ライフサイエンスコーパス: regurgitation

1 gically (high blood pressure and heart-valve regurgitation).

2 in Yorkshire swine by inducing severe mitral regurgitation.

3 ndication for surgery in degenerative mitral regurgitation.

4 nd 40+/-14 mm Hg, whereas 50% had >2+ aortic regurgitation.

5 h GERD present with heartburn and effortless regurgitation.

6 r complications and less paravalvular aortic regurgitation.

7 ur in the 26 patients with persistent aortic regurgitation.

8 ore recurrences of moderate or severe mitral regurgitation.

9 , and incidence of moderate or severe aortic regurgitation.

10 uch patients via reduction of SAM and mitral regurgitation.

11 moderate-to-severe or severe organic mitral regurgitation.

12 lung disease, dialysis, and severe tricuspid regurgitation.

13 dditional balloon dilation to correct aortic regurgitation.

14 DP in order to identify patients with aortic regurgitation.

15 associated with significant neoaortic valve regurgitation.

16 utaneous interventions for functional mitral regurgitation.

17 d in high surgical risk patients with mitral regurgitation.

18 nounced in patients without post-TAVI aortic regurgitation.

19 valve repair in patients with primary mitral regurgitation.

20 ricular function, hemodynamics, and valvular regurgitation.

21 occurred in those with no/trace/mild mitral regurgitation.

22 ricular outflow tract conduit obstruction or regurgitation.

23 all but 1 patient had mild or less pulmonary regurgitation.

24 rum is associated with higher risk of mitral regurgitation.

25 New York Heart Association class with aortic regurgitation.

26 uture repair algorithms for secondary mitral regurgitation.

27 positioning and reduction of residual aortic regurgitation.

28 to improve the lives of patients with mitral regurgitation.

29 d replacement in patients with native mitral regurgitation.

30 re was no residual moderate or severe aortic regurgitation.

31 tion, adverse hemodynamics, or transvalvular regurgitation.

32 of progressive RV dysfunction and tricuspid regurgitation.

33 less severe and subclinical cases of mitral regurgitation.

34 be of importance in the prevention of mitral regurgitation.

35 creased risk of primary and secondary mitral regurgitation.

36 ral valve repair for the treatment of mitral regurgitation.

37 revalence of significant aortic stenosis and regurgitation.

38 intensity was higher in patients with mitral regurgitation (0.15+/-0.03) than in normals (0.11+/-0.02

39 3950 patients with any VHD: 3101 had mitral regurgitation, 1179 with tricuspid regurgitation, 817 ha

40 timers normalized in patients without aortic regurgitation (137 patients).

41 te of moderate or severe paravalvular aortic regurgitation (15.3%) than in-range (6.5%) or above-rang

42 I, 1.02-2.29), and moderate to severe aortic regurgitation (22.4% vs 14.7%; HR, 2.05; 95% CI, 1.28-3.

43 frequency of moderate or severe paravalvular regurgitation (4.3% at 1 year; 4.4% at 2 years) was unch

44 with tricuspid regurgitation, 817 had aortic regurgitation, 471 with aortic stenosis, and 193 with mi

45 tic root dilatation (92% versus 84%), aortic regurgitation (55% versus 36%), and to have undergone pr

46 ss frequent moderate and severe paravalvular regurgitation (6.0% vs. 14.3%; difference, -8.3 percenta

47 h a significantly higher frequency of aortic regurgitation (622 [33.1%] vs 57 [24.1%], P < .001) and

48 ad mitral regurgitation, 1179 with tricuspid regurgitation, 817 had aortic regurgitation, 471 with ao

49 ssociated with the presence of severe aortic regurgitation, abscess, embolization before surgical tre

50 sulted in lower rates of paravalvular aortic regurgitation after self-expanding transcatheter valve r

51 re each predictive of the presence of aortic regurgitation after TAVR and were associated with higher

52 ion for the TAVR group, >/=mild aortic valve regurgitation after TAVR was associated with an increase

53 Patients with aortic regurgitation after the initial implantation, as identif

54 icuspid (31.8% vs. 21.2%) moderate or severe regurgitation (all p < 0.0001).

55 e of SAM and significant reduction in mitral regurgitation, although high systolic LVOT velocities (i

56 d, 28,655 (0.52%) were diagnosed with mitral regurgitation and a further 1,262 (0.02%) were diagnosed

57 It can manifest as mitral regurgitation and is the leading indication for mitral v

58 lopment of clinically important mitral valve regurgitation and mitral valve stenosis.

59 eas TAVR had higher rates of residual aortic regurgitation and need for pacemaker implantation.

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

61 years and 69% men) with >/=3+ primary mitral regurgitation and preserved left ventricular ejection fr

62 tic patients with significant primary mitral regurgitation and preserved left ventricular ejection fr

63 gnition of the risk of progressive tricuspid regurgitation and right heart failure in patients with m

64 Greater than or equal to III+ aortic regurgitation and severe aortic stenosis were seen in 37

65 ocedural and late occurrence of paravalvular regurgitation and transcatheter aortic valve prosthesis

66 with moderate or lesser degrees of tricuspid regurgitation and tricuspid annular dilatation, as well

67 magnetic resonance and no or trivial mitral regurgitation, and 16 (6 female patients; median age: 40

68 ective orifice area, more total aortic valve regurgitation, and higher New York Heart Association fun

69 tenosis populations, in patients with aortic regurgitation, and in patients with bicuspid aortic valv

70 ls and patients with aortic stenosis, mitral regurgitation, and left ventricular assist devices.

71 ft ventricular remodeling, more paravalvular regurgitation, and less right ventricular systolic dysfu

72 ostdilatations, pure aortic stenosis without regurgitation, and possibly more pacing runs, earlier da

73 of Thoracic Surgeons score, degree of aortic regurgitation, and right ventricular systolic pressure)

74 tension, hyperlipidemia, medications, aortic regurgitation, and right ventricular systolic pressure),

75 ited aortopathies, moderate to severe aortic regurgitation, and severe aortic stenosis were seen in 7

76 sonance (CMR) can accurately quantify mitral regurgitation, and we examined whether this was associat

77 ny re-operation/re-intervention," "dysphagia/regurgitation," and "micronutrient status." The main lim

78 tion with right heart failure, and tricuspid regurgitation; and (iii) a typical histopathologic patte

79 evidence of at least moderate aortic/mitral regurgitation, aortic stenosis, or prior valve surgery (

80 lve morphology, dysfunction (aortic stenosis/regurgitation), aortopathy, and complications (endocardi

81 ) incorporates new features to reduce aortic regurgitation (AR) and vascular complications in transca

82 Residual aortic regurgitation (AR) following transcatheter aortic valve

83 and isolated aortic stenosis (AS) or aortic regurgitation (AR) has not been performed, making eviden

84 Chronic severe aortic regurgitation (AR) imposes significant volume and pressu

85 t (TAVR) in patients with pure native aortic regurgitation (AR).

86 aortic valve stenosis (AS) and aortic valve regurgitation (AR).

87 472), adjusting for sex, syndrome, tricuspid regurgitation, arch obstruction, and shunt type.

88 ny patients with unoperated severe tricuspid regurgitation are also deemed at very high or prohibitiv

89 Most operations for tricuspid regurgitation are done at the time of left-sided heart v

90 r tricuspid valve surgery to treat tricuspid regurgitation are related to the cause of the disorder,

91 outcomes after surgical treatment of mitral regurgitation are worse if intervention occurs after det

92 treated with the MitraClip system for mitral regurgitation as a combined procedure.

93 ended in patients with severe primary mitral regurgitation as soon as ejection fraction (EF) </=60% o

94 tricuspid valve disease, primarily valvular regurgitation assessment, with an emphasis on the prepro

95 ns in PHV obstruction and allowed prosthetic regurgitation assessment.

96 f strokes, re-intervention, and aortic valve regurgitation at 1 year after implantation.

97 associated with low mortality, strokes, and regurgitation at 1 year.

98 Paravalvular aortic regurgitation at 30 days was moderate or higher in 0.6%

99 .02), presence of moderate or severe mitral regurgitation at discharge (1.65; 95% CI, 1.21-2.26; P =

100 ismatch (all P<0.001), but more paravalvular regurgitation at discharge, which decreased at 1 year.

101 V had more frequently moderate/severe aortic regurgitation at first presentation compared with women,

102 and 26% had moderate or severe aortic valve regurgitation at the index diagnosis.

103 g annuloplasty repair of secondary tricuspid regurgitation at the time of left-sided valve surgery ha

104 Those with at least troublesome regurgitation (based on the Montreal definition) on PPIs

105 Forty-one patients with severe mitral regurgitation being considered for transcatheter mitral

106 rtic valve surgery, with severe aortic valve regurgitation being the surgical indication in 7 patient

107 rgoing primary repair of degenerative mitral regurgitation between 2003 and 2011, 419 (65%) underwent

108 provided a more durable correction of mitral regurgitation but did not significantly improve survival

109 uced prevalence of moderate or severe mitral regurgitation, but patients had more adverse events.

110 Aortic regurgitation can be difficult to diagnose and quantify.

111 es of moderate or severe paravalvular aortic regurgitation: DAR </=10%, 17.6%; DAR 10% to 15%, 9.9%;

112 re functional, degenerative, or mixed mitral regurgitation deemed at high risk or inoperable.

113 ptoms, particularly in those with persistent regurgitation despite PPI therapy, based on evaluation 6

114 DMD does not incur more severe mitral regurgitation, despite larger prolapse and valve redunda

115 ow-up intervals for TTE assessment of mitral regurgitation, despite risk-adjustment for patient varia

116 he incidence of moderate paravalvular aortic regurgitation did not increase, and no association betwe

117 Proper identification of these severe mitral regurgitation due to these disease valves will help reli

118 f hemostasis could be used to monitor aortic regurgitation during TAVR.

119 and included the following terms: heartburn, regurgitation, dysphagia, gastroesophageal reflux diseas

120 erms included were the following: heartburn, regurgitation, dysphagia, gastroesophageal reflux diseas

121 ejection time, total isovolumic time, mitral regurgitation, ejection fraction, and blood pressure at

122 included the presence of paravalvular aortic regurgitation evaluated by an independent echocardiograp

123 lower-risk patients with severe mitral valve regurgitation (Evaluation of the Safety and Performance

124 ical treatment options for functional mitral regurgitation (FMR) are limited and additional intervent

125 left heart pathologies, functional tricuspid regurgitation (FTR) is often left untreated during left

126 .02), and post-implant periprosthetic aortic regurgitation grade >/=2 of 4 (p < 0.001).

127 Hg to 20 +/- 8 mm Hg; p = 0.06), and mitral regurgitation grade (3.0 +/- 0 vs. 0.8 +/- 0.4; p = 0.00

128 V, both the TV inflow gradient and tricuspid regurgitation grade improved significantly.

129 Aortic regurgitation >/=mild after TAVR was associated with inc

130 Preimplantation aortic regurgitation >/=mild was associated with reduced mortal

131 Paravalvular regurgitation >/=moderate was rare in both groups (4.5%

132 echocardiographic moderate or severe mitral regurgitation had baseline CMR scans and were followed u

133 Patients with organic mitral regurgitation have higher strain than normals.

134 Patients with SERD and complaints of regurgitation have impaired UES and esophageal responses

135 associated with a 26% higher risk of mitral regurgitation (hazard ratio [HR] 1.26; CI 1.23, 1.29).

136 iable analysis, moderate or severe tricuspid regurgitation (hazard ratio [HR], 26.537; 95% confidence

137 acement therapy, severe preimplant tricuspid regurgitation, history of cardiac surgery, and concomita

138 nterval [CI] 2.77-11.33), presence of mitral regurgitation (HR 8.13, 95% CI 4.09-12.16), lower left v

139 In ischemic mitral regurgitation (IMR), ring annuloplasty is associated wit

140 ix (1%), and moderate or severe paravalvular regurgitation in 13 (2%).

141 evice removal was recurrence of heartburn or regurgitation in 5 patients (46%), followed by dysphagia

142 art failure and moderate-to-severe tricuspid regurgitation in 5/6 CRS type II patients.

143 to-treat analysis, TF eliminated troublesome regurgitation in a larger proportion of patients (67%) t

144 Mitral regurgitation in people without prior cardiac disease is

145 gun to emerge for the treatment of tricuspid regurgitation in such patients.

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

147 Despite the anatomical complexity of mitral regurgitation in the patients in this compassionate use

148 of asymptomatic patients with severe mitral regurgitation in valve reference centres, in which succe

149 rtic stenosis and nearly 5 years with aortic regurgitation; independent correlates included smaller L

150 Fetuses with pulmonary regurgitation, indicating circular shunt physiology, are

151 At 1 month after mitral regurgitation induction, pigs developed HF as evidenced

152 One month after mitral regurgitation induction, pigs were randomized to intraco

153 MIDA (Mitral Regurgitation International Database) is a multicenter r

154 Severe mitral regurgitation is a common and complex disease that is as

155 Severe mitral regurgitation is associated with impaired prognosis if l

156 pment of transcatheter approaches for aortic regurgitation is challenging, owing to the absence of va

157 as tricuspid stenosis is uncommon, tricuspid regurgitation is frequently encountered and is most ofte

158 Surgery for severe mitral regurgitation is indicated if symptoms or left ventricul

159 c (TTE) surveillance of patients with mitral regurgitation is indicated to avoid adverse ventricular

160 lthough stroke risk is equivalent and aortic regurgitation is less.

161 t-sided valve surgical intervention, even if regurgitation is mild.

162 nt, thickness, coaptation height, and mitral regurgitation jet height (all P<0.05).

163 o the annulus, coaptation height, and mitral regurgitation jet height in 261 Framingham Offspring par

164 first tested in a preliminary phase, mitral regurgitation jet length>/=2 cm or any aortic regurgitat

165 MVP (17%) had moderate or more severe mitral regurgitation (jet height >/=5 mm) and 5 others (8%) und

166 of reoperative surgery for severe tricuspid regurgitation late after left-sided valve surgery.

167 In patients with secondary mitral regurgitation, mainly a disease of the left ventricle, t

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

169 Quantifying the regurgitation may help, but evidence for its link with o

170 long-term association between SBP and mitral regurgitation (mediator-adjusted HR 1.22; CI 1.20, 1.25;

171 oup had more frequent post-procedural mitral regurgitation moderate or higher (19.4% vs. 6.8%; p = 0.

172 ction fraction, worse post-procedural mitral regurgitation, moderate or severe lung disease, dialysis

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

174 peptide (BNP) may predict outcomes of mitral regurgitation (MR) are plagued by small size, inconsiste

175 gation has been described for primary mitral regurgitation (MR) caused by mitral valve prolapse.

176 tive for patients with severe primary mitral regurgitation (MR) considered at high or prohibitive sur

177 eterminants or its effect on ischemic mitral regurgitation (MR) development.

178 isk for and consequences of recurrent mitral regurgitation (MR) following degenerative mitral valve r

179 fication of patients with significant mitral regurgitation (MR) has not been studied.

180 s and suitable operative strategy for mitral regurgitation (MR) in patients with HOCM.

181 avian artery, misdiagnosed as primary mitral regurgitation (MR) in transthoracic echocardiogram (TTE)

182 Mitral regurgitation (MR) is a complex valve lesion that can po

183 Primary mitral regurgitation (MR) is a growing health problem due to th

184 Symptomatic mitral regurgitation (MR) is associated with high morbidity and

185 Mitral regurgitation (MR) is associated with worse survival in

186 tic stenosis and concomitant relevant mitral regurgitation (MR) is present in 30% to 55% of these pat

187 Severe primary (degenerative) mitral regurgitation (MR) is repaired with durable results when

188 Secondary mitral valve regurgitation (MR) remains a challenging problem in the

189 All patients treated had functional mitral regurgitation (MR) secondary to ischemic cardiomyopathy

190 ive patients with severe degenerative mitral regurgitation (MR) were treated with a mitral valve repa

191 e-to-Edge Repair Study), treatment of mitral regurgitation (MR) with a novel percutaneous device show

192 y displaced papillary muscles induces mitral regurgitation (MR), which doubles mortality.

193 ery for patients with severe ischemic mitral regurgitation (MR).

194 rohibitive-risk patients with primary mitral regurgitation (MR).

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

196 Non-invasive assessment of tricuspid regurgitation must define its cause and severity; advanc

197 erate-severe central prosthetic aortic valve regurgitation (n=13, 28.3%), and moderate-severe parapro

198 l RV revalvulation for significant pulmonary regurgitation (n=21).

199 moderate-severe paraprosthetic aortic valve regurgitation (n=25, 50.0%).

200 tion, 60% [45%-67%]; all </= moderate mitral regurgitation; n=6 with previous cardiac arrest and impl

201 pse are asymptomatic those that cause severe regurgitation need emergent surgical intervention to pre

202 Among the 46 patients with aortic regurgitation, normalization occurred in 20 patients in

203 Moderate or severe aortic regurgitation occurred in 40 (14%) of 280 patients in th

204 Postprocedural aortic regurgitation occurs in 10 to 20% of patients undergoing

205 6 cm(2), with greater than mild paravalvular regurgitation of 1.9%.

206 nts, resulting in procedural residual mitral regurgitation of grade 2+ or less in 22 (96%) patients.

207 he quantitative assessment of organic mitral regurgitation (OMR).

208 MR was defined as >/= mild regurgitation on color Doppler in FHS and from Internati

209 ith plasma endothelin-1 levels and tricuspid regurgitation on echocardiogram (n = 3223) at the time o

210 ed to participants with detectable tricuspid regurgitation on echocardiography.

211 gitation vs 56.6% for those with mild aortic regurgitation or less; p=0.003).

212 in 3.8% (newly identified in 2.2%), valvular regurgitation or stenosis in 28.0% (newly identified in

213 on was associated with worse neoaortic valve regurgitation (OR, 5.29; P=0.0016).

214 s (n=3, 2 with stenosis and 1 with pulmonary regurgitation), or right ventricular dysfunction (n=2).

215 rtic valve function was divided into normal, regurgitation, or stenosis.

216 , severe mitral regurgitation, severe aortic regurgitation, or subaortic stenosis.

217 e of recurrence of moderate or severe mitral regurgitation over 2 years was higher in the repair grou

218 MVP progresses to significant mitral regurgitation over a period of 3 to 16 years in one-four

219 e was 77+/-14 years; 71% male (n=29); mitral regurgitation pathogenesis was functional in 54% (n=22)

220 ated (as distinct from functional) tricuspid regurgitation pose unique challenges.

221 utflow tract (RVOT) obstruction or pulmonary regurgitation (PR).

222 urgitation, pulmonary atrioventricular valve regurgitation, pulmonary and systemic ventricular dysfun

223 ventricle, pulmonary hypertension, pulmonary regurgitation, pulmonary atrioventricular valve regurgit

224 Moderate/severe and even mild paravalvular regurgitation (PVR) are associated with increased mortal

225 Mitral regurgitation recurred more frequently in the repair gro

226 ith hospital mortality of 2% and with mitral regurgitation reduced to grade </=2 in 87% of patients (

227 tubular ascending aorta, presence of mitral regurgitation, reduced left ventricular ejection fractio

228 c core analysis after 6 months showed mitral regurgitation reduction in 50% of treated patients by a

229 s 69%; P=0.003), and in patients with mitral regurgitation, reproducibility was improved with higher

230 for severe, moderate, mild, and trace mitral regurgitation, respectively, with 20% of providers deeme

231 lve, moderate aortic stenosis, severe mitral regurgitation, severe aortic regurgitation, or subaortic

232 ere was an interaction between TR and mitral regurgitation severity (P=0.04); the increased hazard of

233 ing role of tissue paucity of FED) on mitral regurgitation severity.

234 of technical success and reduction of mitral regurgitation severity.

235 icular (LV) dysfunction and secondary mitral regurgitation (SMR) are still controversial.

236 according to atrial fibrillation and mitral regurgitation status.

237 tcomes, mixed data on SMR and primary mitral regurgitation, studies not clearly reporting the outcome

238 In primary mitral regurgitation, surgical repair is the standard of care.

239 atisfied with the treatment of heartburn and regurgitation symptoms, a secondary variable (P = NS).

240 lity, strokes, and moderate or severe aortic regurgitation, TAVR was both non-inferior (pooled weight

241 significantly lower in patients with mitral regurgitation than in healthy control subjects (P < .001

242 ve dysfunction, men had more frequent aortic regurgitation than women (33.8% versus 22.2%, P<0.001),

243 isk Patients with Severe, Symptomatic Mitral Regurgitation - The Twelve Intrepid TMVR Pilot Study; NC

244 After mitral valve repair for primary mitral regurgitation, the preoperative LVEI is a new and simple

245 act (LVOT) obstruction and associated mitral regurgitation, thereby leading to amelioration of heart

246 trial to determine if TF reduced troublesome regurgitation to a greater extent than PPIs in patients

247 e known association between severe tricuspid regurgitation (TR) and mortality.

248 Tricuspid regurgitation (TR) and right ventricular (RV) dysfunctio

249 dical treatment options for severe tricuspid regurgitation (TR) are limited, and additional intervent

250 upright invasive exercise testing, tricuspid regurgitation (TR) Doppler estimates and invasive measur

251 Tricuspid regurgitation (TR) is a common and important comorbidity

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

253 However, significant tricuspid regurgitation (TR) often accompanies left-side heart val

254 Functional tricuspid regurgitation (TR) with a structurally normal tricuspid

255 tricuspid annulus (TA) and reduce tricuspid regurgitation (TR).

256 , 0.89-0.99; P=0.027), and </=mild tricuspid regurgitation (TR; HR, 3.58; 95% CI, 2.04-6.30; P<0.001)

257 for Symptomatic Chronic Functional Tricuspid Regurgitation) trial is a prospective, single-arm, multi

258 patients often present without heartburn or regurgitation typical of GERD.

259 In patients with moderate ischemic mitral regurgitation undergoing CABG, the addition of mitral-va

260 e patient with mild to moderate aortic valve regurgitation underwent aortic valve repair for obstruct

261 tween blood pressure (BP) and risk of mitral regurgitation using Cox regression models.

262 evere (grade 3+) or severe (grade 4+) mitral regurgitation using the Edwards PASCAL TMVr system.

263 ce systolic anterior motion (SAM) and mitral regurgitation using the transcatheter mitral clip system

264 c disorders can result from eccentric mitral regurgitation usually caused by chordae tendinae rupture

265 lished clinical risk factors using tricuspid regurgitation velocity, white blood cell count, history

266 R group (72.4% for moderate or severe aortic regurgitation vs 56.6% for those with mild aortic regurg

267 +/- 5.6 mm Hg, and moderate or severe aortic regurgitation was 1.9% at discharge.

268 Paravalvular regurgitation was assessed in a core laboratory at 30 da

269 CMR quantification of mitral regurgitation was associated with the development of sym

270 egurgitation jet length>/=2 cm or any aortic regurgitation was considered best suited to be FCU crite

271 although moderate or severe residual aortic regurgitation was higher in TAVR patients (6.8% vs. 0.0%

272 r rate of moderate or severe residual mitral regurgitation was higher in the CABG-alone group than in

273 months (19% versus 12%; P=0.01); but aortic regurgitation was less (34% versus 52% mild and 8.9% ver

274 Rate of mild aortic regurgitation was lower with the repositionable and retr

275 More than mild paravalvular regurgitation was more frequent in the self-expandable g

276 Moderate/severe transvalvular regurgitation was noted in 89 patients (3.7%) after TAVR

277 Moderate or greater paravalvular regurgitation was observed in 3.1% of reporting patients

278 y these proximate causes of secondary mitral regurgitation was only 13% (CI 6.1%, 20%), and accountin

279 ning of systemic RV dysfunction or tricuspid regurgitation was seen in 12 patients (57%) and was asso

280 Aortic valve regurgitation was the predominant hemodynamic abnormalit

281 ir in patients with moderate ischemic mitral regurgitation, we found no significant difference in the

282 ment in patients with severe ischemic mitral regurgitation, we found no significant difference in the

283 ir or replacement for severe ischemic mitral regurgitation, we observed no significant between-group

284 patients with </= mild postprocedural mitral regurgitation were 4-fold more likely to experience an i

285 Nonfemoral access and postprocedural aortic regurgitation were also significant predictors of advers

286 itus, and moderate to severe residual aortic regurgitation were significantly associated with an incr

287 damage, and moderate-to-severe paravalvular regurgitation were significantly more frequent after TAV

288 ient and incidence of moderate/severe aortic regurgitation were similar in both groups at 1 year (11%

289 an gradient, valve area, and residual aortic regurgitation were stable during follow-up.

290 rwent mitral valve repair for primary mitral regurgitation were studied.

291 volume was increased in patients with mitral regurgitation when compared with that in healthy volunte

292 rly people, causing both mitral stenosis and regurgitation which are difficult to treat.

293 imary outcome was incident reports of mitral regurgitation, which were identified from hospital disch

294 ood outcomes in patients with primary mitral regurgitation who are at high surgical risk.

295 enrolling patients with degenerative mitral regurgitation with a flail leaflet in 6 tertiary Europea

296 Among patients with degenerative mitral regurgitation with a flail leaflet referred to mitral su

297 pair and replacement for degenerative mitral regurgitation with a flail leaflet.

298 s continuously related to the risk of mitral regurgitation with no evidence of a nadir down to 115 mm

299 , 92.4%, and 98.6%, respectively, for aortic regurgitation, with similar results in the validation co

300 r repair, and 31 patients with native aortic regurgitation without coexisting aortic stenosis.