ischemia induces addiction to NRF2 in cells with NRF2 al

130 e and limit the impact of the prolonged warm ischemia inherent to the uDCD process, and to deal with

131 Breakdown of BBB integrity during cerebral ischemia initiates a devastating cascade of events that

132 also demonstrated significant resistance to ischemia injury compared with their wild-type littermate

133 ssociated with obesity, arrhythmias, cardiac ischemia, insulin resistance, etc.

134 ery for the Treatment of Narrowed Arteries), ISCHEMIA (International Study Of Comparative Health Effe

135 ation of endothelial caspase-9 after hypoxia-ischemia is a critical event in subsequent dysfunction o

136 The expansion of these subsets with ischemia is dependent on activation of innate immune sig

137 When hindlimb ischemia is induced in diabetic mice and QKI-7 is knocke

138 to nonoperative treatment in the absence of ischemia, it is crucial to rapidly detect or predict str

139 nflammatory responses in models of both warm ischemia (kidney clamping) and prolonged cold ischemia (

140 Under TAE-induced ischemia, latent HCC cells demonstrated reduced metaboli

141 S100A9(-/)(-) mice with permanent myocardial ischemia, leading to depressed cardiac function long ter

142 sis platform, UWFA images were segmented for ischemia, leakage, and microaneurysms with manual correc

143 pecified analysis, PAD events (critical limb ischemia, limb revascularization, or amputation for isch

144 ficacy outcome was a composite of acute limb ischemia, major amputation of a vascular cause, myocardi

145 se cohorts where structural heart disease or ischemia may influence repolarization dynamics.

146 ich contains 155 mM [Na(+)](o), with cardiac ischemia may require further investigation.

147 were first detectable 15 minutes after 90-s ischemia (median 43.7% increase) and increased more stee

148 (5 x 10(4) cells) in a preclinical hindlimb ischemia model showing accelerated formation of new bloo

149 In mouse hind limb ischemia model, local intramuscular delivery of CSC over

150 so promotes angiogenesis in a mouse hindlimb ischemia model, with accelerated limb blood flow recover

151 here is limited knowledge on the duration of ischemia necessary to induce a measurable release of cTn

152 ement therapy, occurrence rate of myocardial ischemia, occurrence rate of arrhythmias, and length of

153 nnula was associated with lower odds of limb ischemia (odds ratio, 1.93; 95% CI, 1.17-2.47; p = 0.03)

154 Patients with positive findings for ischemia on stress cardiac MRI or significant coronary s

155 vanced kidney disease and moderate or severe ischemia on stress testing to be treated with an initial

156 COVID-19 who presented with symptoms of leg ischemia only were more likely to avoid amputation or de

157 determine the prognostic value of inducible ischemia or late gadolinium enhancement by CMR.

158 death, myocardial infarction (MI), recurrent ischemia, or thrombotic bailout at 96 h (4-way endpoint)

159 on blood vessels from diabetic critical limb ischemia patients undergoing a lower-limb amputation.

160 patients with colon complications, including ischemia, perforation, fistula, stricture/obstruction, a

161 in human donor lungs starting from the warm-ischemia phase and were associated with increased transc

162 Patients who underwent laparotomy often had ischemia, possibly due to small-vessel thrombosis.

163 -40 kg pig was exposed to 30 minutes of warm ischemia prior to 22 hours of HMP and autotransplantatio

164 abnormal AchFR, and 47% had a normal AchFR; ischemia rates were 83%, 63%, and 14%, respectively.

165 ated the association between the hypothermia/ischemia ratio and functional outcome in a secondary ana

166 estimate the association between hypothermia/ischemia ratio and the primary outcome, adjusting for de

167 Although a larger hypothermia/ischemia ratio was associated with good functional outco

168 comes Consortium site, a greater hypothermia/ischemia ratio was associated with increased survival wi

169 curring during early tumor progression (i.e. ischemia) recruits neutrophils to the site of tissue dam

170 Ischemia reperfusion (IR) injury results in devastating

171 ls and IL-17A play critical roles in hepatic ischemia reperfusion (IR) injury, we tested whether mice

172 eta1 signaling is increased in a profibrotic ischemia reperfusion and cardiotoxin muscle injury model

173 able treatment to prevent muscle fibrosis in ischemia reperfusion and traumatic extremity injury.

174 Ischemia reperfusion injury (IRI) during liver-metastasi

175 Ischemia reperfusion injury (IRI) predisposes to the for

176 jured and repairing kidneys on day two after ischemia reperfusion injury (IRI).

177 This phenomenon is called ischemia reperfusion injury (IRI).

178 izes metabolism to possibly better cope with ischemia reperfusion injury in discarded kidneys.

179 Ischemia reperfusion injury induces a systemic increase

180 Liver ischemia reperfusion injury is associated with coagulati

181 phils in a human-disease-relevant myocardial ischemia reperfusion injury mouse model after i.v. injec

182 unomodulatory properties that could minimize ischemia reperfusion injury.

183 tion of periostin during the repair phase of ischemia reperfusion.

184 As the incidence of ischemia-reperfusion (I-R) injury has substantially incr

185 nhanced susceptibility of steatotic liver to ischemia-reperfusion (I/R) injury is due to impaired rec

186 Intestinal ischemia-reperfusion (IIR) often occurs during and follo

187 Sex differences in responses to intestinal ischemia-reperfusion (IR) have been recognized in animal

188 Lung ischemia-reperfusion (IR) injury is a common clinical pa

189 utrophil-dependent mouse model of intestinal ischemia-reperfusion (IR) injury to investigate the unde

190 In this porcine ischemia-reperfusion autotransplant model, the left kidn

191 te PO2 during continuous HMP in a pig kidney ischemia-reperfusion autotransplant model.

192 ysfunction of antibody-mediated diseases and ischemia-reperfusion conditions.

193 rove mechanical function during baseline and ischemia-reperfusion conditions.

194 Ischemia-reperfusion decreased LVDP in all hearts with r

195 in a preclinical porcine model, we performed ischemia-reperfusion injuries using balloon occlusion fo

196 her/how CEACAM1 signaling may affect hepatic ischemia-reperfusion injury (IRI) and OLT outcomes.

197 Ischemia-reperfusion injury (IRI) is an important risk f

198 Here, genes related to ischemia-reperfusion injury (IRI) or graft rejection may

199 s (DAMPs) released from cells damaged during ischemia-reperfusion injury (IRI), in heart attack or st

200 single dose of agrin is capable of reducing ischemia-reperfusion injury and improving heart function

201 impact of exercise on metabolic parameters, ischemia-reperfusion injury and regeneration after hepat

202 mitigates steatosis; however, its impact on ischemia-reperfusion injury and regeneration is unknown.

203 lly distinct donor macrophage populations in ischemia-reperfusion injury and rejection, including the

204 upregulated within a few hours of bilateral ischemia-reperfusion injury at these sites and new sites

205 drial rupture and cardiomyocyte death during ischemia-reperfusion injury by inducing mitochondrial pe

206 n cardiomyocytes and partial protection from ischemia-reperfusion injury by reducing mitochondrial pe

207 In donor kidneys subjected to ischemia-reperfusion injury during kidney transplant, ph

208 of donor renal macrophages after reversible ischemia-reperfusion injury in a mouse model of congenei

209 plays a pivotal role in the pathogenesis of ischemia-reperfusion injury in solid organ transplantati

210 d quantified and compared renal responses to ischemia-reperfusion injury in the presence and absence

211 ion molecule 1 (CEACAM1) exhibited increased ischemia-reperfusion injury inflammation and decreased f

212 Ischemia-reperfusion injury is inevitable during intesti

213 ce lacking periostin expression in the renal ischemia-reperfusion injury model, and primary cultures

214 u- and (68)Ga-DOTA-ECL1i were compared in an ischemia-reperfusion injury mouse model.

215 ic brain or spinal cord injury, glaucoma and ischemia-reperfusion injury of the eye.

216 regarding the effects of transplant-induced ischemia-reperfusion injury on the ability of donor-deri

217 We subjected SerpinB2 knockout mice to ischemia-reperfusion injury or unilateral ureteral obstr

218 Ischemia-reperfusion injury was modeled in vitro by plac

219 mammalian 'deactive transition' (relevant to ischemia-reperfusion injury) and their effects on the ub

220 in the normal kidney and following bilateral ischemia-reperfusion injury, and quantified and compared

221 or of donor renal macrophage functions after ischemia-reperfusion injury, crucial to guiding the phen

222 After ischemia-reperfusion injury, periostin-overexpressing mi

223 iency of endothelial HIF-2 exacerbated renal ischemia-reperfusion injury, whereas inactivation of end

224 inal organs have a higher risk of developing ischemia-reperfusion injury, which can lead to posttrans

225 le of detecting both nephrotoxin-induced and ischemia-reperfusion injury-induced AKI in live mice.

226 of diseases such as chronic inflammation and ischemia-reperfusion injury.

227 h the transcriptional changes observed after ischemia-reperfusion injury.

228 p are reported to have a detrimental role in ischemia-reperfusion injury.

229 line, but mRNA and protein are induced after ischemia-reperfusion injury.

230 esponse and improved tissue repair following ischemia-reperfusion injury.

231 lial immune defense and highly vulnerable to ischemia-reperfusion injury.

232 seq) with the clinically relevant unilateral ischemia-reperfusion murine model of AKI at days 1, 2, 4

233 ion of SULT1E1 expression to bilateral renal ischemia-reperfusion or sham surgery, either in the abse

234 Ischemia-reperfusion triggered marked unilateral CX3CR1-

235 It is also overexpressed after renal ischemia-reperfusion, an event that induces kidney injur

236 In hearts subjected to ischemia-reperfusion, Nox4 limits infarct size through t

237 hearts have an impaired recovery from acute ischemia/reperfusion (I/R) injury ex vivo, the role of d

238 The latter trigger a version of ischemia/reperfusion (I/R) pathobiology that is singular

239 Renal FoxM1 expression increased after renal ischemia/reperfusion (I/R)-induced AKI in mouse kidneys.

240 itus (DM) significantly increases myocardial ischemia/reperfusion (MI/R) injury.

241 Here we used cerebral ischemia/reperfusion as a model to investigate the inter

242 Here, using a murine renal ischemia/reperfusion injury (IRI) model, we show that in

243 idence of the important role of platelets in ischemia/reperfusion injury and SEC injury.

244 Therapeutic trials aimed at prevention of ischemia/reperfusion injury to allografts based on anima

245 , in vivo kidney fibrosis induced via UUO or ischemia/reperfusion injury was ameliorated by systemic

246 At 33 days after ischemia/reperfusion injury, LNA-21-treated hearts exhib

247 Similarly, in a rat model of renal ischemia/reperfusion injury, SAR247799 preserved renal s

248 New data demonstrate that ischemia/reperfusion is necessary and sufficient to indu

249 In vitro-simulated ischemia/reperfusion showed that NGAL-deficient CD4(+) T

250 ise in response to nephrotoxins, sepsis, and ischemia/reperfusion, and in chronic kidney diseases.

251 /GFRalpha1 signaling to sensory neurons from ischemia/reperfusion-affected muscle directly modulated

252 omal dominant polycystic kidney disease, and ischemia/reperfusion-induced acute kidney injury.

253 nor bacterial pneumonia promotes PGD through ischemia/reperfusion-primed donor TRAMs.

254 tion in mouse and porcine models of hindlimb ischemia rescues severely damaged tissues by the ingrowt

255 -34%], respectively; P < .001) and confirmed ischemia resistance in NRF2-overexpressing HCC cell line

256 Purpose To test whether ischemia resistance is present in individuals with NRF2-

257 hat reflect inflammation, depolarization and ischemia respectively, mimicking events after brain inju

258 The angiogenic response to ischemia restores perfusion so as to preserve tissue.

259 mputation were obtained including acute limb ischemia, revascularization, and all-cause mortality.

260 We conclude that PTPRG is an ischemia susceptibility locus; and RPTPgamma-dependent s

261 schemia (kidney clamping) and prolonged cold ischemia (syngeneic renal transplant).

262 of retinal capillary changes associated with ischemia that correlated with visual acuity and radiatio

263 For chronic limb-threatening ischemia, the mortality difference was not significant;

264 lthough it is thought to result from chronic ischemia, the underlying nature and mechanisms driving t

265 ine oxide (17) is a novel agent for cerebral ischemia therapy as it is able to scavenge different typ

266 Cold ischemia time (CIT) was 10.8 +/- 4.1 hours and anastomos

267 d include the vital importance of donor warm ischemia time (DWIT) on outcome for both recipients as w

268 an operative time was 159 (54) minutes, warm ischemia time 180 (90) seconds, estimated blood loss 50

269 Warm ischemia time and cold ischemia times were 38 and 466 mi

270 yzed following challenge with 45 min of warm ischemia time and either 4 h of reperfusion or 24 h of c

271 Longer cold ischemia time and large droplet macrovesicular steatosis

272 mediation analysis was used to evaluate warm ischemia time as a potential mediator of this associatio

273 no-flow time, functional warm time, and cold ischemia time did not affect the risk of PNF or poor ren

274 Cold as well as warm ischemia time resulted in a significant decrease in cell

275 Mean functional warm ischemia time was 135 minutes.

276 ity, cause of liver disease, donor age, cold ischemia time, and waiting time.

277 lities emerged in donor selection (age, cold ischemia time, intensive care unit length, amylase conce

278 Longer cold/warm ischemia time, recipient/donor hypertension, and having

279 t times can impact logistics as well as cold ischemia time; our findings motivate an exploration of c

280 donor/recipient case-mix and increased cold ischemia times under the Kidney Allocation System (KAS),

281 Warm ischemia time and cold ischemia times were 38 and 466 minutes, respectively.

282 ocured from older donors and had longer warm ischemia times, and consequently achieved higher utiliza

283 ficant increase in door-to-balloon and total ischemia times, which may have contributed to the higher

284 signed 5179 patients with moderate or severe ischemia to an initial invasive strategy (angiography an

285 Although hypoxic or ischemia tolerance in AGS involves physiological adaptat

286 us insults including glaucoma, inflammation, ischemia, trauma, and genetic deficits, which are charac

287 ttish Computed Tomography of the Heart), and ISCHEMIA trial (International Study of Comparative Healt

288 rst-line test for the evaluation of CAD, the ISCHEMIA trial also resulted in some interesting finding

289 In the ISCHEMIA trial, an invasive strategy with angiographic a

290 The ISCHEMIA trial, presented in November 2019, was eligible

291 In ISCHEMIA, type 1 MI events using the primary and seconda

292 In multivariable Cox regression, inducible ischemia was an independent predictor of a higher incide

293 Ischemia was assessed by quantitative 3-Tesla stress per

294 Ischemia was induced by inflating a balloon in the left

295 able coronary disease and moderate or severe ischemia, we did not find evidence that an initial invas

296 total of 20 938 veterans with critical limb ischemia were hospitalized between 2005 and 2014.

297 stium-and symptoms or evidence of myocardial ischemia) were offered surgery or exercise restriction (

298 able coronary disease and moderate or severe ischemia, whether clinical outcomes are better in those

299 increased among veterans with critical limb ischemia, which was accompanied by a reduction in mortal

300 d was collected directly after 45 minutes of ischemia without reperfusion (45I-0R), after 30 minutes