ライフサイエンスコーパス: mitral

1 .7 to 117.6 g/m(2)), with reductions in both mitral (34.9% vs. 12.7%) and tricuspid (31.8% vs. 21.2%)

2 bability of ORNs (0.7) was equivalent across mitral and external tufted cells and could be explained

3 s, indicating that the distinct responses of mitral and external tufted cells to high frequency stimu

4 Transcatheter interventions to treat mitral and tricuspid valve disease are becoming increasi

5 scuss the role of cross-sectional imaging in mitral and tricuspid valve disease, primarily valvular r

6 ngly being integrated into the evaluation of mitral and tricuspid valve disease.

7 bition.SIGNIFICANCE STATEMENT Olfactory bulb mitral and tufted cells display different odor-evoked re

8 w that these circuit-level differences allow mitral and tufted cells to best discriminate odors in se

9 ry bulb contains excitatory principal cells (mitral and tufted cells) that project to cortical target

10 t excitation and feedforward inhibition onto mitral and tufted cells, the principal neurons.

11 ut neuron layers in the olfactory bulb (OB), mitral and tufted cells, using chronic two-photon calciu

12 in piriform cortex but not in olfactory bulb mitral and tufted cells.

13 ate transporter 1, a presynaptic protein, in mitral and tufted projection neurons, and 5T4 in granule

14 tation and suppression in OB output neurons (mitral and tufted, MT cells).

15 Mitral annular calcification is an increasing problem in

16 ral stenosis, developing secondary to severe mitral annular calcification.

17 Mitral annular calcium (MAC), commonly identified by car

18 tio between early mitral inflow velocity and mitral annular early diastolic velocity (E/e') ratio, ha

19 ventricular (LV) long-axis function-lateral mitral annular plane systolic excursion (MAPSE)-in a lar

20 had decreased longitudinal motion (decreased mitral annular systolic peak velocities: control median,

21 diastolic function, and E to early diastolic mitral annular tissue velocity (E/e') to estimate LV fil

22 mitral flow velocity to peak early diastolic mitral annular velocity [E/e'] <13 both at rest and exer

23 the area under the curve of early diastolic mitral annular velocity and left ventricular longitudina

24 e approximation with undersizing restrictive mitral annuloplasty (PMA) associated with complete surgi

25 randomized to either undersizing restrictive mitral annuloplasty (RA) or papillary muscle approximati

26 ting the left-sided pulmonary veins with the mitral annulus along the posterior base of the left atri

27 tology of the mitral annulus showed a longer mitral annulus disjunction in 50 sudden death patients w

28 Histology of the mitral annulus showed a longer mitral annulus disjunctio

29 the right pulmonary vein (PV) in 3 patients, mitral annulus, crista terminalis, tricuspid annulus, an

30 ng the left inferior pulmonary vein with the mitral annulus.

31 Perfect coupling between mitral-aortic flow reversal and ejection flow in the lef

32 the outcomes of TMVR in patients with failed mitral bioprosthetic valves (valve-in-valve [ViV]) and a

33 during active odor discrimination learning, mitral but not tufted cells exhibited improved pattern s

34 ctory bulb and its neuromodulatory effect on mitral cell (MC) first-order neurons.

35 ary granule cell EPSPs evoked in response to mitral cell action potentials in rat (both sexes) brain

36 fting the balance of principal tufted versus mitral cell activity across large expanses of the MOB in

37 onic dose-response relationship, suppressing mitral cell activity at high and low, but not intermedia

38 e combination of large olfactory bulbs, high mitral cell counts and a greatly enlarged nasal cavity l

39 The direct inhibitory synaptic input engages mitral cell intrinsic membrane properties to generate in

40 ve been hypothesized to represent tufted and mitral cell networks, respectively.

41 nce, the AOB network topology, in which each mitral cell receives input from multiple glomeruli, enab

42 this slow current in mitral cells converted mitral cell responses to a transient response profile, t

43 and mGluR1 receptor antagonists, converting mitral cell responses to transient response profiles.

44 tions in a cell-type-specific manner between mitral cells (MCs) and GCs or between MCs and EPL intern

45 ivity, population-level interactions between mitral cells (MCs) and granule cells (GCs) can generate

46 ence-dependent plasticity between excitatory mitral cells (MCs) and inhibitory internal granule cells

47 nd inhibition at reciprocal synapses between mitral cells (MCs) and local interneurons.

48 In the mouse olfactory system, mitral cells (MCs) and tufted cells (TCs) comprise paral

49 classes of the mammalian olfactory bulb, the mitral cells (MCs) and tufted cells (TCs), differ marked

50 illatory synchrony in the activity of output mitral cells (MCs) appears to result from interactions w

51 ABSTRACT: Mitral cells (MCs) contained in the main (MOB) and acces

52 onergic afferents are largely excitatory for mitral cells (MCs) in the MOB where 5-HT2A receptors med

53 e tested how background odors are encoded by mitral cells (MCs) in the olfactory bulb (OB) of male mi

54 evident in the spontaneous synaptic input in mitral cells (MCs) separated up to 220 mum (300 mum with

55 Here we report that Nrp2-positive (Nrp2(+)) mitral cells (MCs, second-order neurons) play crucial ro

56 Specifically, we measured how mitral cells adapt to continuous background odors and ho

57 ther, distinct temporal response profiles in mitral cells and external tufted cells could be attribut

58 Here, we show that assemblies of AOB mitral cells are synchronized by lateral interactions th

59 that are 4x larger and contain twice as many mitral cells as those of the sympatric black vulture (Co

60 While mitral cells at rest were also excited by raphe activati

61 ry bulb slices elicited the GABAergic LTP in mitral cells by enhancing postsynaptic GABA receptor res

62 tral cells, as blocking this slow current in mitral cells converted mitral cell responses to a transi

63 t of dendrodendritic synapses of granule and mitral cells in the olfactory bulb.

64 or brain size among birds, but the number of mitral cells is proportional to the size of their olfact

65 synchronous infra-slow bursting activity in mitral cells of the mouse accessory olfactory bulb (AOB)

66 tic depression, dendrodendritic circuitry in mitral cells produces robust amplification of brief affe

67 Mitral cells responded to high frequency ORN stimulation

68 In cell-attached recordings, mitral cells responded to high frequency stimulation wit

69 The sustained response in mitral cells resulted from dendrodendritic amplification

70 slow intracellular Na(+) dynamics endow AOB mitral cells with a weak tendency to burst, which is fur

71 ributed to slow dendrodendritic responses in mitral cells, as blocking this slow current in mitral ce

72 re, we find that longer-latency responses in mitral cells, compared with tufted cells, are due to wea

73 membrane excitability of projection neurons (mitral cells, MCs) that dramatically curtailed their res

74 0, the Ca(2+) sensor for IGF1 secretion from mitral cells, or deletion of IGF1 receptor in the olfact

75 ritic circuitry in external tufted cells and mitral cells, respectively, tunes the postsynaptic respo

76 One view suggests that mitral cells, the primary output neuron of the olfactory

77 Functionally, odor-evoked responses of mitral cells, which are normally inhibited by abGCs, wer

78 size of their olfactory bulbs and numbers of mitral cells, which provide the primary output of the ol

79 sulted from dendrodendritic amplification in mitral cells, which was blocked by NMDA and mGluR1 recep

80 me that some rodent accessory olfactory bulb mitral cells-the direct link between vomeronasal sensory

81 5 patients were identified with degenerative mitral disease who underwent mitral valve operations bet

82 s, db/db mice had reduced ejection fraction, mitral E/A ratio, endothelium-dependent relaxation of co

83 d as stage C1 (ratio of peak early diastolic mitral flow velocity to peak early diastolic mitral annu

84 us studies reported monosynaptically coupled mitral/granule cell connections and neither attempted to

85 athway requirement likely enables the sparse mitral/granule cell interconnections to develop highly o

86 ular (LV) mass index and ratio between early mitral inflow velocity and mitral annular early diastoli

87 Predictors for unsuccessful bidirectional mitral isthmus blockade were the need for epicardial abl

88 The mitral isthmus is a critical part of perimitral reentran

89 Deployment of an endocardial mitral isthmus line (MIL) with the end point of bidirect

90 e 2,556 patients who underwent transcatheter mitral leaflet clip in 2015 were similar to patients fro

91 Changes in mitral leaflet morphology are associated with both NDM a

92 Systolic anterior motion of mitral leaflets caused the MR in most patients.

93 ded polytetrafluoroethylene (ePTFE) cords on mitral leaflets in the beating heart.

94 or surgeons with total annual volumes of >50 mitral operations (p < 0.001).

95 decrease in reoperation risk until 25 total mitral operations annually; and improved 1-year survival

96 surgeons with total annual volumes of </=10 mitral operations to 77% (n = 1,710 of 2,216) for surgeo

97 Median annual surgeon volume of any mitral operations was 10 (range 1 to 230), with a mean r

98 surgeons with a total annual volume of </=25 mitral operations, repair rates were higher (63.8%; n =

99 dds ratio [OR]: 1.13 for every additional 10 mitral operations; 95% confidence interval [CI]: 1.10 to

100 y, in inhibitory interneurons and excitatory mitral projection neurons of the main olfactory bulb; he

101 sis dysfunction and in 5 of 19 patients with mitral prosthesis/repair dysfunction and was associated

102 secutive patients who underwent percutaneous mitral PVL closure at Mayo Clinic, Rochester, MN, betwee

103 e cohort of patients undergoing percutaneous mitral PVL closure, successful percutaneous reduction of

104 total of 231 patients underwent percutaneous mitral PVL repair at a mean age of 67+/-12 years.

105 strain intensity was higher in patients with mitral regurgitation (0.15+/-0.03) than in normals (0.11

106 and medical treatment options for functional mitral regurgitation (FMR) are limited and additional in

107 SBP was associated with a 26% higher risk of mitral regurgitation (hazard ratio [HR] 1.26; CI 1.23, 1

108 In ischemic mitral regurgitation (IMR), ring annuloplasty is associa

109 on the long-term association between SBP and mitral regurgitation (mediator-adjusted HR 1.22; CI 1.20

110 lve (MV) disease is a common cause of severe mitral regurgitation (MR) and accounts for the majority

111 uretic peptide (BNP) may predict outcomes of mitral regurgitation (MR) are plagued by small size, inc

112 l aggregation has been described for primary mitral regurgitation (MR) caused by mitral valve prolaps

113 alternative for patients with severe primary mitral regurgitation (MR) considered at high or prohibit

114 g its determinants or its effect on ischemic mitral regurgitation (MR) development.

115 ications and suitable operative strategy for mitral regurgitation (MR) in patients with HOCM.

116 Mitral regurgitation (MR) is a complex valve lesion that

117 Primary mitral regurgitation (MR) is a growing health problem du

118 Symptomatic mitral regurgitation (MR) is associated with high morbid

119 onsecutive patients with severe degenerative mitral regurgitation (MR) were treated with a mitral val

120 herapy for patients with symptomatic, severe mitral regurgitation (MR).

121 nd surgery for patients with severe ischemic mitral regurgitation (MR).

122 d for the quantitative assessment of organic mitral regurgitation (OMR).

123 t ventricular (LV) dysfunction and secondary mitral regurgitation (SMR) are still controversial.

124 High Risk Patients with Severe, Symptomatic Mitral Regurgitation - The Twelve Intrepid TMVR Pilot St

125 p period, 28,655 (0.52%) were diagnosed with mitral regurgitation and a further 1,262 (0.02%) were di

126 In asymptomatic patients with >/=3+ mitral regurgitation and preserved left ventricular (LV)

127 linical outcomes after surgical treatment of mitral regurgitation are worse if intervention occurs af

128 e also treated with the MitraClip system for mitral regurgitation as a combined procedure.

129 06; P = .02), presence of moderate or severe mitral regurgitation at discharge (1.65; 95% CI, 1.21-2.

130 c, severe functional, degenerative, or mixed mitral regurgitation deemed at high risk or inoperable.

131 Proper identification of these severe mitral regurgitation due to these disease valves will he

132 Mitral regurgitation in people without prior cardiac dis

133 (mean age, 61 years +/- 19; nine male) with mitral regurgitation in the 24 hours before mitral valve

134 Despite the anatomical complexity of mitral regurgitation in the patients in this compassiona

135 eatment of asymptomatic patients with severe mitral regurgitation in valve reference centres, in whic

136 At 1 month after mitral regurgitation induction, pigs developed HF as evi

137 One month after mitral regurgitation induction, pigs were randomized to

138 MIDA (Mitral Regurgitation International Database) is a multic

139 Severe mitral regurgitation is a common and complex disease tha

140 Severe mitral regurgitation is associated with impaired prognos

141 ographic (TTE) surveillance of patients with mitral regurgitation is indicated to avoid adverse ventr

142 placement, thickness, coaptation height, and mitral regurgitation jet height (all P<0.05).

143 ViR group had more frequent post-procedural mitral regurgitation moderate or higher (19.4% vs. 6.8%;

144 l patients, resulting in procedural residual mitral regurgitation of grade 2+ or less in 22 (96%) pat

145 2014, with hospital mortality of 2% and with mitral regurgitation reduced to grade </=2 in 87% of pat

146 h rate of technical success and reduction of mitral regurgitation severity.

147 nd then according to atrial fibrillation and mitral regurgitation status.

148 AS) was significantly lower in patients with mitral regurgitation than in healthy control subjects (P

149 ship between blood pressure (BP) and risk of mitral regurgitation using Cox regression models.

150 te-to-severe (grade 3+) or severe (grade 4+) mitral regurgitation using the Edwards PASCAL TMVr syste

151 PERM) by these proximate causes of secondary mitral regurgitation was only 13% (CI 6.1%, 20%), and ac

152 d that patients with </= mild postprocedural mitral regurgitation were 4-fold more likely to experien

153 stolic volume was increased in patients with mitral regurgitation when compared with that in healthy

154 egistry enrolling patients with degenerative mitral regurgitation with a flail leaflet in 6 tertiary

155 Among patients with degenerative mitral regurgitation with a flail leaflet referred to mi

156 r MV repair and replacement for degenerative mitral regurgitation with a flail leaflet.

157 SBP was continuously related to the risk of mitral regurgitation with no evidence of a nadir down to

158 re were 3950 patients with any VHD: 3101 had mitral regurgitation, 1179 with tricuspid regurgitation,

159 absence of SAM and significant reduction in mitral regurgitation, although high systolic LVOT veloci

160 cardiac magnetic resonance and no or trivial mitral regurgitation, and 16 (6 female patients; median

161 ography evidence of at least moderate aortic/mitral regurgitation, aortic stenosis, or prior valve su

162 in follow-up intervals for TTE assessment of mitral regurgitation, despite risk-adjustment for patien

163 time, ejection time, total isovolumic time, mitral regurgitation, ejection fraction, and blood press

164 lar ejection fraction, worse post-procedural mitral regurgitation, moderate or severe lung disease, d

165 % versus 69%; P=0.003), and in patients with mitral regurgitation, reproducibility was improved with

166 months for severe, moderate, mild, and trace mitral regurgitation, respectively, with 20% of provider

167 spid valve, moderate aortic stenosis, severe mitral regurgitation, severe aortic regurgitation, or su

168 with outcomes, mixed data on SMR and primary mitral regurgitation, studies not clearly reporting the

169 flow tract (LVOT) obstruction and associated mitral regurgitation, thereby leading to amelioration of

170 ve repair in patients with moderate ischemic mitral regurgitation, we found no significant difference

171 our primary outcome was incident reports of mitral regurgitation, which were identified from hospita

172 able to less severe and subclinical cases of mitral regurgitation.

173 ol may be of importance in the prevention of mitral regurgitation.

174 h an increased risk of primary and secondary mitral regurgitation.

175 ter mitral valve repair for the treatment of mitral regurgitation.

176 f the indication for surgery in degenerative mitral regurgitation.

177 reated in Yorkshire swine by inducing severe mitral regurgitation.

178 antly more recurrences of moderate or severe mitral regurgitation.

179 ef in such patients via reduction of SAM and mitral regurgitation.

180 ts with moderate-to-severe or severe organic mitral regurgitation.

181 l spectrum is associated with higher risk of mitral regurgitation.

182 rategy to improve the lives of patients with mitral regurgitation.

183 pair and replacement in patients with native mitral regurgitation.

184 on fraction, 60% [45%-67%]; all </= moderate mitral regurgitation; n=6 with previous cardiac arrest a

185 Mitral repair rates, mitral reoperations within 12 months of repair, and surv

186 .2% (interquartile range: 6.0% to 14.1%) for mitral repair and replacement, respectively.

187 surgeon volume is a determinant of not only mitral repair rates, but also freedom from reoperation,

188 Mitral repair rates, mitral reoperations within 12 month

189 for procedural guidance during transcatheter mitral repair.

190 Degenerative mitral stenosis (DMS) is an important cause of mitral st

191 e was no association between SBP and risk of mitral stenosis (HR per 20 mmHg higher SBP 1.03; CI 0.93

192 sing problem in elderly people, causing both mitral stenosis and regurgitation which are difficult to

193 Patients with moderate to severe mitral stenosis or mechanical heart valves were excluded

194 farin excluded patients with moderate/severe mitral stenosis or mechanical heart valves, but variably

195 tral stenosis (DMS) is an important cause of mitral stenosis, developing secondary to severe mitral a

196 471 with aortic stenosis, and 193 with mild mitral stenosis.

197 a further 1,262 (0.02%) were diagnosed with mitral stenosis.

198 concept of reference referral to experienced mitral surgeons to improve outcomes in patients with deg

199 gurgitation with a flail leaflet referred to mitral surgery, MV repair was associated with lower oper

200 Three patients required conversion to open mitral surgery.

201 Transcatheter mitral technologies have potential as solutions for unme

202 ill help to define the role of transcatheter mitral therapy as a potentially exciting new strategy to

203 tly, multiple technologies for transcatheter mitral therapy have emerged, with the potential for both

204 receptor neuron nerve terminals (input) and mitral/tufted cell apical dendrites (output).

205 Concerning mitral valve (MV) annular geometry, we found significant

206 Degenerative mitral valve (MV) disease is a common cause of severe mi

207 Conventional mitral valve (MV) operations allow direct anatomic asses

208 Mitral valve (MV) repair is preferred over replacement i

209 ume with hospital performance for aortic and mitral valve (MV) surgical procedures.

210 itral ViV and ViR were compared according to Mitral Valve Academic Research Consortium criteria.

211 success 30 days after implantation using the Mitral Valve Academic Research Consortium definitions.

212 t of cardiac development but, along with the mitral valve and trabeculae, their developmental traject

213 that experimental tethering alone increases mitral valve area in association with endothelial-to-mes

214 ds, and outcomes of transcatheter aortic and mitral valve catheter-based valve procedures in the Unit

215 othesized that percutaneous plication of the mitral valve could reduce left ventricular outflow tract

216 Mean mitral valve diameter z score was lower (P<0.001) and th

217 with increased repair rates of degenerative mitral valve disease (adjusted odds ratio [OR]: 1.13 for

218 ial tissues from the patients with rheumatic mitral valve disease in either sinus rhythm or persisten

219 ower the incidence of clinically significant mitral valve disease requires further study.

220 AC, a risk factor for clinically significant mitral valve disease, suggesting a causal association.

221 o promote the development of AF in rheumatic mitral valve disease.

222 prove outcomes in patients with degenerative mitral valve disease.

223 ase category, younger age, and morphological mitral valve features were risk factors for an unfavorab

224 Mean mitral valve gradients were similar between groups (6.4

225 ing prostheses specifically designed for the mitral valve is warranted.

226 ickness, morphology, left atrial volume, and mitral valve leaflet lengths (all P=non-significant).

227 oint of a line connecting the origins of the mitral valve leaflets at end systole and end diastole.

228 ium, biatrial enlargement, thickening of the mitral valve leaflets, and interatrial septum and mild p

229 ence between peak twisting and untwisting at mitral valve opening (%untwMVO) using speckle-tracking e

230 th degenerative mitral disease who underwent mitral valve operations between 2002 and 2013.

231 Percutaneous closure of prosthetic mitral valve paravalvular leak (PVL) has emerged as an a

232 Precise definition of the mitral valve plane (VP) during segmentation of the left

233 This is a report of percutaneous mitral valve plication as a primary therapy in the manag

234 nitial experience suggests that percutaneous mitral valve plication may be effective for symptom reli

235 Longitudinal studies of mitral valve prolapse (MVP) progression among unselected

236 disease valves will help relieve symptomatic mitral valve prolapse patients.

237 07-0.23), 0.12 (95% CI, 0.04-0.20) excluding mitral valve prolapse, and 0.44 (95% CI, 0.15-0.73) for

238 higher rates of scoliosis, pectus excavatum, mitral valve prolapse, and mutations in the CFTR gene.

239 primary mitral regurgitation (MR) caused by mitral valve prolapse.

240 levance when referring patients with complex mitral valve prolapse.

241 er, transapical delivery of a self-expanding mitral valve prosthesis and were examined in a prospecti

242 n of TMVR in lower-risk patients with severe mitral valve regurgitation (Evaluation of the Safety and

243 Secondary mitral valve regurgitation (MR) remains a challenging pr

244 s to the development of clinically important mitral valve regurgitation and mitral valve stenosis.

245 e devices currently available, transcatheter mitral valve repair (TMVr) remains challenging in comple

246 the commercial experience with transcatheter mitral valve repair for the treatment of mitral regurgit

247 gs demonstrate that commercial transcatheter mitral valve repair is being performed in the United Sta

248 uence of surgeon case volume on degenerative mitral valve repair rates and outcomes.

249 nnual mitral volumes of >50 and degenerative mitral valve repair rates of >70%, compared with surgeon

250 Degenerative mitral valve repair rates remain highly variable, despit

251 itral regurgitation (MR) were treated with a mitral valve repair system (MVRS) via small left thoraco

252 me in which patients underwent transcatheter mitral valve repair using the Edwards PASCAL TMVr system

253 cic Surgeons predicted risk of mortality for mitral valve repair was 4.8% (2.1-9.0) and 6.8% (2.9-10.

254 ents commercially treated with transcatheter mitral valve repair were analyzed.

255 tery bypass graft, aortic valve replacement, mitral valve repair) using an interrupted time series mo

256 st- atrial fibrillation ablation or surgical mitral valve repair).

257 Transcatheter mitral valve repair, particularly edge-to-edge leaflet r

258 Limited data exist regarding transcatheter mitral valve replacement (TMVR) for patients with failed

259 More recently, transcatheter mitral valve replacement (TMVR) has emerged as a potenti

260 Transcatheter mitral valve replacement (TMVR) is a potential therapy f

261 Transcatheter mitral valve replacement (TMVR) may be an option for sel

262 replacement (TMVR) for patients with failed mitral valve replacement and repair.

263 cedures were high risk, with an STS PROM for mitral valve replacement of 11%.

264 85 (74-96) seconds compared to dysfunctional mitral valve replacement or repair, 143 (128-192) second

265 , P < .001, and also in normally functioning mitral valve replacement or repair, 85 (74-96) seconds c

266 ormance of the Twelve Intrepid Transcatheter Mitral Valve Replacement System in High Risk Patients wi

267 Mean time from mitral valve replacement to percutaneous PVL repair was

268 for elective isolated or combined aortic and mitral valve replacement were included.

269 r was 4.8% (2.1-9.0) and 6.8% (2.9-10.1) for mitral valve replacement.

270 oup at high or extreme risk for conventional mitral valve replacement.

271 lly important mitral valve regurgitation and mitral valve stenosis.

272 Diastolic mitral valve surface area was quantified by 3-dimensiona

273 ation with the development of indication for mitral valve surgery (0.83).

274 re associated with higher mortality, whereas mitral valve surgery (HR: 0.82) was associated with impr

275 mitral regurgitation in the 24 hours before mitral valve surgery and 13 age- and sex-matched healthy

276 Mitral valve surgery is also challenging in these patien

277 Prophylactic aortic root replacement and mitral valve surgery were rare during childhood versus a

278 Perioperative bleeding, aortic and mitral valve surgery, and septal surgery increased the o

279 ricular (LV) ejection fraction who underwent mitral valve surgery, we sought to discover whether base

280 41%) either died or developed indication for mitral valve surgery.

281 arranting close follow-up and perhaps, early mitral valve surgery.

282 (Early Feasibility Study of the Tendyne Mitral Valve System [Global Feasibility Study]; NCT02321

283 s on the basis of valve position (aortic vs. mitral valve).

284 Following surgical repair of the mitral valve, the dyspnea and palpitations resolved.

285 ents who underwent mitral valve-in-valve and mitral valve-in-ring procedures were high risk, with an

286 The 349 patients who underwent mitral valve-in-valve and mitral valve-in-ring procedure

287 ct through rotating reversal flow around the mitral valve.

288 phied septum and the anterior leaflet of the mitral valve.

289 bypass grafting (CABG) alone with CABG plus mitral-valve repair in patients with moderate ischemic m

290 il 70 years of age among patients undergoing mitral-valve replacement and until 55 years of age among

291 nderwent primary aortic-valve replacement or mitral-valve replacement with a mechanical or biologic p

292 In patients undergoing aortic-valve or mitral-valve replacement, either a mechanical or biologi

293 increased substantially for aortic-valve and mitral-valve replacement, from 11.5% to 51.6% for aortic

294 Among patients who underwent mitral-valve replacement, receipt of a biologic prosthes

295 alve replacement and from 16.8% to 53.7% for mitral-valve replacement.

296 Mitral valves (MVs) are larger in such patients but fibr

297 prostheses or failed annuloplasty rings, but mitral ViR was associated with higher rates of procedura

298 egistry, procedural and clinical outcomes of mitral ViV and ViR were compared according to Mitral Val

299 cations and mid-term mortality compared with mitral ViV.

300 e institution as a surgeon with total annual mitral volumes of >50 and degenerative mitral valve repa