ライフサイエンスコーパス: tricuspid

1 Of the concurrent valve procedures, 56 were tricuspid, 13 aortic, and 6 mitral.

2 uctions in both mitral (34.9% vs. 12.7%) and tricuspid (31.8% vs. 21.2%) moderate or severe regurgita

3 6 cases of BPVT (11.6%; aortic 29, mitral 9, tricuspid 7, pulmonary 1), mean age was 63 years, and 68

4 The following review will describe tricuspid anatomy, define echocardiographic views for ev

5 specific models of severe aortic stenosis (6 tricuspid and 2 bicuspid) were created using dual-materi

6 smutase 3 in ascending aorta samples from 50 tricuspid and 70 patients with BAV undergoing surgery fo

7 icular tachycardia originating from the peri-tricuspid and mitral annuli.

8 Tricuspid and neoaortic regurgitation, diastolic functio

9 esser degrees of tricuspid regurgitation and tricuspid annular dilatation, as well as with appreciati

10 ity of TR, but also pays strict attention to tricuspid annular dilation (size), the mode of tricuspid

11 Routine treatment of moderate TR or tricuspid annular dilation at the time of MV repair appe

12 for moderate tricuspid regurgitation (TR) or tricuspid annular dilation in patients undergoing degene

13 lasty, and the growing consensus that FTR or tricuspid annular dilation should be more aggressively a

14 In patients with moderate TR or tricuspid annular dilation who were undergoing degenerat

15 ricuspid annuloplasty for moderate TR and/or tricuspid annular dilation.

16 a of the left ventricular outflow tract, and tricuspid annular geometry.

17 Tricuspid annular plane excursion and RV strain did not

18 , end-systolic area, fractional area change, tricuspid annular plane excursion, and RV speckle-tracki

19 as defined by semiquantitative assessment or tricuspid annular plane systolic excursion </=15 mm, HFp

20 including 1 point for each of the following: tricuspid annular plane systolic excursion <15 mm, ratio

21 7+/-0.6 versus 2.3+/-0.8; P=0.003) and lower tricuspid annular plane systolic excursion (16+/-4 mm ve

22 IQR 8.9-2.4]; P < 0.0001) and mean ( +/- SD) tricuspid annular plane systolic excursion (2.2 +/- 0.12

23 ; P=0.002) and further increased by exercise tricuspid annular plane systolic excursion (chi(2), 52.2

24 n a Cox proportional-hazards model, exercise tricuspid annular plane systolic excursion (hazard ratio

25 ce interval, 1.01-1.11; P=0.01) and exercise tricuspid annular plane systolic excursion (odds ratio,

26 icuspid valve offset (r=0.583; P=0.004), and tricuspid annular plane systolic excursion (r=0.554; P=0

27 baseline in 17beta-estradiol levels (E2) and tricuspid annular plane systolic excursion (TAPSE) at 3

28 ble Cox proportional-hazards model, exercise tricuspid annular plane systolic excursion (TAPSE; hazar

29 re examined relative to the severity of RVD (tricuspid annular plane systolic excursion [TAPSE]) and

30 RV function was categorized by tertiles of tricuspid annular plane systolic excursion and by semiqu

31 d assessment of RV chamber function included tricuspid annular plane systolic excursion and fractiona

32 ; the strongest predictors of mortality were tricuspid annular plane systolic excursion and peak syst

33 Tricuspid annular plane systolic excursion and systolic

34 Tricuspid annular plane systolic excursion correlated wi

35 RV fractional area change and tricuspid annular plane systolic excursion index were ev

36 uctive pulmonary disease (P = 0.034) and the tricuspid annular plane systolic excursion to systolic p

37 valvular heart disease (P = 0.046), and the tricuspid annular plane systolic excursion to systolic p

38 RVD defined by tricuspid annular plane systolic excursion values showed

39 Tricuspid annular plane systolic excursion was not diffe

40 le analysis: (1) right ventricular function (tricuspid annular plane systolic excursion) (P=0.002), (

41 bnormalities were frequent: 28% had abnormal tricuspid annular plane systolic excursion, 15% had redu

42 troke volume/pulmonary pulse pressure ratio, tricuspid annular plane systolic excursion, 6-minute wal

43 cise mitral regurgitation, rest and exercise tricuspid annular plane systolic excursion, exercise sys

44 left ventricular ejection fraction and lower tricuspid annular plane systolic excursion.

45 s to show the feasibility of a transcatheter tricuspid annular repair.

46 correlated significantly with late diastolic tricuspid annular velocity (A'), tissue Doppler imaging-

47 03 and 2011, 419 (65%) underwent concomitant tricuspid annuloplasty for moderate TR and/or tricuspid

48 to compare a strategy of routine concomitant tricuspid annuloplasty for moderate tricuspid regurgitat

49 Associated tricuspid annuloplasty is recommended during left-heart

50 oing degenerative mitral repair, concomitant tricuspid annuloplasty is safe, effective, and associate

51 e indications for and results of concomitant tricuspid annuloplasty remain controversial.

52 roups, but multivariate analysis showed that tricuspid annuloplasty was independently associated with

53 ocalized to the mitral annulus and 37 to the tricuspid annulus (including 9 para-Hisian), and all wer

54 a novel transcatheter device to plicate the tricuspid annulus (TA) and reduce tricuspid regurgitatio

55 ded during left-heart valve surgery when the tricuspid annulus (TA) is dilated but methodology for th

56 ide the scars, between scars, or between the tricuspid annulus and a scar.

57 mmend TV repair in the presence of a dilated tricuspid annulus at the time of a left-sided valve surg

58 18 ARVD patients versus 4 of 6 controls and tricuspid annulus in 5 of 18 ARVD patients versus 2 of 6

59 e inferior vena cava, superior vena cava, or tricuspid annulus or by ablating focally in the lateral

60 End-diastolic short-/long-axis ratio <0.6, tricuspid annulus peak systolic velocity >/= 8 cm/s, and

61 nd-diastolic short-/long-axis ratio >/= 0.6, tricuspid annulus peak systolic velocity <8 cm/s, and pe

62 /long-axis and long-axis/length-area ratios, tricuspid annulus peak systolic velocity, RV peak longit

63 mpact of RV fractional area change (FAC) and tricuspid annulus plane systolic excursion (TAPSE) for t

64 ricle (RV) and left ventricle (LV) may alter tricuspid annulus size and papillary muscle (PM) positio

65 lar geometry can lead to TR by altering both tricuspid annulus size and PM position.

66 ed isthmuses included (1A) ventriculotomy-to-tricuspid annulus, (1B) ventriculotomy-to-ventricular se

67 ricular tachycardia, 3 were localized to the tricuspid annulus, and 6 to the mitral annulus.

68 patients, mitral annulus, crista terminalis, tricuspid annulus, and right-sided PV via a posterior co

69 , and (4) ventricular septal defect patch-to-tricuspid annulus.

70 ion between vena cavae and right atrium; the tricuspid annulus; or between TV leaflets, improving coa

71 n patients undergoing surgery for BAV versus tricuspid aortic valve (TAV) stenosis.

72 rum concentration significantly decreased in tricuspid aortic valve and BAVnon-dil patients versus he

73 In this series of patients with tricuspid aortic valve and similar AS severity, women ha

74 tion-based MI registry (n=403).Compared with tricuspid aortic valve disease, CAE occurred more than t

75 spected aortic valve disease (n=94 BAV, n=83 tricuspid aortic valve) underwent both cardiac magnetic

76 lot in ascending aorta samples from other 10 tricuspid aortic valve, 10 BAVnon-dil, and 10 BAVdil pat

77 distinct valve morphologies were identified: tricuspid aortic valve, 64% (n=133); partially fused aor

78 /-3.3, and 19.8+/-3.9 mm/m(2) (P<0.0001) for tricuspid aortic valve, partially fused aortic valve, an

79 AV, 39.6+/-7.2 mm); aorta size controls with tricuspid aortic valves (n=30, 41.0+/-4.4 mm); healthy v

80 cification than those Npr2(+/-) with typical tricuspid aortic valves or all wild-type littermate cont

81 Explanted stenotic tricuspid aortic valves were weighed, and fibrosis degre

82 3-dimensional echocardiogram focused on the tricuspid apparatus.

83 ies: tetralogy of Fallot (15 patients, 25%), tricuspid atresia (12 patients, 20%), Ebstein's anomaly

84 was previously identified in a patient with tricuspid atresia and large secundum atrial septal defec

85 ct ventricular septum, single ventricle, and tricuspid atresia born in 1996 to 2003 were identified f

86 l Wnt signaling in the myocardium results in tricuspid atresia with hypoplastic right ventricle assoc

87 (95% confidence interval, 45.8 to 64.4); and tricuspid atresia, 74.6% (95% confidence interval, 62.4

88 e significantly greater in both bicuspid and tricuspid CAS cases with more severe valve calcification

89 analysis we confirmed that the repertoire of tricuspid CAS valves contains numerous expanded T cell c

90 onse is occurring in cases with bicuspid and tricuspid CAS, involving circulating CD8 T cell activati

91 ficant correlations were found among tau and tricuspid deceleration time, E', E/E', TimeE-E', A wave

92 On multivariate analysis, tricuspid deceleration time, TimeE-E', and global early

93 were atrioventricular septal defects (n=22), tricuspid hypoplasia/atresia (n=13), and coronary artery

94 RHF for patients with significant preimplant tricuspid insufficiency.

95 g the feasibility of pulmonary vein and cavo-tricuspid isthmus ablation.

96 e, 13+/-2.2 minutes) were formed at the cavo-tricuspid isthmus, with the end point of bidirectional b

97 s were formed at the pulmonary vein and cavo-tricuspid isthmus.

98 We hypothesized that tricuspid leaflet area (TLA) is increased in PH, and tha

99 icuspid annular dilation (size), the mode of tricuspid leaflet coaptation, and tricuspid leaflet teth

100 and underwent device implantation to improve tricuspid leaflet coaptation, thereby reducing TR.

101 he mode of tricuspid leaflet coaptation, and tricuspid leaflet tethering-factors often influenced by

102 ckening of the mitral and aortic but not the tricuspid or pulmonary valves, accompanied by inflammato

103 All mitral (including tricuspid, or atrial fibrillation ablation) operations p

104 ients enrolled in the CARE-HF study, 688 had tricuspid plane systolic excursion (TAPSE) measured at b

105 Tricuspid regurgitant (TR) jet velocity and its relation

106 An elevated tricuspid regurgitant jet velocity (TRV) is associated w

107 Abnormal tricuspid regurgitant jet velocity (TRV) was defined as

108 We assessed vascular complications (elevated tricuspid regurgitant jet velocity [TRV], microalbuminur

109 Elevated tricuspid regurgitant jet velocity, pulmonary hypertensi

110 ery systolic pressure (PASP) >35 mmHg and/or tricuspid regurgitant velocity (TRV) >2.5 m/s.

111 with sickle cell disease (SCD), an increased tricuspid regurgitant velocity (TRV) measured by Doppler

112 Tricuspid regurgitant velocity and creatinine levels als

113 Baseline tricuspid regurgitant velocity, a measure of pulmonary s

114 ly associated with anemia, endothelin-1, and tricuspid regurgitant velocity; the latter is reflective

115 d severe atrial dilatation (5 cases), mitral/tricuspid regurgitation (5), atrial mural thrombus (3),

116 t of the etiology and severity of functional tricuspid regurgitation (FTR) has many limitations, espe

117 Functional tricuspid regurgitation (FTR) is an important clinical e

118 ated with left heart pathologies, functional tricuspid regurgitation (FTR) is often left untreated du

119 Functional tricuspid regurgitation (FTR) with structurally normal v

120 n multivariable analysis, moderate or severe tricuspid regurgitation (hazard ratio [HR], 26.537; 95%

121 hreshold (r=0.426; P=0.048), the severity of tricuspid regurgitation (r=0.692; P=0.009), tricuspid va

122 Functional or secondary tricuspid regurgitation (STR) is the most frequent etiol

123 e is known about the incidence of prosthetic tricuspid regurgitation (TR) after lead placement.

124 despite the known association between severe tricuspid regurgitation (TR) and mortality.

125 Tricuspid regurgitation (TR) and right ventricular (RV)

126 cal and medical treatment options for severe tricuspid regurgitation (TR) are limited, and additional

127 face for native leaflet coaptation to reduce tricuspid regurgitation (TR) by occupying the regurgitan

128 ndergoing upright invasive exercise testing, tricuspid regurgitation (TR) Doppler estimates and invas

129 Patients with severe tricuspid regurgitation (TR) frequently present with exe

130 Tricuspid regurgitation (TR) is a common and important c

131 Tricuspid regurgitation (TR) is a risk factor for mortal

132 Functional tricuspid regurgitation (TR) is increasingly recognized

133 (FTR) has many limitations, especially when tricuspid regurgitation (TR) is more than severe.

134 Functional or secondary tricuspid regurgitation (TR) is the most common cause of

135 Significant tricuspid regurgitation (TR) late after left heart valve

136 However, significant tricuspid regurgitation (TR) often accompanies left-side

137 left heart syndrome who develop significant tricuspid regurgitation (TR) or require tricuspid valve

138 comitant tricuspid annuloplasty for moderate tricuspid regurgitation (TR) or tricuspid annular dilati

139 Functional tricuspid regurgitation (TR) with a structurally normal

140 stood that annular dilatation contributes to tricuspid regurgitation (TR), other factors are less cle

141 licate the tricuspid annulus (TA) and reduce tricuspid regurgitation (TR).

142 94; 95% CI, 0.89-0.99; P=0.027), and </=mild tricuspid regurgitation (TR; HR, 3.58; 95% CI, 2.04-6.30

143 nferior outcomes in the presence of residual tricuspid regurgitation after cardiac surgery, surgical

144 ith restrictive myocardial disease or severe tricuspid regurgitation after constrictive pericarditis

145 with recognition of the risk of progressive tricuspid regurgitation and right heart failure in patie

146 late outcomes because of the progression of tricuspid regurgitation and right heart failure.

147 patients with moderate or lesser degrees of tricuspid regurgitation and tricuspid annular dilatation

148 ntation if preoperative RV pressure load and tricuspid regurgitation are also considered.

149 owever, many patients with unoperated severe tricuspid regurgitation are also deemed at very high or

150 Most operations for tricuspid regurgitation are done at the time of left-sid

151 id valve replacement in patients with severe tricuspid regurgitation are poorly understood.

152 cations for tricuspid valve surgery to treat tricuspid regurgitation are related to the cause of the

153 ictive ring annuloplasty repair of secondary tricuspid regurgitation at the time of left-sided valve

154 Increased recognition and correction of tricuspid regurgitation at the time of surgery is increa

155 Tricuspid valve replacement for severe tricuspid regurgitation can be performed with an accepta

156 lines recommend a more proactive approach to tricuspid regurgitation correction and highlight the shi

157 me ratio, ejection fraction, and severity of tricuspid regurgitation did not differ by shunt type.

158 First, tricuspid regurgitation does not simply go away after co

159 during jugular venous examination and severe tricuspid regurgitation during transthoracic ECG.

160 d predictive for RV failure in patients with tricuspid regurgitation grade >2 and pulmonary arterial

161 After TVIV, both the TV inflow gradient and tricuspid regurgitation grade improved significantly.

162 We advocate the measurement of the tricuspid regurgitation gradient, pulmonary regurgitatio

163 , right heart failure and moderate-to-severe tricuspid regurgitation in 5/6 CRS type II patients.

164 Whether the surgical correction of tricuspid regurgitation in left heart disease can defini

165 es have begun to emerge for the treatment of tricuspid regurgitation in such patients.

166 tanding of the natural history of functional tricuspid regurgitation in the setting of left heart dis

167 PURPOSE OF REVIEW: The presence of tricuspid regurgitation in the setting of right ventricu

168 Second, functional tricuspid regurgitation is a progressive disorder charac

169 Severe tricuspid regurgitation is associated with poor prognosi

170 Whereas tricuspid stenosis is uncommon, tricuspid regurgitation is frequently encountered and is

171 high risks of reoperative surgery for severe tricuspid regurgitation late after left-sided valve surg

172 Worsening systemic RV function and tricuspid regurgitation may develop after LVOT TPVR.

173 Non-invasive assessment of tricuspid regurgitation must define its cause and severi

174 ividuals with plasma endothelin-1 levels and tricuspid regurgitation on echocardiogram (n = 3223) at

175 was limited to participants with detectable tricuspid regurgitation on echocardiography.

176 f lead-related (as distinct from functional) tricuspid regurgitation pose unique challenges.

177 cal events comprised death, vascular events, tricuspid regurgitation requiring surgery, worsening hea

178 interval, 1.2-3.3; P=0.0053]) and preimplant tricuspid regurgitation severity (odds ratio=2.9 [95% co

179 Tricuspid regurgitation severity was the most important

180 for years, because of the misconception that tricuspid regurgitation should disappear once the primar

181 was significantly higher in the groups with tricuspid regurgitation velocity >/=2.7 m/s.

182 er pulmonary artery pressure assessed by the tricuspid regurgitation velocity (hazard ratio, 1.23 per

183 .0001), LV lateral E/e' ratio (P=0.014), and tricuspid regurgitation velocity (P=0.019) were independ

184 with sickle cell disease (SCD), an increased tricuspid regurgitation velocity (TRV) by Doppler echoca

185 Tricuspid regurgitation velocity, which reflects systoli

186 with established clinical risk factors using tricuspid regurgitation velocity, white blood cell count

187 t between RV and right atrium (DeltaPRV-RA), tricuspid regurgitation velocity-time integral, and pulm

188 e independently associated with an increased tricuspid regurgitation velocity.

189 Worsening of systemic RV dysfunction or tricuspid regurgitation was seen in 12 patients (57%) an

190 ermore, patients with significant preimplant tricuspid regurgitation who did not receive a TVP experi

191 ty System for Symptomatic Chronic Functional Tricuspid Regurgitation) trial is a prospective, single-

192 HD: 3101 had mitral regurgitation, 1179 with tricuspid regurgitation, 817 had aortic regurgitation, 4

193 weight (n=472), adjusting for sex, syndrome, tricuspid regurgitation, arch obstruction, and shunt typ

194 renal replacement therapy, severe preimplant tricuspid regurgitation, history of cardiac surgery, and

195 ght ventricular dysfunction, moderate-severe tricuspid regurgitation, low cardiac index, and raised r

196 The severity of tricuspid regurgitation, myocardial performance index, p

197 o describe the pathophysiology of functional tricuspid regurgitation, summarize the current reports f

198 The presence of significant tricuspid regurgitation, whether in the context of mitra

199 or severe lung disease, dialysis, and severe tricuspid regurgitation.

200 nscatheter tricuspid valve repair for severe tricuspid regurgitation.

201 ificantly associated with mortality, but not tricuspid regurgitation.

202 om restrictive myocardial disease and severe tricuspid regurgitation.

203 om restrictive myocardial disease and severe tricuspid regurgitation.

204 res of RV size and function, or magnitude of tricuspid regurgitation.

205 on because of progressive RV dysfunction and tricuspid regurgitation.

206 ading to further annular dilatation and more tricuspid regurgitation.

207 rwent tricuspid valve replacement for severe tricuspid regurgitation.

208 in combination with right heart failure, and tricuspid regurgitation; and (iii) a typical histopathol

209 nths), 70 patients (37%) died, 6 (3%) needed tricuspid reoperation, and 41 (21.7%) were readmitted fo

210 were free from cardiovascular events (death, tricuspid reoperation, or heart failure admissions).

211 Surgical tricuspid repair has been avoided for years, because of

212 n, 6.5 mm [interquartile range, 6.1-7.1 mm]; tricuspid ring displacement in ART: 5.5 mm [interquartil

213 dial walls, decreased longitudinal function (tricuspid ring displacement in controls: median, 6.5 mm

214 Tricuspid S' was 9.6+/-2.8 cm/s (mean+/-SD).

215 d 2005, 48 patients with ES, all with a post-tricuspid shunt, were enrolled in a prospective, longitu

216 Whereas tricuspid stenosis is uncommon, tricuspid regurgitation

217 Few patients undergo isolated tricuspid surgery, which remains associated with high in

218 ator leads on the incidence of bioprosthetic tricuspid valve (BTV) regurgitation compared with BTV pa

219 ntation (TVIV) within dysfunctional surgical tricuspid valve (TV) bioprostheses has been described in

220 assess the remodeling potential of a tubular tricuspid valve (TV) bioprosthesis made of SIS-ECM by ev

221 Tricuspid valve (TV) disease has been relatively neglect

222 Severe tricuspid valve (TV) dysfunction may lead to surgical TV

223 le electronic device leads to interfere with tricuspid valve (TV) function has gained increasing reco

224 Severe isolated disease of the tricuspid valve (TV) is increasing and results in intrac

225 egurgitation (TR) with a structurally normal tricuspid valve (TV) may occur secondary to chronic atri

226 cant tricuspid regurgitation (TR) or require tricuspid valve (TV) surgery in the medium term have det

227 rmined by factors in the right ventricle and tricuspid valve and not the timing of or the type of sur

228 cardiographic dataset at baseline revealed a tricuspid valve annular area of 14.1 cm(2), and effectiv

229 ly Feasibility of the Mitralign Percutaneous Tricuspid Valve Annuloplasty System (PTVAS) Also Known a

230 The SCOUT (Percutaneous Tricuspid Valve Annuloplasty System for Symptomatic Chro

231 ve surgery, and discuss the emerging role of tricuspid valve annuloplasty with left ventricular assis

232 increasingly supports the use of corrective tricuspid valve annuloplasty, and the growing consensus

233 95% confidence interval, 3.5-21.0; P<0.001), tricuspid valve annulus diameter z-score (odds ratio, 1.

234 ices of RV size and function, neo-aortic and tricuspid valve annulus dimensions and function, and aor

235 ining the lateral tunnel suture line and the tricuspid valve annulus.

236 f correcting pathological alterations of the tricuspid valve apparatus may lead to more robust repair

237 ve regurgitation (<5% at each time), indexed tricuspid valve area, and >/=moderate tricuspid valve re

238 he optimal ICD configuration in a paediatric tricuspid valve atresia patient; (3) establish whether t

239 ter z score was lower (P<0.001) and the mean tricuspid valve diameter z score was higher in fetuses w

240 isease who may also concurrently suffer from tricuspid valve disease and atrial fibrillation.

241 nscatheter interventions to treat mitral and tricuspid valve disease are becoming increasingly availa

242 The assessment and management of tricuspid valve disease have evolved substantially durin

243 tients who have mitral valve with or without tricuspid valve disease with a significant history of at

244 ole of cross-sectional imaging in mitral and tricuspid valve disease, primarily valvular regurgitatio

245 integrated into the evaluation of mitral and tricuspid valve disease.

246 Ebstein anomaly and tricuspid valve dysplasia are rare congenital tricuspid

247 Fetuses diagnosed with Ebstein anomaly and tricuspid valve dysplasia from 2005 to 2011 were include

248 y series of fetuses with Ebstein anomaly and tricuspid valve dysplasia, perinatal mortality remained

249 ed recipient also had pulmonary stenosis and tricuspid valve dysplasia.

250 ar-old woman who had received a diagnosis of tricuspid valve endocarditis caused by MRSA was evaluate

251 lip device was successfully implanted in the tricuspid valve in 97% of the cases.

252 5% CI, 30.2%-44.9%]) patients, predominantly tricuspid valve infection (43/177 [24.3%]), with associa

253 year later the patient developed mitral and tricuspid valve insufficiency and subsequently underwent

254 Surgical mortality for isolated tricuspid valve interventions remains higher than for an

255 ricuspid valve dysplasia are rare congenital tricuspid valve malformations associated with high perin

256 efine echocardiographic views for evaluating tricuspid valve morphology and function, and discuss ima

257 tricuspid regurgitation (r=0.692; P=0.009), tricuspid valve offset (r=0.583; P=0.004), and tricuspid

258 ation (STR) is the most frequent etiology of tricuspid valve pathology in Western countries.

259 propose a new staging system for functional tricuspid valve pathology using 3 parameters that may mo

260 ) as independent predictors while concurrent tricuspid valve procedures (TVP) were not predictors.

261 ndexed tricuspid valve area, and >/=moderate tricuspid valve regurgitation (<20% at each time).

262 pressure, and more severe RV enlargement and tricuspid valve regurgitation.

263 lasty (n=3), recoarctation repair (n=2), and tricuspid valve repair (n=1).

264 after excluding the 3 patients who underwent tricuspid valve repair as part of their HF procedure.

265 rgery, and concomitant procedures other than tricuspid valve repair at the time of LVAD.

266 Transcatheter tricuspid valve repair could become an effective treatme

267 the first-in-human successful transcatheter tricuspid valve repair for severe tricuspid regurgitatio

268 s such as cardiac resynchronization therapy, tricuspid valve repair or replacement, pulmonary artery

269 Patients undergoing tricuspid valve repair were older (mean age 59.2 years v

270 ciency and subsequently underwent mitral and tricuspid valve repair, pulmonary valve replacement, and

271 to benefit from leaflet augmentation during tricuspid valve repair.

272 All had tricuspid valve replacement (159 bioprostheses, 36 mecha

273 Tricuspid valve replacement for severe tricuspid regurgi

274 % men; age, 67.5+/-11.3 years) who underwent tricuspid valve replacement for severe tricuspid regurgi

275 increased mortality and worse outcome after tricuspid valve replacement in patients with severe tric

276 In 68 patients with isolated tricuspid valve replacement, the associations between sh

277 roperatively in 120 patients who underwent a tricuspid valve surgery and using TTE (A4C) in 66 health

278 Isolated tricuspid valve surgery is associated with high morbidit

279 RECENT FINDINGS: The rationale for offering tricuspid valve surgery is based upon an understanding o

280 The indications for tricuspid valve surgery to treat tricuspid regurgitation

281 Tricuspid valve surgery was necessary in 87 of the 89 pr

282 s favoring a more aggressive approach toward tricuspid valve surgery, and discuss the emerging role o

283 Finally, operative mortality for isolated tricuspid valve surgery, particularly re-operative surge

284 now include echocardiographic parameters of tricuspid valve tenting area, and associated right ventr

285 The mean (SD) initial z-score for the tricuspid valve was -5.1 (+/-3.4), and a further 142 set

286 The tricuspid valve was virtually ignored for a long time in

287 septal defects, Ebstein malformation of the tricuspid valve, and perimembranous and muscular ventric

288 orm the transcatheter bicuspidization of the tricuspid valve, the Mitralign system was used to place

289 er aortic and pulmonary valve prostheses for tricuspid valve-in-valve implantation (TVIV) within dysf

290 es, good operator technique, and a competent tricuspid valve.

291 by MRSA was evaluated for replacement of the tricuspid valve.

292 that extends posteriorly to the plane of the tricuspid valve.

293 Patients with a tricuspid-valve regurgitant jet velocity >/=3.2 m/s (3.6

294 The positive predictive value for the tricuspid-valve regurgitant jet velocity >/=3.2 m/s thre

295 Porcine tricuspid valves (n=16) were studied in an in vitro righ

296 uspid valves, and in all 12 AR patients with tricuspid valves unassociated with the Marfan syndrome.

297 onconduit positions such as in bioprosthetic tricuspid valves, branch pulmonary arteries, aortic and

298 red with age- and size-matched controls with tricuspid valves.

299 with bicuspid aortic valves than those with tricuspid valves.

300 ater gives rise to the septum and mitral and tricuspid valves.