ライフサイエンスコーパス: Marfan syndrome

1 ere forms of the Marfan syndrome ("neonatal" Marfan syndrome).

2 iated with thoracic aortic aneurysm (TAA) in Marfan syndrome.

3 mal bone growth activity in a mouse model of Marfan syndrome.

4 not previously reported as causing classical Marfan syndrome.

5 ration and regurgitation in a mouse model of Marfan syndrome.

6 nd long-term clinical outcomes in women with Marfan syndrome.

7 with tricuspid valves unassociated with the Marfan syndrome.

8 tions lead to clinical features unrelated to Marfan syndrome.

9 atients) had physical features suggestive of Marfan syndrome.

10 lt in the dominant connective tissue disease Marfan syndrome.

11 stress contributes to the disease, including Marfan syndrome.

12 ad to alternative therapeutic strategies for Marfan syndrome.

13 , which recapitulate the most severe form of Marfan syndrome.

14 ecapitulates the pulmonary features of human Marfan syndrome.

15 tic wall of a mouse model of neonatal lethal Marfan syndrome.

16 ted individuals meets the Ghent criteria for Marfan syndrome.

17 families with familial TAAD who did not have Marfan syndrome.

18 erlying connective tissue disorders like the Marfan syndrome.

19 ween age groups were not entirely related to Marfan syndrome.

20 Fifty patients had Marfan syndrome.

21 ficient in fibrillin-1, an accepted model of Marfan syndrome.

22 ortic dilatation in children and adults with Marfan syndrome.

23 rs evaluated met the diagnostic criteria for Marfan syndrome.

24 l density has been reported in patients with Marfan syndrome.

25 ey shifted inferiorly with gaze elevation in Marfan syndrome.

26 nts in the genetic and orthopedic aspects of Marfan syndrome.

27 sponsible for the clinical manifestations of Marfan syndrome.

28 ndings in elastic vessels from patients with Marfan syndrome.

29 om fibrillin-1, the defective protein in the Marfan syndrome.

30 ; and physical stigmata or family history of Marfan syndrome.

31 f outcome of this operation in patients with Marfan syndrome.

32 cellular matrix protein that is defective in Marfan syndrome.

33 isrupted in all three zones in patients with Marfan syndrome.

34 rt rhythm, peripheral pulses, or stigmata of Marfan syndrome.

35 lly similar to but genetically distinct from Marfan syndrome.

36 sorder that is phenotypically related to the Marfan syndrome.

37 dissections in patients who do not have the Marfan syndrome.

38 ic aneurysms in patients who do not have the Marfan syndrome.

39 oracic aortic aneurysms who did not have the Marfan syndrome.

40 drives the development of aortic aneurysm in Marfan syndrome.

41 cular, ocular, and skeletal abnormalities in Marfan syndrome.

42 ase, and arrhythmias) following diagnosis of Marfan syndrome.

43 ent occurred in 4 eyes (10%), 3 of which had Marfan syndrome.

44 was used to identify patients diagnosed with Marfan syndrome.

45 re more prevalent in adults than children in Marfan syndrome.

46 d tested 248 probands with aortic disease or Marfan syndrome.

47 ential for noninvasive clinical diagnosis of Marfan syndrome.

48 Recurrent AD is strongly associated with Marfan syndrome.

49 ved ORA variables successfully discriminated Marfan syndrome.

50 ervation was accentuated among patients with Marfan syndrome.

51 ic valve-sparing operations in patients with Marfan syndrome.

52 re a major clinical problem in patients with Marfan syndrome.

53 ly different from that seen in patients with Marfan syndrome.

54 ct type B aortic dissection in patients with Marfan syndrome.

55 risk for type B dissection in patients with Marfan syndrome.

56 n reduces aortic dilatation in patients with Marfan syndrome.

57 e arterial tree and phenotypically resembles Marfan syndrome.

58 dissection in multiple disorders, including Marfan syndrome.

59 hypertension, bicuspid aortic valve, and the Marfan syndrome.

60 lerated aneurysm growth in a murine model of Marfan syndrome.

61 tection of aortic expansion in patients with Marfan syndrome.

62 calculated in a subgroup of 22 patients with Marfan syndrome.

63 fter previous aortic repair in patients with Marfan syndrome.

64 All 9 patients (2 with Marfan syndrome, 1 with Takayasu's disease) with undiagn

65 diagnosed in late follow-up in patients with Marfan syndrome (10.8 +/- 4.4%) compared with those with

66 es type I and II (12q13.1-q13.3 and 6p21.3), Marfan syndrome (15q21.1), and juvenile glaucoma (chromo

67 ry or idiopathic ectopia lentis, 5 (29%) had Marfan syndrome, 2 (12%) were aphakic after pars plana v

68 s with recurrent AD were more likely to have Marfan syndrome (21.5% versus 3.1%; P<0.001) but not bic

69 st lone disease predictor was Concavity Min (Marfan syndrome 47.5 +/- 20, control 69 +/- 14, P = .003

70 on was significantly higher in patients with Marfan syndrome (5.5 +/- 2.7%) compared with those with

71 ients with aortic dissection type A, 74 with Marfan syndrome (58% men; median age, 37 years [first an

72 t has been known for more than a decade that Marfan syndrome - a dominantly inherited connective tiss

73 of the known mutations in fibrillin-1 cause Marfan syndrome, a number of other mutations lead to cli

74 ession of aortic aneurysm in mouse models of Marfan syndrome, a systemic disorder of the connective t

75 Marfan syndrome accounted for 37% cases.

76 The vascular structural defects of Marfan syndrome, Alagille syndrome, neurofibromatosis, a

77 ations in the FBN1 gene are the cause of the Marfan syndrome, an autosomal dominant disorder with ske

78 2.8% (35 patients) had genetically confirmed Marfan syndrome and an additional 17.8% (232 patients) h

79 complications during pregnancy in women with Marfan syndrome and an aortic diameter <4.5 cm.

80 In addition to Marfan syndrome and aorta diameter, a large entry tear l

81 rtic dissection remains low in patients with Marfan syndrome and aortic diameter between 45 and 49 mm

82 fibrils, cause pleiotropic manifestations in Marfan syndrome and congenital contractural arachnodacty

83 implying distinct mechanisms of bone loss in Marfan syndrome and congenital contractural arachnodacty

84 Fibrillin-based human diseases such as Marfan syndrome and congenital contractural arachnodacty

85 dilatation in children and young adults with Marfan syndrome and could reduce the incidence of aortic

86 risk has not been evaluated in patients with Marfan syndrome and documented pathogenic variants in th

87 sue have major cardiovascular complications, Marfan syndrome and Ehlers-Danlos syndrome type IV.

88 Patients undergoing AVS had higher rates of Marfan syndrome and lower rates of bicuspid aortic valve

89 Patients with the diagnosis of Marfan syndrome and magnetic resonance imaging or comput

90 In people with Marfan syndrome and no previous aortic surgery, ARBs red

91 Furthermore, patients with Marfan syndrome and other forms of inherited thoracic ao

92 opi infection in a patient with a history of Marfan syndrome and recreational feral swine hunting.

93 tations in the fibrillin-1 gene (FBN1) cause Marfan syndrome and related connective tissue disorders

94 In 81 patients with Marfan syndrome and seven healthy control subjects, aort

95 w discusses mutant-fibrillin mouse models of Marfan syndrome and SSc (Tsk mice), and studies suggesti

96 g a common pathogenesis of aortic disease in Marfan syndrome and STAAD.

97 ortic valves should not be extrapolated from Marfan syndrome and support discrete treatment algorithm

98 ated with aneurysm and dissection, including Marfan syndrome and the role of transforming growth fact

99 outcomes in a series of young patients with Marfan syndrome and to define the prevalence of ventricu

100 tions cause IEL or syndromic ectopia lentis (Marfan syndrome and Weill-Marchesani syndrome).

101 (2,079 with bicuspid aortic valves, 73 with Marfan syndrome, and 11,053 control patients with acquir

102 rs-Danlos syndrome, osteogenesis imperfecta, Marfan syndrome, and Larsen syndrome, are characterized

103 Ingenuity pathway analysis identified Marfan syndrome, aneurysm formation, LV dilatation, and

104 ces of osteoporosis and a single instance of Marfan syndrome are also the result of mutations at thes

105 to the pathophysiologic alterations seen in Marfan syndrome are highlighted.

106 rd type A aortic dissection in patients with Marfan syndrome are limited.

107 tegies to block TGF-beta, used in those with Marfan syndrome, are unlikely to be beneficial and could

108 The cardiovascular complications of Marfan syndrome arise due to alterations in the structur

109 (HLA) provided the best predictive value for Marfan syndrome (AUROC = 0.85).

110 treat aortic root aneurysm in patients with Marfan syndrome, based on relatively short-term outcomes

111 luding timing of surgery, remains debated in Marfan syndrome because of a lack of data on aortic risk

112 eness of familial aortic disease such as the Marfan syndrome, bicuspid aortic valve disease, and here

113 r, younger patients were more likely to have Marfan syndrome, bicuspid aortic valve, and prior aortic

114 an also be subject to abnormalities (such as Marfan syndrome, bicuspid aortic valve, inflammatory vas

115 nts have unique risk factors for dissection: Marfan syndrome, bicuspid aortic valves, and larger aort

116 AD) occur as part of known syndromes such as Marfan syndrome but can also be inherited in families in

117 identified relevant trials of patients with Marfan syndrome by systematically searching MEDLINE, Emb

118 s of constituents such as fibrillin-1, as in Marfan syndrome, can compromise both elastic fiber integ

119 amount of fibrillin expression in normal and Marfan syndrome capsules.

120 s of intact fibrillin-1, the consequences of Marfan syndrome causing mutations, and the ultrastructur

121 We have studied Marfan syndrome-causing mutations which affect calcium b

122 neal resistance factor (CRF) were decreased (Marfan syndrome CH 9.45 +/- 1.62, control CH 11.24 +/- 1

123 mes 12q13.1-q13.3 and 6p21.3, respectively), Marfan syndrome (chromosome 15q21.1), and juvenile glauc

124 e in age at surgery, dissection, or death in Marfan syndrome compared with LDS.

125 ications after AVR observed in patients with Marfan syndrome compared with those with bicuspid aortic

126 /- 1.62, control CH 11.24 +/- 1.21, P = .01; Marfan syndrome CRF 9.77 +/- 1.65, control CRF 11.03 +/-

127 (defective in coagulation factor IX) and the Marfan syndrome (defective in the connective tissue prot

128 as Klippel-Feil, familial dysautonomia, and Marfan syndrome demonstrate high rates of scoliotic defo

129 Mutations in fibrillin-1 (FBN1) result in Marfan syndrome, demonstrating a critical requirement fo

130 d has been extrapolated from experience with Marfan syndrome, despite the absence of comparative long

131 Seventy patients with Marfan syndrome diagnosed at birth to 52 years were foll

132 os syndrome, but arterial events are rare in Marfan syndrome due to PVs in FBN1, and poorly character

133 idia, albinism, anterior segment dysgenesis, Marfan syndrome, ectopia lentis, neurofibromatosis, reti

134 rs for Stickler syndrome types 1, 2, and 2B; Marfan syndrome; Ehlers-Danlos syndrome type 4; and juve

135 e the most severe phenotypes associated with Marfan syndrome (fibrillin-1) and congenital contractura

136 f echocardiograms, changing drug therapy for Marfan syndrome, follow-up of infant with complex corona

137 ckers (CCBs) are prescribed to patients with Marfan syndrome for prophylaxis against aortic aneurysm

138 ay underlie one of the major features of the Marfan syndrome: fragmentation of aortic elastic lamella

139 A total of 146 patients with Marfan syndrome had aortic valve-sparing operations.

140 Marfan syndrome has a variable phenotype, even within fa

141 enosis and the heart disease associated with Marfan syndrome has been clearly established.

142 ing technique, but its role in patients with Marfan syndrome has not previously been defined.

143 Both bicuspid aortic valve (BAV) and Marfan syndrome have been associated with aortic dissect

144 New insights regarding the pathogenesis of Marfan syndrome have developed from investigation of mur

145 A distinct subgroup of individuals with Marfan syndrome have distal airspace enlargement, histor

146 s of age and sex with phenotypic features of Marfan syndrome have not been systematically examined in

147 Fibrillin-1 mutations associated with Marfan syndrome have recently been shown to induce genes

148 ear size (HR: 1.1 [1.04-1.16]; P=0.001), and Marfan syndrome (HR: 3.66 [1.65-8.13]; P=0.001).

149 ents with a history of ectopia lentis due to Marfan syndrome, idiopathic causes, or hereditary causes

150 Mitral valve prolapse was present in 5.4%, Marfan syndrome in 1.1% and scoliosis in 29%.

151 minating connective tissue disorders such as Marfan syndrome in the not-too-distant future.

152 ving or preventing several manifestations of Marfan syndrome in these mice, including aortic aneurysm

153 Cardiac manifestations of Marfan syndrome include aortic root dilation and mitral

154 The major orthopedic manifestations of Marfan syndrome include scoliosis, chest wall deformity,

155 features of corneal deformation responses in Marfan syndrome, including increased deformation, decrea

156 In multivariate analysis, the diagnosis of Marfan syndrome independently predicted recurrent AD (ha

157 observed in aneurysms forming in those with Marfan syndrome, inhibition of TGF-beta would worsen inf

158 predictors of late death (P< or =0.005), and Marfan syndrome, initial valve-preserving aortic root re

159 Marfan syndrome is a common inherited disorder of connec

160 Marfan syndrome is a connective tissue disorder caused b

161 Marfan syndrome is a connective tissue disorder caused b

162 Marfan syndrome is an autosomal dominant disorder of con

163 Marfan syndrome is an autosomal dominant disorder of con

164 Type B dissection in patients with Marfan syndrome is associated with a high need for exten

165 Marfan syndrome is associated with early death due to ao

166 rgery for type A dissection in patients with Marfan syndrome is associated with low in-hospital morta

167 Pathogenesis of Marfan syndrome is currently thought to be driven by mec

168 ept of pharmaceutical aorta stabilization in Marfan syndrome is supported by a wealth of promising st

169 and corneas were flatter in Marfan syndrome (Marfan syndrome Kmean 41.25 +/- 2.09 diopter, control Km

170 lysis of 90 patients </=50 years of age with Marfan syndrome, LDS, Ehlers-Danlos syndrome, or nonspec

171 In Fbn1(C1041G/+) mice, a model of Marfan syndrome, MAGP1 deposition is reduced, endothelia

172 A subset of patients with Marfan syndrome manifested multiple forms of vasculopath

173 - 1.72, P = .01) and corneas were flatter in Marfan syndrome (Marfan syndrome Kmean 41.25 +/- 2.09 di

174 ess of the clinical features associated with Marfan syndrome may facilitate earlier diagnosis and opt

175 ic dissections occurred in 600 patients with Marfan syndrome (mean age 36 +/- 14 years, 52% male).

176 In 22 patients with Marfan syndrome, mean aortic volume was increased at 3 y

177 er were assessed for discriminative value in Marfan syndrome, measuring right eyes of 24 control and

178 Bicuspid aortic valve (BAV) (39%) and Marfan syndrome (MFS) (22%) were the leading diagnoses i

179 aortic valve (BAV) with aneurysm (n = 879), Marfan syndrome (MFS) (n = 861), nonsyndromic heritable

180 Mice that harbor both a mutant Marfan syndrome (MFS) allele (Fbn1(C1039G/+)) and Tgfb2

181 NS-TAA) are incompletely defined compared to Marfan syndrome (MFS) and bicuspid aortic valve (BAV).

182 the autosomal dominant microfibrillopathies Marfan syndrome (MFS) and congenital contractural arachn

183 FBN1 gene, which encodes fibrillin-1, cause Marfan syndrome (MFS) and have been associated with a wi

184 presentations of aortic aneurysm, including Marfan syndrome (MFS) and Loeys-Dietz syndrome (LDS).

185 Marfan syndrome (MFS) and other type 1 fibrillinopathies

186 ons in the fibrillin-1 (FBN1) gene cause the Marfan syndrome (MFS) and related connective tissue diso

187 g is a major contributor to the pathology of Marfan syndrome (MFS) and related diseases.

188 issecting aortic aneurysm is the hallmark of Marfan syndrome (MFS) and the result of mutations in fib

189 ctor (TGF)-beta bioavailability/signaling in Marfan syndrome (MFS) changed the view of the extracellu

190 educed quality of life (QOL) for people with Marfan syndrome (MFS) compared with those without MFS.

191 Marfan syndrome (MFS) is a connective tissue disorder ca

192 Marfan syndrome (MFS) is a connective tissue disorder ca

193 Marfan syndrome (MFS) is a connective tissue disorder th

194 Marfan syndrome (MFS) is a dominantly inherited disorder

195 Marfan syndrome (MFS) is a hereditary connective tissue

196 Marfan syndrome (MFS) is a heritable connective tissue d

197 Marfan syndrome (MFS) is a heritable connective tissue d

198 Marfan syndrome (MFS) is a heritable disorder of connect

199 Marfan syndrome (MFS) is a highly variable genetic conne

200 Marfan syndrome (MFS) is a systemic connective tissue di

201 Marfan syndrome (MFS) is a systemic disorder of connecti

202 Marfan syndrome (MFS) is an autosomal dominant disorder

203 Marfan syndrome (MFS) is an autosomal dominant disorder

204 Marfan syndrome (MFS) is an autosomal dominant, age-rela

205 Marfan syndrome (MFS) is associated with TGF (transformi

206 Marfan syndrome (MFS) is caused by mutations in the fibr

207 Marfan syndrome (MFS) is known to cause ascending thorac

208 Marfan syndrome (MFS) is the most common inherited conne

209 egnancy-associated vascular complications in Marfan syndrome (MFS) is uncertain because of ascertainm

210 mutation in the fibrillin-1 (FBN1) gene of a Marfan syndrome (MFS) patient induces in-frame exon skip

211 ice with reduced Fbn1 gene expression and of Marfan syndrome (MFS) patients with heterozygous fibrill

212 is the most life-threatening complication in Marfan syndrome (MFS) patients.

213 ometric findings of adults and children with Marfan syndrome (MFS) recruited from 2 annual National M

214 inical significance of MAD for patients with Marfan syndrome (MFS) remains largely unexplored.

215 the human fibrillin-1 gene, FBN1, result in Marfan syndrome (MFS), a common connective tissue disord

216 tations in the FBN1 gene are associated with Marfan syndrome (MFS), a common developmental disorder.

217 tations in the FBN1 gene are responsible for Marfan syndrome (MFS), a common systemic disorder of the

218 neurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in

219 rmalities that are similar to those found in Marfan syndrome (MFS), a heritable connective tissue dis

220 Marfan syndrome (MFS), a heritable connective tissue dis

221 stature is the most evident manifestation in Marfan syndrome (MFS), a multisystem condition caused by

222 pediatric and adult patients afflicted with Marfan syndrome (MFS), a multisystem disorder caused by

223 Patients with Marfan syndrome (MFS), a multisystem disorder caused by

224 in the human fibrillin-1 (FBN-1) gene cause Marfan syndrome (MFS), an autosomal dominant disease of

225 FBN1 mutations cause Marfan syndrome (MFS), an autosomal dominant disorder of

226 rmalities with many clinical features of the Marfan syndrome (MFS), an autosomal dominant disorder of

227 the context of genetic syndromes, including Marfan syndrome (MFS), an autosomal-dominant connective

228 progression in multiple disorders, including Marfan syndrome (MFS), and therapies that inhibit this s

229 ithin these proteins have been linked to the Marfan syndrome (MFS), CADASIL, protein S deficiency, ha

230 Many individuals with Marfan syndrome (MFS), caused by a deficiency of extrace

231 aneurysms and dissections (TAAD), including Marfan syndrome (MFS), currently lack a cure, and causat

232 In individuals with Marfan Syndrome (MFS), fibrillin-1 gene (FBN1) mutations

233 as recently exemplified through the study of Marfan syndrome (MFS), including aortic aneurysm and ske

234 The Marfan syndrome (MFS), initially described just over 100

235 onnective tissue disorders (CTDs), including Marfan syndrome (MFS), systemic sclerosis (SSc) and Tigh

236 , telmisartan was able to inhibit aging- and Marfan syndrome (MFS)-associated aortic root widening in

237 disorders associated with EL, in particular Marfan syndrome (MFS).

238 and rupture of the aorta in a mouse model of Marfan syndrome (MFS).

239 llular matrix (ECM) protein defective in the Marfan syndrome (MFS).

240 three disulfide bonds are frequent causes of Marfan syndrome (MFS).

241 an fibrillin-1, the protein defective in the Marfan syndrome (MFS).

242 nents of several genetic diseases, including Marfan syndrome (MFS).

243 -two patients (44% of the CVG group) had the Marfan syndrome (MFS).

244 ne lens is a common finding in patients with Marfan syndrome (MFS).

245 p of families exhibits traits reminiscent of Marfan syndrome (MFS).

246 not included in the diagnostic criteria for Marfan syndrome (MFS); however, their prevalence and eve

247 lective angiotensin-1 receptor inhibitor, in Marfan syndrome might reduce aortic dilatation, which is

248 in the gene for fibrillin 1 (FBN1) underlie Marfan syndrome (MS), a disorder characterized by lens d

249 The VTI was higher in Marfan syndrome (n=57, median 26; interquartile range 10

250 his region can result in severe forms of the Marfan syndrome ("neonatal" Marfan syndrome).

251 action, and five capsules from patients with Marfan syndrome obtained at intracapsular lens extractio

252 a large and diverse cohort of patients with Marfan syndrome, ocular manifestations of the disorder a

253 All patients with Marfan syndrome operated on for aortic root aneurysm fro

254 After excluding individuals with Marfan syndrome or bicuspid aortic valve, a family histo

255 ng aorta: dissection, 28 patients (19%); the Marfan syndrome or its forme fruste variety, 15 patients

256 diseases such as polycystic kidney disease, Marfan syndrome, or Ehlers-Danlos syndrome; body mass in

257 for the Stickler syndrome types 1 and 2, the Marfan syndrome, or the juvenile glaucoma loci.

258 nce (MR) images obtained in 48 patients with Marfan syndrome over a period of 2.3-9.4 years (mean, 5.

259 The Marfan syndrome patient undergoes care by many different

260 Retrospective analysis of 86 consecutive Marfan syndrome patients fulfilling Ghent criteria that

261 Marfan syndrome patients were more likely to dissect at

262 , aortic valve function, and aortic shape in Marfan syndrome patients with and without BAV and report

263 No aortic dissection was observed in Marfan syndrome patients with BAV.

264 omplications are rare in young patients with Marfan syndrome receiving medical therapy and close clin

265 of promising studies in the murine models of Marfan syndrome-related aortapathy.

266 This distinguishes MSSE from the Marfan syndrome-related disorders in which missense muta

267 Marfan syndrome remains primarily a clinical diagnosis.

268 subluxated lenses in Egyptian patients with Marfan Syndrome, resulting in improved visual acuity wit

269 Marfan syndrome results from mutations in the FBN1 gene,

270 e, measuring right eyes of 24 control and 13 Marfan syndrome subjects.

271 ression in the lens capsule of patients with Marfan syndrome supported a causal relationship to lens

272 verlaps a previously mapped second locus for Marfan syndrome, termed the MFS2 locus.

273 e was significantly greater in patients with Marfan syndrome than in control subjects (104 mL/m(2); 9

274 a may be more relevant in the development of Marfan syndrome than mechanisms previously proposed in a

275 es of many of the genetic syndromes, such as Marfan syndrome, that predispose persons to thoracic aor

276 c aneurysms and aortic root stabilization in Marfan syndrome, these claims are not consistently confi

277 perations are feasible in most patients with Marfan syndrome; they are applicable to patients with bo

278 variants do not meet diagnostic criteria for Marfan syndrome, though variants are associated with tal

279 blockers are widely used in the treatment of Marfan syndrome to try to reduce the rate of progressive

280 t data exist describing MVP in patients with Marfan syndrome undergoing aortic root replacement.

281 979, 82 patients (73.2% of all patients with Marfan syndrome undergoing resection of aneurysm of the

282 yndromes, including Birt-Hogg-Dube syndrome, Marfan syndrome, vascular (type IV) Ehlers-Danlos syndro

283 sudden death is a well-recognized outcome in Marfan syndrome, ventricular arrhythmias are not well de

284 Marfan syndrome was exclusively associated with dissecti

285 adult females with a confirmed diagnosis of Marfan syndrome was performed.

286 ic valve-sparing operations in patients with Marfan syndrome were associated with low rates of valve-

287 ls aged 6-40 years with clinically confirmed Marfan syndrome were eligible for inclusion.

288 Seven hundred thirty-two patients with Marfan syndrome were followed up for a mean of 6.6 years

289 sports, family history of heart disease, or Marfan syndrome were included in 0% to 56% of the state

290 Patients with Marfan syndrome were significantly more likely to underg

291 cause autosomal dominant disorders including Marfan Syndrome, which is characterized by disrupted TGF

292 nd long-term clinical outcomes in women with Marfan syndrome who are followed prospectively during pr

293 rgery and long-term results in patients with Marfan syndrome who suffered aortic dissection.

294 Although the majority of patients with Marfan syndrome who undergo elective aortic root replace

295 FBN1 mutations cause Marfan syndrome, whose major cardiovascular complication

296 g of the pathogenesis of vascular disease in Marfan syndrome will facilitate the development of thera

297 tution is reported to be pathogenic, causing Marfan syndrome with a dominant mode of inheritance, of

298 to describe aortic risk in a population with Marfan syndrome with pathogenic variants in the FBN1 gen

299 Patients with Marfan syndrome with prior prophylactic aortic surgery a

300 Most mutations in fibrillin-1 cause Marfan syndrome with severe cardiovascular and ocular sy