ライフサイエンスコーパス: tricuspid regurgitation

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

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

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

4 RV compression did not induce or exacerbate tricuspid regurgitation.

5 nscatheter tricuspid valve repair for severe tricuspid regurgitation.

6 ificantly associated with mortality, but not tricuspid regurgitation.

7 om restrictive myocardial disease and severe tricuspid regurgitation.

8 om restrictive myocardial disease and severe tricuspid regurgitation.

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

10 ading to further annular dilatation and more tricuspid regurgitation.

11 on because of progressive RV dysfunction and tricuspid regurgitation.

12 rwent tricuspid valve replacement for severe tricuspid regurgitation.

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

14 60% vs. 4%, p < 0.0001), moderate or greater tricuspid regurgitation (4% vs. 0%, p = 0.06), and aorti

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

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

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

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

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

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

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

22 Tricuspid regurgitation and RV function did not change b

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

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

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

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

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

28 RV failure and tricuspid regurgitation are common.

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

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

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

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

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

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

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

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

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

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

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

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

41 Changes observed in tricuspid regurgitation Doppler echocardiographic variab

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

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

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

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

46 Functional tricuspid regurgitation (FTR) with structurally normal v

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

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

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

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

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

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

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

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

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

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

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

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

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

60 Tricuspid regurgitation is a frequent echocardiographic

61 Second, functional tricuspid regurgitation is a progressive disorder charac

62 Severe tricuspid regurgitation is associated with poor prognosi

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

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

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

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

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

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

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

70 Progressive tricuspid regurgitation occurs with age and is associate

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

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

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

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

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

76 Tricuspid regurgitation preceded third-degree block in 1

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

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

79 The tricuspid regurgitation resulting from this disease has

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

81 Tricuspid regurgitation severity was the most important

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 Tricuspid regurgitation (TR) is an important predictor o

103 Functional tricuspid regurgitation (TR) is increasingly recognized

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

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

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

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

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

109 Tricuspid regurgitation (TR) occurs mainly from tricuspi

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

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

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

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

114 Functional tricuspid regurgitation (TR) with a structurally normal

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

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

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

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

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

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

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

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

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

124 94; 95% CI, 0.89-0.99; P=0.027), and </=mild tricuspid regurgitation (TR; HR, 3.58; 95% CI, 2.04-6.30

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

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

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

128 .0001), LV lateral E/e' ratio (P=0.014), and tricuspid regurgitation velocity (P=0.019) were independ

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

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

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

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

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

134 Tricuspid regurgitation velocity, which reflects systoli

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

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

137 e independently associated with an increased tricuspid regurgitation velocity.

138 PASP was measured from the tricuspid regurgitation velocity.

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

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

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

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

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

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

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