ライフサイエンスコーパス: PFO

1 PFO binds both to sterols that tend to localize in order

2 PFO closure did not meet the primary endpoint of reducti

3 PFO closure seems as effective as medical therapy for se

4 PFO closure was associated with a low rate of ischemic e

5 PFO closure was associated with an increased risk of atr

6 PFO conformational behavior in asymmetric vesicles was f

7 PFO forms a multimeric barrel with many TM segments.

8 PFO is a potential route for embolic transit from the sy

9 PFO is believed to interact with liquid ordered lipid do

10 PFO is found more frequently in stroke patients than in

11 PFO presence was assessed by transthoracic echocardiogra

12 PFO prevalence was similar in 50 patients with COPD and

13 PFO was considered present if both studies were positive

14 PFO was present in 164 participants (14.9%).

15 PFO+ subjects had a higher oesophageal temperature (T(oe

16 (3) a residual pool that does not bind 125I-PFO* even after sphingomyelinase treatment.

17 lesterol: (1) a pool accessible to bind 125I-PFO*, a mutant form of bacterial Perfringolysin O, which

18 omyelin(SM)-sequestered pool that binds 125I-PFO* only after SM is destroyed by sphingomyelinase; and

19 Thirty well-matched males (15 PFO-, 8 large PFO+, 7 small PFO+) completed cycle ergome

20 point of stroke/TIA was met in 30/364 (8.2%) PFO versus 117/5711 (2.0%) non-PFO patients (hazard rati

21 Surgical closure was performed in 639 PFO patients (28%), and surgeons were more likely to clo

22 uently in patients more likely to have had a PFO-attributable stroke (n=637) compared with those less

23 7) compared with those less likely to have a PFO-attributable stroke (n=657).

24 cardiac implantable electronic devices; if a PFO is detected, PFO closure, anticoagulation, or nonvas

25 data suggest that the presence and size of a PFO are associated with T(oesoph) in healthy humans but

26 ts with endocardial leads, the presence of a PFO on routine echocardiography is associated with a sub

27 were screened for the presence and size of a PFO using saline contrast echocardiography.

28 a cryptogenic ischemic stroke, closure of a PFO was associated with a lower rate of recurrent ischem

29 We sought to determine whether a PFO increases the risk of stroke/transient ischemic atta

30 Among patients with a PFO who had had a cryptogenic stroke, the risk of subseq

31 ultinational trial involving patients with a PFO who had had a cryptogenic stroke, we randomly assign

32 d two perfluorinated ether carboxylic acids (PFO(4)DA and PFO(5)DoDA; PFO(5)DoDA range: 5-30 ng/g).

33 llation occurred in 29 patients (6.6%) after PFO closure.

34 losure, the presence of residual shunt after PFO closure was associated with an increased incidence o

35 first recurrent ischemic stroke or TIA after PFO closure.

36 During exercise breathing cold and dry air, PFO+ subjects achieved a higher T(oesoph) than PFO- subj

37 , Inc., Boston, Massachusetts] and Amplatzer PFO Occluder [disc occluder] [AGA Medical/St. Jude Medic

38 l therapy and PFO closure with the Amplatzer PFO Occluder device (St.

39 the patent foramen ovale with the Amplatzer PFO Occluder or to receive medical therapy.

40 ts With Migraine and PFO Using the AMPLATZER PFO Occluder to Medical Management [PREMIUM]; NCT0035505

41 ts With Migraine and PFO Using the AMPLATZER PFO Occluder to Medical Management) was a double-blind s

42 n of important toxins, such as CPA, CPB, and PFO, is controlled by the C. perfringens Agr-like (CpAL)

43 rinated ether carboxylic acids (PFO(4)DA and PFO(5)DoDA; PFO(5)DoDA range: 5-30 ng/g).

44 ache Reduction in Subjects With Migraine and PFO Using the AMPLATZER PFO Occluder to Medical Manageme

45 ache Reduction in Subjects With Migraine and PFO Using the AMPLATZER PFO Occluder to Medical Manageme

46 y explain the differing abilities of SLO and PFO to efficiently penetrate target cell membranes in th

47 unresolved issues related to PFO stroke and PFO migraine pathophysiology, and to identify the patien

48 ents each year have a cryptogenic stroke and PFO.

49 reating patients with cryptogenic stroke and PFO.

50 catheterization) versus medical therapy and PFO closure with the Amplatzer PFO Occluder device (St.

51 for the concerted action of alpha-toxin and PFO during C. perfringens pathogenesis.

52 esophageal echocardiography features such as PFO size, associated hypermobile septum, and presence of

53 ented with arrhythmia (no difference between PFO and non-PFO groups).

54 nt difference in all-cause mortality between PFO and non-PFO patients (hazard ratio, 0.91; 95% confid

55 This suggests a causal relationship between PFO and cryptogenic stroke.

56 ll established, and the relationship between PFO and silent brain infarcts (SBI) is not known.

57 rises mobile cholesterol, accessible to both PFO and ALOD4, that is rapidly transported to the endopl

58 n, and data for percutaneous closure of both PFOs and ASDs.

59 ered by sphingomyelin and cannot be bound by PFO* unless the sphingomyelin is destroyed with sphingom

60 te that accessible cholesterol, as judged by PFO* or ALO-D4 binding, is not evenly distributed over t

61 In this community-based cohort, PFO was not associated with an increased risk of clinica

62 In an expanded COPD cohort, PFO prevalence was similar in 31 hypoxemic (Pao2 </= 7.3

63 a from completed randomized trials comparing PFO closure versus medical therapy in patients with cryp

64 ull mutants exhibited reduced levels of CPB, PFO, and CPA in their culture supernatants, and this eff

65 ocardiography was used to establish definite PFO and non-PFO cohorts.

66 Additional tools to describe PFOs may be useful in helping to determine whether an ob

67 le electronic devices; if a PFO is detected, PFO closure, anticoagulation, or nonvascular lead placem

68 , although the pathogenicity of a discovered PFO in the setting of CS is typically unclear.

69 s displaces it from rafts, does not displace PFO from ordered domains.

70 r carboxylic acids (PFO(4)DA and PFO(5)DoDA; PFO(5)DoDA range: 5-30 ng/g).

71 effect would be dependent upon the estimated PFO size and inspired air temperature.

72 ta exist on the long-term outcomes following PFO closure.

73 ast to the 5% threshold previously found for PFO binding to endoplasmic reticulum membranes.

74 oup further improved the detection limit for PFO(-) to 1.7 x 10(-10) M (0.070 ppb).

75 of cholesterol required in the membrane for PFO binding and pore formation.

76 ction limits of 2.3 x 10(-9) M (1.0 ppb) for PFO(-) and 8.6 x 10(-10) M (0.43 ppb) for PFOS(-).

77 The adjusted hazard ratio for PFO and stroke was 1.10 (95% confidence interval [CI]: 0

78 With their higher selectivity for PFO(-) over OH(-), membranes containing the alternative

79 These changes were much weaker for PFO(W165T) lipo where substantial stabilization was obse

80 his finding suggests a role of screening for PFOs in patients who require cardiac implantable electro

81 presenting risk of stroke would benefit from PFO closure or anticoagulation, as compared with antipla

82 patients who would most likely benefit from PFO closure.

83 Procedural complications from PFO closure occurred in 14 patients (5.9%).

84 scence resonance energy transfer (FRET) from PFO Trp to domain-localized acceptors indicated that PFO

85 he biochemical properties of the homodimeric PFO of C. reinhardtii expressed in Escherichia coli.

86 gned to antiplatelet therapy alone; however, PFO closure was associated with higher rates of device c

87 y relate cholesterol concentration to (125)I-PFO binding.

88 The (125)I-PFO probe also proved useful in monitoring the movement

89 ography and transcranial Doppler to identify PFO.

90 mpelling circumstantial evidence implicating PFO, the precise role of PFO in the pathogenesis of cryp

91 In PFO, the strongest changes accompanying binding to the m

92 y (MS), we have mapped structural changes in PFO and its variant bearing a point mutation during inco

93 postimplantation follow-up were compared in PFO versus non-PFO patients with the use of Cox proporti

94 There was no difference in PFO prevalence in those with migraine with aura and thos

95 represent an important intermediate stage in PFO pore formation.

96 An analysis reveals that, in PFO, there are complementary interactions between the mo

97 Incidental PFO is common in patients undergoing cardiothoracic surg

98 cholesterol concentration required to induce PFO binding, whereas phosphatidylethanolamine and phosph

99 Intraoperative PFO was diagnosed in 2277 patients in the study populati

100 rafts is poorly understood, we investigated PFO raft affinity in vesicles having coexisting ordered

101 th clinical features suggesting that a CS is PFO-attributable.

102 d CS by the probability that their stroke is PFO-attributable.

103 Thirty well-matched males (15 PFO-, 8 large PFO+, 7 small PFO+) completed cycle ergometer exercise t

104 Subjects with a large PFO, but not those with a small PFO, had a higher T(oeso

105 ageal echocardiography risk markers of large PFO size, hypermobile septum, and presence of right-to-l

106 h COPD with no shunt and patients with large PFO underwent cardiopulmonary exercise tests with contra

107 Both mutant and wild type length PFO exhibited cholesterol-dependent membrane insertion.

108 included iOCT after perfluorocarbon liquid (PFO) placement, visualization of the foveal center on iO

109 By using a non-lytic PFO derivative, we showed that the sensitivity of the pr

110 Maximal PFO-induced pore formation occurred in vesicles with wid

111 30/364 (8.2%) PFO versus 117/5711 (2.0%) non-PFO patients (hazard ratio, 3.49; 95% confidence interva

112 y was used to establish definite PFO and non-PFO cohorts.

113 rrhythmia (no difference between PFO and non-PFO groups).

114 e in all-cause mortality between PFO and non-PFO patients (hazard ratio, 0.91; 95% confidence interva

115 re frequent in the PFO group than in the non-PFO group (9 of 42 patients [21.4%] vs. 15 of 273 patien

116 on follow-up were compared in PFO versus non-PFO patients with the use of Cox proportional hazards mo

117 ype B strains also produce perfringolysin O (PFO) and beta2 toxin (CPB2).

118 bacterial toxin proteins, perfringolysin O (PFO) and domain 4 of anthrolysin O (ALOD4), have shown t

119 cholesterol-binding CDCs, perfringolysin O (PFO) and streptolysin O (SLO), were found to exhibit str

120 sterol-dependent cytolysin Perfringolysin O (PFO) constitutes a powerful tool to detect cholesterol i

121 e structures at the tip of perfringolysin O (PFO) domain 4 reveals that a threonine-leucine pair medi

122 eraction with cholesterol, perfringolysin O (PFO) inserts into membranes and forms a rigid transmembr

123 Perfringolysin O (PFO) is a toxic protein that binds to cholesterol-contai

124 The sterol-binding protein perfringolysin O (PFO) was used to test this hypothesis.

125 -labeled mutant version of Perfringolysin O (PFO), a cholesterol-binding protein, and use it to measu

126 s (rafts) was tested using perfringolysin O (PFO), a pore-forming cholesterol-dependent cytolysin.

127 the well-characterized CDC perfringolysin O (PFO), although the sequences in this region are identica

128 f the pore-forming protein Perfringolysin O (PFO), potent silencing was achieved in vitro with no det

129 sterol-dependent cytolysin perfringolysin O (PFO).

130 rticularly alpha-toxin and perfringolysin O (PFO).

131 d version of the cytolysin perfringolysin O (PFO*), whereas another pool is sequestered by sphingomye

132 in helping to determine whether an observed PFO is incidental or pathogenically related to CS.

133 al technique using a sub-perfluoro-n-octane (PFO) injection of ocular viscoelastic device (OVD) to st

134 na cystic alterations were found in 58.3% of PFO eyes and 17.2% of perfluorodecalin eyes; outer retin

135 g membrane contraction was found in 58.4% of PFO and in none of perfluorodecalin eyes; inner retina c

136 na cystic alterations were found in 39.6% of PFO eyes and 13.8% of perfluorodecalin eyes; retinal hol

137 n eyes; retinal holes were found in 14.6% of PFO eyes and in none of the perfluorodecalin eyes; and o

138 etinal atrophic areas were found in 41.7% of PFO and in none of the perfluorodecalin eyes; inner limi

139 er retinal inclusions were found in 20.8% of PFO eyes and in 3.45% of perfluorodecalin eyes.

140 It has been suggested that the ability of PFO to perforate the membrane of target cells is dictate

141 The association of PFO with stroke/TIA remained significant after multivari

142 Unfortunately, the benefit of PFO closure in patients with stroke has not been demonst

143 SIMS images revealed preferential binding of PFO* and ALO-D4 to microvilli on the plasma membrane; lo

144 d new insight into conformational changes of PFO associated with the membrane binding, oligomerizatio

145 The comparison of PFO closure plus antiplatelet therapy with antiplatelet

146 pecific compared to TTE for the detection of PFO in patients with cryptogenic cerebral ischemia.

147 c echocardiography (TTE) in the detection of PFO in patients with cryptogenic ischemic stroke or tran

148 We investigated the effect of PFO closure combined with antiplatelet therapy versus an

149 The effect of PFO on the association between migraine and CIS was anal

150 trials comparing the safety and efficacy of PFO closure with that of medical therapy.

151 d lipid domains, both TM and non-TM forms of PFO were found to concentrate in ordered domains in vesi

152 ith CIS remained significant irrespective of PFO.

153 The pore-forming mechanism of PFO exhibits an absolute requirement for membrane choles

154 nt ferredoxin, is thus likely the partner of PFO in C. reinhardtii.

155 M form, demonstrating that the TM portion of PFO interacts unfavorably with rafts.

156 tween migraine headaches and the presence of PFO by use of a large case-control study.

157 tween migraine headaches and the presence of PFO in this large case-control study.

158 Presence of PFO was determined by transthoracic echocardiogram with

159 ent of vascular risk factors and presence of PFO.

160 se-control study to assess the prevalence of PFO in subjects with and without migraine.

161 In the matched analysis, the prevalence of PFO was similar in case and control subjects (26.4% vers

162 with COPD do not have a higher prevalence of PFO.

163 The properties of PFO mutants with lengthened or shortened TM segments wer

164 vidence implicating PFO, the precise role of PFO in the pathogenesis of cryptogenic stroke is not yet

165 This can be explained by shielding of PFO-bound cholesterol from water.

166 s pertaining to the clinical significance of PFO.

167 tened TM segments were compared with that of PFO with wild type TM sequences.

168 ect cholesterol in membranes, and the use of PFO-based probes has flourished in recent years.

169 years of age who had a patent foramen ovale (PFO) and had had a cryptogenic ischemic stroke to underg

170 olism in patients with patent foramen ovale (PFO) and otherwise unexplained ischemic stroke, in a pro

171 presumably related to patent foramen ovale (PFO) are at risk for recurrent cerebrovascular events.

172 Patent foramen ovale (PFO) can be detected in up to 43% of patients with crypt

173 ose for catheter-based patent foramen ovale (PFO) closure are still evolving.

174 Patent foramen ovale (PFO) closure is the gold standard for treating patients

175 Trials of patent foramen ovale (PFO) closure to prevent recurrent stroke have been incon

176 25% of patients after patent foramen ovale (PFO) closure, but its long-term influence on stroke recu

177 Patent foramen ovale (PFO) has been associated with migraine, but its role in

178 ficacy of closure of a patent foramen ovale (PFO) in the prevention of recurrent stroke after cryptog

179 The patent foramen ovale (PFO) is a normal interatrial communication during fetal

180 Patent foramen ovale (PFO) is associated with cryptogenic stroke (CS), althoug

181 A patent foramen ovale (PFO) may permit arterial embolization of thrombi that ac

182 ercutaneous closure of patent foramen ovale (PFO) plus medical therapy versus medical therapy alone f

183 xical embolism through patent foramen ovale (PFO) should be the main mechanism.

184 d blood flow through a patent foramen ovale (PFO) would not be cooled.

185 oms in patients with a patent foramen ovale (PFO), both of which conditions are highly prevalent, hav

186 e relationship between patent foramen ovale (PFO), ischemic stroke, and subclinical cerebrovascular d

187 ncidentally discovered patent foramen ovale (PFO).

188 The prevalence of patent foramena ovale (PFOs) in the general population is around 25%, but it is

189 ists) is pyruvate:ferredoxin oxidoreductase (PFO), which decarboxylates pyruvate and forms acetyl-coe

190 related to PFO underwent either percutaneous PFO closure (150 patients) or medical treatment (158 pat

191 g Adults), who underwent either percutaneous PFO closure or medical therapy for comparative analysis.

192 study examined the efficacy of percutaneous PFO closure as a therapy for migraine with or without au

193 trials question the benefit of percutaneous PFO closure, but concern has also been raised about the

194 propensity score-matched study, percutaneous PFO closure was more effective than medical treatment fo

195 enic stroke who were undergoing percutaneous PFO closure were followed for up to 11 years.

196 pairs of patients who underwent percutaneous PFO closure or medical treatment.

197 red in 15 patients treated with percutaneous PFO closure (7.3%) versus 33 patients medically treated

198 nvestigated among patients with percutaneous PFO closure and those who received medical treatment.

199 entiometric detection of perfluorooctanoate (PFO(-)) and perfluorooctanesulfonate (PFOS(-)) were deve

200 chemic stroke to undergo closure of the PFO (PFO closure group) or to receive medical therapy alone (

201 hs (interquartile range 6 to 14 months) post-PFO closure, and none of them had any ischemic or bleedi

202 iod (the majority within the first-year post-PFO closure), and this was not associated with any incre

203 detected more often in those with a probable PFO-attributable stroke (OR, 0.80; P=0.45; OR, 1.15; P=0

204 re frequently seen among those with probable PFO-attributable strokes (odds ratio [OR], 0.92; P=0.53)

205 (15)N-labeled cholesterol-binding proteins (PFO* and ALO-D4, a modified anthrolysin O), to generate

206 Many physicians recommend PFO closure, an intuitively attractive mechanical soluti

207 fter a short lag, it also increases the ER's PFO-accessible regulatory pool.

208 es: first, it is unclear whether a patient's PFO is causally related to the event ('pathogenic') or n

209 holesterol leaves lysosomes, it expands PM's PFO-accessible pool and, after a short lag, it also incr

210 conclusive in 324 of 361 patients and showed PFO in 43 patients (13%).

211 atched males (15 PFO-, 8 large PFO+, 7 small PFO+) completed cycle ergometer exercise trials on three

212 with a large PFO, but not those with a small PFO, had a higher T(oesoph) than PFO- subjects (P < 0.05

213 lyzes phosphatidylcholine and sphingomyelin, PFO forms large transmembrane pores on cholesterol-conta

214 The use of sub-PFO injection of OVD in MHRD surgery could stabilize inv

215 Patients who underwent MHRD surgery with sub-PFO injection of OVD to stabilize inverted ILM flap onto

216 In the MRI subcohort, PFO was not associated with SBI (adjusted odds ratio: 1.

217 geal temperature (T(oesoph)) (P < 0.05) than PFO- subjects on Trial 1.

218 ith a small PFO, had a higher T(oesoph) than PFO- subjects (P < 0.05) during Trial 1 and increased T(

219 O+ subjects achieved a higher T(oesoph) than PFO- subjects (P < 0.05).

220 ts would have a higher core temperature than PFO- subjects due, in part, to absence of respiratory sy

221 in giant unilamellar vesicles confirmed that PFO exhibits intermediate raft affinity, and showed that

222 Long-term analysis demonstrated that PFO repair was associated with no survival difference (P

223 Accordingly, we hypothesized that PFO+ subjects would have a higher core temperature than

224 to domain-localized acceptors indicated that PFO generally has a raft affinity between that of LW pep

225 Taken together, our studies reveal that PFO binding to membranes is triggered when the concentra

226 Finally, FRET showed that PFO affinity for ordered domains was higher in its non-T

227 The PFO closure device was successfully implanted in all cas

228 differences in VA were observed between the PFO and perfluorodecalin patients.

229 action on membrane bilayers facilitates the PFO-cholesterol interaction as evidenced by a reduction

230 However, the PFO-related stroke risk in the general population is not

231 e was no difference in responder rate in the PFO closure (45 of 117) versus control (33 of 103) group

232 occurred in 6 of 441 patients (1.4%) in the PFO closure group and in 12 of 223 patients (5.4%) in th

233 ermined cause occurred in 10 patients in the PFO closure group and in 23 patients in the medical-ther

234 nts occurred in 23.1% of the patients in the PFO closure group and in 27.8% of the patients in the an

235 chemic stroke occurred in 18 patients in the PFO closure group and in 28 patients in the medical-ther

236 Subjects in the PFO closure group had a significantly greater reduction

237 n infarctions was significantly lower in the PFO closure group than in the antiplatelet-only group (2

238 ate of atrial fibrillation was higher in the PFO closure group than in the antiplatelet-only group (4

239 deep-vein thrombosis) was more common in the PFO closure group than in the medical-therapy group.

240 milar in the 2 treatment groups (6.3% in the PFO closure group versus 10.2% in the medically treated

241 roups was unequal (3141 patient-years in the PFO closure group vs. 2669 patient-years in the medical-

242 events occurred in 6 patients (1.4%) in the PFO closure group, and atrial fibrillation occurred in 2

243 troke occurred among the 238 patients in the PFO closure group, whereas stroke occurred in 14 of the

244 ent ischemic stroke was more frequent in the PFO group than in the non-PFO group (9 of 42 patients [2

245 roke was 10.1% (standard error: 2.5%) in the PFO+ and 10.4% (standard error: 1.1%) in the PFO- group

246 c strokes occurred (10.1%), 15 (9.2%) in the PFO+ and 96 (10.3%) in the PFO- groups.

247 PFO+ and 10.4% (standard error: 1.1%) in the PFO- group (p = 0.46).

248 15 (9.2%) in the PFO+ and 96 (10.3%) in the PFO- groups.

249 ic ischemic stroke to undergo closure of the PFO (PFO closure group) or to receive medical therapy al

250 ay between the structural arrangement of the PFO C-terminal domain and the distribution of cholestero

251 th the increased binding and affinity of the PFO L3 mutant, suggesting that selection of a compatible

252 dergo PFO closure plus antiplatelet therapy (PFO closure group) or to receive antiplatelet therapy al

253 closure plus long-term antiplatelet therapy (PFO closure group), antiplatelet therapy alone (antiplat

254 known whether right-to-left shunting through PFO increases during exercise impairing exercise perform

255 nity, and showed that TM PFO (but not non-TM PFO) concentrated at the edges of liquid ordered domains

256 termediate raft affinity, and showed that TM PFO (but not non-TM PFO) concentrated at the edges of li

257 recurrence was lower among those assigned to PFO closure combined with antiplatelet therapy than amon

258 mic stroke was lower among those assigned to PFO closure combined with antiplatelet therapy than amon

259 ad a recent cryptogenic stroke attributed to PFO with an associated atrial septal aneurysm or large i

260 ge who had had a recent stroke attributed to PFO, with an associated atrial septal aneurysm or large

261 myelin (SM)-sequestered pool inaccessible to PFO and ALOD4 but that becomes accessible by treatment w

262 rd is an essential pool also inaccessible to PFO and ALOD4 that cannot be liberated by SMase treatmen

263 ne in a manner that makes it inaccessible to PFO until its concentration exceeds a threshold of 35 mo

264 th contraindications to anticoagulants or to PFO closure were randomly assigned to the alternative no

265 address several unresolved issues related to PFO stroke and PFO migraine pathophysiology, and to iden

266 cerebrovascular events presumably related to PFO underwent either percutaneous PFO closure (150 patie

267 te outcome occurred in 11 patients slated to PFO closure (11%) and 22 patients slated to medical trea

268 p conferred the binding properties of SLO to PFO and vice versa.

269 hemorrhagic events) following transcatheter PFO closure.

270 Several randomized trials of transcatheter PFO closure versus medical management are ongoing.

271 or large interatrial shunt, to transcatheter PFO closure plus long-term antiplatelet therapy (PFO clo

272 with the lipid environment both in wild-type PFO, thus providing new experimental constraints for mol

273 traoperative subretinal fluid persists under PFO tamponade with high frequency in eyes undergoing ret

274 intraoperative subretinal fluid volume under PFO tamponade also may be linked to visual outcomes.

275 intraoperative subretinal fluid volume under PFO tamponade trended toward significantly worse visual

276 ssigned patients, in a 2:1 ratio, to undergo PFO closure plus antiplatelet therapy (PFO closure group

277 Among patients undergoing PFO closure to prevent future stroke, the presence of re

278 e: 47 +/- 12 years, 51% women) who underwent PFO closure due to a cryptogenic embolism (stroke: 76%,

279 tion) occurred in 205 subjects who underwent PFO closure.

280 Thus far, it has been unclear whether PFO* and related cholesterol-binding proteins bind unifo

281 We analyzed 6075 patients (364 with PFO) followed for a mean 4.7 +/- 3.1 years.

282 evaluated the risk of stroke associated with PFO after adjusting for established stroke risk factors

283 Patients with COPD with PFO do not perform less well either on a 6-minute walk o

284 d during exercise in patients with COPD with PFO.

285 2max was 574 (178) seconds for patients with PFO and 534 (279) seconds for those without (P = ns).

286 Among patients with PFO and cryptogenic stroke, closure reduced recurrent st

287 roimaging features to stratify patients with PFO and CS by the probability that their stroke is PFO-a

288 nting had lower Pao2 than both patients with PFO and those with no right-to-left shunt (7.7 vs. 8.6 v

289 h symptomatic PE was higher in patients with PFO than in those without PFO.

290 t cerebrovascular events among patients with PFO-related transient ischemic attack or stroke.

291 of the right-to-left shunt in patients with PFO.

292 echanism of ischemic stroke in patients with PFO.

293 tient-years, respectively (hazard ratio with PFO closure vs. medical therapy, 0.55; 95% confidence in

294 ons were found in 60.4% of eyes treated with PFO and in 10.3% of perfluorodecalin-treated eyes; retin

295 al of 48 eyes that underwent vitrectomy with PFO were compared to 29 eyes that underwent vitrectomy w

296 mic stroke patients aged 18 to 45 years with PFO and no other cause of brain ischemia, as part of the

297 ecutive patients (mean age, 49.3 years) with PFO-attributable cryptogenic stroke who were undergoing

298 s of having SBI among those with and without PFO.

299 ke were similar in patients with and without PFO.

300 r in patients with PFO than in those without PFO.