ライフサイエンスコーパス: tricuspid regurgitation

1 uropean Registry of Transcatheter Repair for Tricuspid Regurgitation).

2 om restrictive myocardial disease and severe tricuspid regurgitation.

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

4 ading to further annular dilatation and more tricuspid regurgitation.

5 rwent tricuspid valve replacement for severe tricuspid regurgitation.

6 ight-sided filling pressures, and functional tricuspid regurgitation.

7 he right ventricle (RV) and right atrium and tricuspid regurgitation.

8 RV compression did not induce or exacerbate tricuspid regurgitation.

9 riven by less frequent progression to severe tricuspid regurgitation.

10 e in adult patients with severe, symptomatic tricuspid regurgitation.

11 dimension >7 cm, home oxygen use, or severe tricuspid regurgitation.

12 ht ventricular dilation and dysfunction, and tricuspid regurgitation.

13 easures in patients with severe, symptomatic tricuspid regurgitation.

14 reatment of patients with symptomatic severe tricuspid regurgitation.

15 ent implantation for the treatment of severe tricuspid regurgitation.

16 tricuspid valve repair system, for reducing tricuspid regurgitation.

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

18 on because of progressive RV dysfunction and tricuspid regurgitation.

19 nscatheter tricuspid valve repair for severe tricuspid regurgitation.

20 ificantly associated with mortality, but not tricuspid regurgitation.

21 om restrictive myocardial disease and severe tricuspid regurgitation.

22 upper body flushing (70%), asthma (38%), and tricuspid regurgitation (23%).

23 ive patients with severe isolated functional tricuspid regurgitation (33 centres, 10 countries), surv

24 60% vs. 4%, p < 0.0001), moderate or greater tricuspid regurgitation (4% vs. 0%, p = 0.06), and aorti

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

26 %] versus 0 [0%] versus 0 [0%], P=0.012) and tricuspid regurgitation (6 [46%] versus 1 [8%] versus 2

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

28 Atrial secondary tricuspid regurgitation (A-STR) is a distinct phenotype

29 (PASCAL for Tricuspid Regurgitation-a European registry [PASTE]; NCT

30 The PASTE (PASCAL for Tricuspid Regurgitation-a European registry) study is an

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

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

33 Importantly, moderate or severe mitral and tricuspid regurgitation also decreased (33.7% vs. 8.6% [

34 ic function and RV-PA coupling and increased tricuspid regurgitation and Eed as compared to patients

35 accounts for 10%-15% of clinically relevant tricuspid regurgitation and has better outcomes compared

36 ibrillator were more likely to develop >mild tricuspid regurgitation and larger structural and functi

37 r ICD leads may result in severe symptomatic tricuspid regurgitation and may not be overtly visualize

38 oppler echocardiography variables (including tricuspid regurgitation and pulmonary regurgitation) and

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

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

41 Tricuspid regurgitation and RV function did not change b

42 In patients with severe tricuspid regurgitation and RVD/PH, transcatheter tricus

43 The severity of tricuspid regurgitation and safety were also assessed.

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

45 eroidal shape was associated with >=moderate tricuspid regurgitation and tricuspid annular dilation.

46 ic pressure >=50 mmHg and moderate to severe tricuspid regurgitation) and their impact on post-operat

47 ar remodeling, greater coexisting mitral and tricuspid regurgitation, and a higher prevalence of left

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

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

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

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

52 RV failure and tricuspid regurgitation are common.

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

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

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

56 Mitral regurgitation and tricuspid regurgitation are the most common valvular hea

57 nction, are independent of RV-PA coupling or tricuspid regurgitation, are associated with exercise-in

58 ntricular systolic dysfunction > or =3+, and tricuspid regurgitation area > or =1.8 cm2).

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

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

61 Atrial functional tricuspid regurgitation (atrial TR) has received growing

62 appears to be safe and effective at reducing tricuspid regurgitation by at least one grade.

63 2011, to August 28, 2013) and had measurable tricuspid regurgitation by spectral Doppler.

64 for tricuspid regurgitation, progression of tricuspid regurgitation by two grades from baseline or t

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

66 Severe tricuspid regurgitation caused by a PPM or ICD lead is a

67 derwent tricuspid valve operation for severe tricuspid regurgitation caused by previously placed PPM

68 PASCAL TrAnScatheter Valve RePair System in Tricuspid Regurgitation [CLASP TR] Early Feasibility Stu

69 PASCAL TrAnScatheter Valve RePair System in Tricuspid Regurgitation [CLASP TR] Early Feasibility Stu

70 right ventricular function, and less mitral/tricuspid regurgitation compared with high NP HFpEF.

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

72 pulmonary artery pressure assessed from the tricuspid regurgitation derived maximal pressure gradien

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

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

75 Changes observed in tricuspid regurgitation Doppler echocardiographic variab

76 actor for mortality in patients with chronic tricuspid regurgitation due to acquired heart disease.

77 One patient developed severe tricuspid regurgitation due to entrapment of the anterio

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

79 Overall, tricuspid regurgitation estimated systolic pressure grad

80 terest in the treatment of severe functional tricuspid regurgitation (FTR) due to the awareness of it

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

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

83 Functional tricuspid regurgitation (FTR) is common in heart failure

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

85 Functional tricuspid regurgitation (FTR) with structurally normal v

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

87 tricular diastolic area (17 to 18.7 cm2) and tricuspid regurgitation grade (2 + to 3 +; p < 0.0001 be

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

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

90 ad >=2 severe native VHDs (left-sided and/or tricuspid regurgitation, Group C).

91 asive parameter was associated with residual tricuspid regurgitation >=3+.

92 Patients with a moderate or severe degree of tricuspid regurgitation (> or =2+) demonstrated by color

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

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

95 Conclusions In significant tricuspid regurgitation, impaired RV free wall longitudi

96 ER) for the treatment of severe, symptomatic tricuspid regurgitation improved quality of life compare

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

98 ssigned 400 patients with severe symptomatic tricuspid regurgitation in a 2:1 ratio to undergo either

99 anomaly is the most common cause of primary tricuspid regurgitation in adults with congenital heart

100 medically managed patients with >= moderate tricuspid regurgitation in Europe and North America (n =

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

102 nd function in all subjects, as well as mild tricuspid regurgitation in nine subjects, with normal es

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

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

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

106 rain in patients with significant functional tricuspid regurgitation, in comparison with tricuspid an

107 sed and the percentage of moderate or severe tricuspid regurgitation increased from baseline to 1 yea

108 ghting the effectiveness of TTVR in reducing tricuspid regurgitation, inducing reverse right ventricu

109 Severe tricuspid regurgitation is a debilitating condition that

110 Tricuspid regurgitation is a frequent echocardiographic

111 Tricuspid regurgitation is a prevalent disease associate

112 Second, functional tricuspid regurgitation is a progressive disorder charac

113 AF-tricuspid regurgitation is also discussed.

114 Severe tricuspid regurgitation is associated with disabling sym

115 Severe tricuspid regurgitation is associated with increased mor

116 Tricuspid regurgitation is associated with increased rat

117 Severe tricuspid regurgitation is associated with poor prognosi

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

119 Marked tricuspid regurgitation is frequently present in patient

120 unction and stiffness associations with ECV, tricuspid regurgitation jet velocity (TRV) and exercise

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

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

123 ogistic regression models revealed that only tricuspid regurgitation, LV ejection fraction and 3D RV

124 Tricuspid regurgitation maximal velocity greater than 2.

125 Tricuspid regurgitation maximal velocity pressure gradie

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

127 Decreasing tricuspid regurgitation may reduce symptoms and improve

128 Echodensities and moderate/severe tricuspid regurgitation merit attention as early signs o

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

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

131 evere right ventricular (RV) dysfunction and tricuspid regurgitation (n = 110, 31 events) and uncommo

132 n in those with mild/less RV dysfunction and tricuspid regurgitation (n = 181, 13 events, P < .001).

133 System in Patients With Moderate or Greater Tricuspid Regurgitation]; n=85) is an international, pro

134 Atrial secondary tricuspid regurgitation occurs most commonly in elderly

135 Progressive tricuspid regurgitation occurs with age and is associate

136 p and 4.8% of those in the control group had tricuspid regurgitation of no greater than moderate seve

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

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

139 -valve surgery in patients who have moderate tricuspid regurgitation or less-than-moderate regurgitat

140 ades from baseline or the presence of severe tricuspid regurgitation, or death.

141 atation, pulmonary hypertension, severity of tricuspid regurgitation, or individual mitral regurgitat

142 ncidence of preoperative acidosis (P:=0.02), tricuspid regurgitation (P:=0.001), and ventricular dysf

143 ation) and in spontaneous restoration of SR (tricuspid regurgitation) (P < 0.05).

144 rvational Real-World Study Evaluating Severe Tricuspid Regurgitation Patients Treated With the Abbott

145 rvational Real-world Study Evaluating Severe Tricuspid Regurgitation Patients Treated With the Abbott

146 rvational Real-World Study Evaluating Severe Tricuspid Regurgitation Patients Treated With the Abbott

147 rvational Real-World Study Evaluating Severe Tricuspid Regurgitation Patients Treated With the Abbott

148 functional status and no impact on residual tricuspid regurgitation, patients with higher mean pulmo

149 ease in E/e'(lat) (P=0.045), and decrease in tricuspid regurgitation peak velocity (P=0.024) than pat

150 ges in Doppler echocardiographically derived tricuspid regurgitation peak velocity and velocity durat

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

152 Tricuspid regurgitation preceded third-degree block in 1

153 Patients with severe tricuspid regurgitation present late and are often ineli

154 al velocity greater than 2.82 m/s as well as tricuspid regurgitation pressure gradient greater than 3

155 end point was a composite of reoperation for tricuspid regurgitation, progression of tricuspid regurg

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

157 moderate (2 patients) or severe (6 patients) tricuspid regurgitation recorded at either initial or re

158 se (aortic/mitral stenosis or regurgitation, tricuspid regurgitation), reduced ejection fraction <50%

159 nt analysis and correlated with RV function, tricuspid regurgitation, remnant left ventricular morpho

160 (TrIcuspid Regurgitation RePAIr With CaRdioband Transcath

161 R in 30 patients enrolled in the TRI-REPAIR (TrIcuspid Regurgitation RePAIr With CaRdioband Transcath

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

163 l haemodynamic abnormalities (more than mild tricuspid regurgitation, residual ventricular septal def

164 The tricuspid regurgitation resulting from this disease has

165 ocardiographic measurements (>mild degree of tricuspid regurgitation, RV outflow tract diameter in pa

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

167 T-TEER reduces tricuspid regurgitation severity and improves a composit

168 primary efficacy endpoint was a reduction in tricuspid regurgitation severity by at least one grade a

169 7.2 [-19.3, -15.8]%; P<0.001) raise, whereas tricuspid regurgitation severity improved only in transp

170 Tricuspid regurgitation severity was reduced by at least

171 Tricuspid regurgitation severity was the most important

172 id TEER appeared safe, significantly reduced tricuspid regurgitation severity, and decreased rates of

173 better LV and RV function, lower mitral and tricuspid regurgitation severity, were using smaller dos

174 ea, right ventricular systolic pressure, and tricuspid regurgitation severity.

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

176 ctively (p < 0.0001); mean percent change in tricuspid regurgitation signal duration was 18% +/- 2% a

177 lyzing Doppler echocardiographically derived tricuspid regurgitation signals and that this informatio

178 lyzing Doppler echocardiographically derived tricuspid regurgitation signals during respiration in re

179 ulmonary hypertension or moderate or greater tricuspid regurgitation (stage 3), and significant right

180 Secondary tricuspid regurgitation (STR) in heart failure with pres

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

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

183 ctively (p < 0.0001); mean percent change in tricuspid regurgitation time velocity integral was 27% +

184 ound In patients with significant functional tricuspid regurgitation, timely detection of right ventr

185 olic dimension and volume index, >= moderate tricuspid regurgitation (TR) (7%, 35%, and 53%, respecti

186 12.5%, persistent or new moderate or severe tricuspid regurgitation (TR) 20.8%, and new atrial fibri

187 ation of mechanisms of recurrent or residual tricuspid regurgitation (TR) after annuloplasty is neces

188 udy was to examine mortality associated with tricuspid regurgitation (TR) after controlling for left

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

190 We compared the predictive ability of tricuspid regurgitation (TR) and end-diastolic pulmonary

191 atheter edge-to-edge repair (T-TEER) reduced tricuspid regurgitation (TR) and improved health status

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

193 association between periprocedural change in tricuspid regurgitation (TR) and outcomes in patients un

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

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

196 Incidence and types of secondary tricuspid regurgitation (TR) are not well defined in atr

197 A new grading of tricuspid regurgitation (TR) beyond severe has been prop

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

199 Benefit of tricuspid regurgitation (TR) correction and timing of in

200 and EDT lengthened (by 43 ms and 46 ms), and tricuspid regurgitation (TR) decreased (by 26 mm Hg, p <

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

202 Severe tricuspid regurgitation (TR) exhibits high 1-year morbid

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

204 y, management, and outcomes of patients with tricuspid regurgitation (TR) has grown in the wake of mu

205 theter edge-to-edge repair (TEER) for severe tricuspid regurgitation (TR) has shown promise as an alt

206 The determinants of tricuspid regurgitation (TR) hemodynamic severity remain

207 Patients with isolated tricuspid regurgitation (TR) in the absence of left-side

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

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

210 Tricuspid regurgitation (TR) is an important predictor o

211 In hypoplastic left heart syndrome, tricuspid regurgitation (TR) is associated with circulat

212 Surgical management of isolated tricuspid regurgitation (TR) is associated with high mor

213 Severe tricuspid regurgitation (TR) is associated with high mor

214 Tricuspid regurgitation (TR) is common among adults with

215 Functional tricuspid regurgitation (TR) is increasingly recognized

216 implantable electronic device (CIED)-related tricuspid regurgitation (TR) is increasingly recognized

217 Severe tricuspid regurgitation (TR) is known to be associated w

218 Severe tricuspid regurgitation (TR) is known to be associated w

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

220 Accurate assessment of tricuspid regurgitation (TR) is necessary for identifica

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

222 o 8.4, p < 0.001), even after adjustment for tricuspid regurgitation (TR) jet velocity.

223 ed for only 10% to 20% of the variability in tricuspid regurgitation (TR) jet velocity.

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

225 The presence of tricuspid regurgitation (TR) may affect prognosis in pat

226 Tricuspid regurgitation (TR) occurs mainly from tricuspi

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

228 Severe tricuspid regurgitation (TR) often causes substantial im

229 The impact of tricuspid regurgitation (TR) on cardiac remodeling has n

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

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

232 Isolated tricuspid regurgitation (TR) remains a management dilemm

233 atification in aortic (AR), mitral (MR), and tricuspid regurgitation (TR) remains a significant clini

234 sided cardiac lesions, associated functional tricuspid regurgitation (TR) that was surgically ignored

235 c magnetic resonance (CMR) quantification of tricuspid regurgitation (TR) to identify high-risk patie

236 clinical benefits for patients with >=severe tricuspid regurgitation (TR) treated with the EVOQUE tra

237 ct of sexuality in patients with significant tricuspid regurgitation (TR) undergoing transcatheter tr

238 Functional tricuspid regurgitation (TR) with a structurally normal

239 ught to evaluate the effect of PTE on severe tricuspid regurgitation (TR) without tricuspid annulopla

240 Respiratory dependence of tricuspid regurgitation (TR), a long-held concept sugges

241 on (PR), 71 with multivalve disease, 73 with tricuspid regurgitation (TR), and 40 with aortic regurgi

242 rVHDs), including mitral regurgitation (MR), tricuspid regurgitation (TR), and aortic regurgitation (

243 milar to risk factors for the progression of tricuspid regurgitation (TR), and both conditions freque

244 een shown to be highly effective in reducing tricuspid regurgitation (TR), and interest in this thera

245 For patients with symptomatic, severe tricuspid regurgitation (TR), early results of transcath

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

247 ients with significant (moderate and severe) tricuspid regurgitation (TR), the decision to intervene

248 ) annuloplasty is recommended for functional tricuspid regurgitation (TR), which is caused by TV annu

249 thy subjects and in patients with functional tricuspid regurgitation (TR).

250 derate, and 69 severe PR; 55 had significant tricuspid regurgitation (TR).

251 h inadequate continuous wave (CW) signals of tricuspid regurgitation (TR).

252 ing color Doppler as an index of severity of tricuspid regurgitation (TR).

253 clinical implications of TVP with regard to tricuspid regurgitation (TR).

254 e primary endpoint and in-hospital worsening tricuspid regurgitation (TR).

255 ed, controlled study of patients with severe tricuspid regurgitation (TR).

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

257 94; 95% CI, 0.89-0.99; P=0.027), and </=mild tricuspid regurgitation (TR; HR, 3.58; 95% CI, 2.04-6.30

258 For patients with severe tricuspid regurgitation, transcatheter tricuspid-valve r

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

260 Correction of tricuspid regurgitation using tricuspid transcatheter ed

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

262 ion mediated 19%-35%), E/e' ratio (18%-29%), tricuspid regurgitation velocity (27%-41%), and tricuspi

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

264 .0001), LV lateral E/e' ratio (P=0.014), and tricuspid regurgitation velocity (P=0.019) were independ

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

266 pants underwent echocardiography; those with tricuspid regurgitation velocity 2.5 m/s proceeded to ri

267 F were independently associated with higher tricuspid regurgitation velocity after adjustment for de

268 ystolic pressure (PASP) was derived from the tricuspid regurgitation velocity and PH defined as PASP

269 molysis (P < or = .002) but no difference in tricuspid regurgitation velocity compared with those not

270 Mean (+/- SD) percent change in maximal tricuspid regurgitation velocity was 13% +/- 6% and -8%

271 abnormal parameters (medial e', medial E/e', tricuspid regurgitation velocity, and left atrial volume

272 Tricuspid regurgitation velocity, which reflects systoli

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

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

275 e independently associated with an increased tricuspid regurgitation velocity.

276 PASP was measured from the tricuspid regurgitation velocity.

277 increased mitral E velocity, E/e' ratio, and tricuspid regurgitation velocity; and worse right ventri

278 icular tachycardia and sudden death, whereas tricuspid regurgitation was for those with atrial flutte

279 Massive or torrential tricuspid regurgitation was found in 6.8% of patients in

280 During surgery, severe tricuspid regurgitation was found to be caused by the PP

281 Tricuspid regurgitation was graded using a five-class gr

282 ome, higher FTR degree compared with trivial tricuspid regurgitation was independently associated wit

283 The 2-year prevalence of progression of tricuspid regurgitation was lower in the surgery-plus-TA

284 Tricuspid regurgitation was massive (46 mL) (Figs 1-4).

285 Moderate or less tricuspid regurgitation was present in 84% at 2 years in

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

287 Analysis of right ventricular adaptation to tricuspid regurgitation was studied in 10 heart transpla

288 cular enlargement, systolic dysfunction, and tricuspid regurgitation were all associated with the pri

289 ars; 67% female) with severe or higher grade tricuspid regurgitation were analyzed.

290 s [62-78 years]) with significant functional tricuspid regurgitation were divided according to the pr

291 Patients with symptomatic severe tricuspid regurgitation were enrolled at 65 centers in t

292 id valve edge-to-edge repair for significant tricuspid regurgitation were included.

293 tal of 572 patients with severe, symptomatic tricuspid regurgitation were randomized to either tricus

294 out CP (restrictive cardiomyopathy or severe tricuspid regurgitation) were identified.

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

296 ation; inclusions bias related to detectable tricuspid regurgitation, which may limit generalizabilit

297 ht ventricular systolic function and greater tricuspid regurgitation, which persisted at 1 year.

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

299 , abnormal septal curvature, and significant tricuspid regurgitation with a high regurgitant velocity

300 (A-STR) is a distinct phenotype of secondary tricuspid regurgitation with predominant dilation of the