ライフサイエンスコーパス: right ventricular

1 in comparison with zero patients undergoing right ventricular ablation (P=0.04).

2 red with a control group of those undergoing right ventricular ablation only.

3 ventricular tachycardia, n=2; PVC, n=10) and right ventricular ablation was performed exclusively in

4 data from various epicardial and endocardial right ventricular activation mapping procedures in 6 BrS

5 p = 0.023) as well as parameters reflecting right ventricular afterload (diastolic pulmonary artery

6 e respiratory distress syndrome treatment on right ventricular afterload and outcome.

7 pling between right ventricular function and right ventricular afterload.

8 ty for ventricular tachycardia on programmed right ventricular and burst stimulation and spontaneousl

9 prognostic significance of left ventricular, right ventricular, and LA strain measures was assessed b

10 Of the left ventricular, right ventricular, and LA strain measures, LA reservoir

11 ny and improves cardiac function relative to right ventricular apex (RVA) pacing in animals.

12 Standard right ventricular apex+LV and LV-only pacing enhanced sy

13 In comparison with the AAI, right ventricular apex+LV and LV-only pacing resulted in

14 ematically assessed: standard biventricular (right ventricular apex+LV), LV-only, HIS, simultaneous H

15 eads were placed in the right atrium, at the right ventricular apex, and in a coronary vein.

16 Pacing leads were placed into the right ventricular apex/outflow tract through a subclavia

17 electrogram at the initiation of continuous right ventricular apical pacing during tachycardia effec

18 reimplant risk factors associated with early right ventricular assist device (RVAD) use in patients u

19 is (59% left ventricular assist devices, 23% right ventricular assist devices, 18% biventricular assi

20 entricular volumes (LV: beta=0.26, P<0.0001; right ventricular: beta=0.26, P<0.0001).

21 atrial capture threshold (4%), increases in right ventricular capture threshold (4%), and increases

22 Our data demonstrated that right ventricular cardiac myocytes exhibited reduced cel

23 nd cellular electrophysiology in left versus right ventricular cardiac myocytes.

24 ventricular tachycardia (4%), arrhythmogenic right ventricular cardiomyopathy (4%), and Brugada syndr

25 nd/or fibrosis (n = 59, 16%); arrhythmogenic right ventricular cardiomyopathy (ARVC) (13%); and hyper

26 Although overlap with arrhythmogenic right ventricular cardiomyopathy (ARVC) has been suggest

27 Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetically

28 Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a leading cau

29 Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a significant

30 Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited

31 e overt structural disease in arrhythmogenic right ventricular cardiomyopathy (ARVC).

32 cardiomyopathy, specifically arrhythmogenic right ventricular cardiomyopathy (ARVC).

33 a (rTFC) for the diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC).

34 s to screen 315 patients with arrhythmogenic right ventricular cardiomyopathy (n = 111), DCM (n = 95)

35 brillator (ICD) in males with arrhythmogenic right ventricular cardiomyopathy caused by a p.S358L mut

36 thesis of an exercise-induced arrhythmogenic right ventricular cardiomyopathy has to be questioned.

37 ntricular tachycardia (VT) in arrhythmogenic right ventricular cardiomyopathy improves short-term VT-

38 In diagnosed channelopathy or arrhythmogenic right ventricular cardiomyopathy index cases, 44 patient

39 I substrate ablation of VT in arrhythmogenic right ventricular cardiomyopathy is good.

40 thies occur infrequently; and arrhythmogenic right ventricular cardiomyopathy is rare.

41 primary electric syndrome or arrhythmogenic right ventricular cardiomyopathy were analyzed.

42 3; short QT syndrome, 1; and arrhythmogenic right ventricular cardiomyopathy, 23).

43 Long-QT, arrhythmogenic right ventricular cardiomyopathy, and catecholaminergic

44 In patients with arrhythmogenic right ventricular cardiomyopathy, those demonstrating an

45 n in alphaT-catenin linked to arrhythmogenic right ventricular cardiomyopathy, V94D, promotes homodim

46 ic cardiomyopathy and none to arrhythmogenic right ventricular cardiomyopathy.

47 rt failure (HF) prevalence in arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) vari

48 ed in patients with inherited arrhythmogenic right ventricular cardiomyopathy/dysplasia, although the

49 hypothesis of the crucial role of intrinsic right ventricular conduction in optimal cardiac resynchr

50 ed on echocardiography, and 40% reduction in right ventricular contractile function in isolated perfu

51 thesia resulted in a significant decrease in right ventricular contractility (DeltaESV25: +25.5 mL, P

52 Thoracic epidural anesthesia impairs right ventricular contractility but does not inhibit the

53 In response, right ventricular contractility increased (DeltaESV25: -

54 Based on our results, chronic right ventricular damage in elite endurance master athle

55 RA and right ventricular deformation indices were obtained usin

56 Primary endpoint was the right ventricular diameter at the third rhythm analysis.

57 ltrasonographic images were obtained and the right ventricular diameter was measured.

58 d conduit functions is related to changes in right ventricular diastolic dysfunction.

59 ion (adjusted odds ratio 2.2; P<0.0001), and right ventricular dilatation (adjusted odds ratio 2.2; P

60 centric left ventricular remodeling, greater right ventricular dilatation (base, 34+/-7 versus 31+/-6

61 These findings challenge the paradigm that right ventricular dilatation on ultrasound during cardio

62 g left ventricular dilatation and 20% having right ventricular dilatation.

63 Right atrial and right ventricular dimensions correlated with WHO-FC and

64 esulting in acute pulmonary hypertension and right ventricular distension.

65 osis and 1 with pulmonary regurgitation), or right ventricular dysfunction (n=2).

66 n of LGE (14+/-11 versus 5+/-5%, P<0.01) and right ventricular dysfunction (right ventricular EF 45+/

67 Right ventricular dysfunction and congestive states may

68 y was to further explore the significance of right ventricular dysfunction and investigate potential

69 icular diameter ratio on CT as indicators of right ventricular dysfunction and reported that recurren

70 Increased LGE burden and right ventricular dysfunction can identify LGE+ patients

71 goal-directed echocardiography in diagnosing right ventricular dysfunction in acute pulmonary embolis

72 intensivists' interpretations for evaluating right ventricular dysfunction in acute pulmonary embolis

73 The REDEFINE trial (Right Ventricular Dysfunction in Tetralogy of Fallot: In

74 In patients with pulmonary embolism, right ventricular dysfunction is associated with early m

75 pulmonary embolism using imaging presence of right ventricular dysfunction is essential for triage; h

76 ort class, use of multiple inotropes, severe right ventricular dysfunction on echocardiography, ratio

77 increased pulmonary vascular resistance, and right ventricular dysfunction that promotes heart failur

78 Screening for right ventricular dysfunction using goal-directed echoca

79 versus 61+/-7 and 61+/-7 mm, P<0.0001), more right ventricular dysfunction, increased epicardial fat

80 pulmonary arterial pressure and resistance, right ventricular dysfunction, left ventricular compress

81 slightly higher in patients with HF-PH with right ventricular dysfunction, pulmonary vascular remode

82 ents with pulmonary embolism and evidence of right ventricular dysfunction.

83 n were compared in patients with and without right ventricular dysfunction.

84 in most), and only 5.1% of patients had mild right ventricular dysfunction.

85 the pulmonary microvasculature culminated in right ventricular dysfunction.

86 ion was 31%, and 60% had moderate or greater right ventricular dysfunction.

87 racterized diseases including arrhythmogenic right ventricular dysplasia 3.

88 ibed the arrhythmic course of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C).

89 , P<0.01) and right ventricular dysfunction (right ventricular EF 45+/-12 versus 53+/-28%, P=0.04).

90 RV dysfunction was defined as right ventricular ejection fraction </=45%.

91 distensibility was associated with change in right ventricular ejection fraction (RVEF, rho=0.39, P<0

92 Both right ventricular ejection fraction and left ventricular

93 Right ventricular ejection fraction did not differ betwe

94 xamined the incremental value of considering right ventricular ejection fraction for the prediction o

95 action was 32+/-12% (range, 6-54%) with mean right ventricular ejection fraction of 48+/-15% (range,

96 Right ventricular ejection fraction was an independent p

97 olume increased by 4.87 ml/m(2) (P = 0.003); right ventricular ejection fraction was unchanged.

98 ncreased risk of mortality (lowest quartile: right ventricular ejection fraction, <40%; hazard ratio,

99 wer pulmonary arterial compliance, depressed right ventricular ejection fraction, and shorter life ex

100 entricular ejection fraction, and especially right ventricular ejection fraction-associated with prog

101 of late gadolinium enhancement, and left and right ventricular ejection fractions.

102 n) underwent combined endocardial-epicardial right ventricular electroanatomical mapping and ablation

103 Right ventricular end diastolic volume increased by 49.4

104 body mass index was associated with greater right ventricular end-diastolic area and worse right ven

105 ed left ventricular end-diastolic volume and right ventricular end-diastolic volume (left ventricular

106 h a concomitant small stable increase in the right ventricular end-diastolic volume index (P<0.001).

107 P < 0.001) increase in change from baseline right ventricular end-diastolic volume index and a 429 m

108 Primary outcome was change from baseline in right ventricular end-diastolic volume index versus plac

109 pared with published normal values, left and right ventricular end-diastolic volume z scores were mil

110 area, 104+/-13 and 69+/-18 mL/m(2); P<0.001; right ventricular end-diastolic volume/body surface area

111 correlated with the right atrial volume than right ventricular end-systolic volume in AF-TR (P<0.001)

112 ependent MRI predictors of death (P < 0.01): right ventricular end-systolic volume index adjusted for

113 an be successfully salvaged with fenestrated right ventricular exclusion and systemic to pulmonary sh

114 Three patients underwent nonfenestrated right ventricular exclusion, 2 (67%) of whom died.

115 ectively, whereas for those with fenestrated right ventricular exclusion, survival at 1, 5, and 10 ye

116 erioperative period were not attributable to right ventricular failure (chronic thromboembolic pulmon

117 pulmonary perfusion, ultimately resulting in right ventricular failure and dilation.

118 of RA size and pressure, and likely reflect right ventricular failure and overload.

119 ermine if patient survival and mechanisms of right ventricular failure in pulmonary hypertension coul

120 d, TR can progress and result in progressive right ventricular failure.

121 swings (obliteration during inspiration) in right ventricular filling and pulmonary perfusion, ultim

122 ght ventricular end-diastolic area and worse right ventricular fractional area change (P</=0.001).

123 oth global left ventricular longitudinal and right ventricular free wall longitudinal strain via an i

124 Global left ventricular longitudinal and right ventricular free wall longitudinal strain were cal

125 ent of left ventricular longitudinal strain, right ventricular free wall strain, and LA booster, cond

126 tricular size (94% versus 80%; P=0.001), and right ventricular function (87% versus 73%; P=0.006).

127 hazard ratio: 1.655; p < 0.001) and impaired right ventricular function (hazard ratio: 2.360; p = 0.0

128 was an independent predictor of recovery of right ventricular function (p=0.02).

129 f MBG were associated with measures of worse right ventricular function (RV s', r=-0.39, P<0.0001) an

130 s by thoracic epidural anesthesia may affect right ventricular function and interfere with the coupli

131 In 10 patients scheduled for lung resection, right ventricular function and its response to increased

132 Parameters of left and right ventricular function and LGE burden were measured

133 tion and interfere with the coupling between right ventricular function and right ventricular afterlo

134 e effects of thoracic epidural anesthesia on right ventricular function and ventricular-pulmonary cou

135 3) developing standard methods for assessing right ventricular function and, hopefully, its coupling

136 unction at discharge and 1 month with normal right ventricular function at 1 year.

137 ignificantly compromise left ventricular and right ventricular function through different mechanisms

138 proved right ventricular systolic pressures, right ventricular function, and survival.

139 he provision of volumes, diastolic function, right ventricular function, hemodynamics, and valvular r

140 proving pulmonary hemodynamic parameters and right ventricular function.

141 ncountered, its severity, and its effects on right ventricular function.

142 hy, measuring annulus diameter and valve and right ventricular function.

143 d pulmonary arterial compliance, and reduced right ventricular function.

144 city, biomarkers, invasive hemodynamics, and right ventricular functional indices, and (3) evaluate t

145 Anatomic and right ventricular-functional variables were obtained by

146 AH, Egln1(Tie2) mice exhibited unprecedented right ventricular hypertrophy and failure and progressiv

147 n of right ventricular systolic pressure and right ventricular hypertrophy and pulmonary vascular rem

148 ry resistance, functional residual capacity, right ventricular hypertrophy index, and total cell coun

149 ization of peripheral pulmonary arteries and right ventricular hypertrophy.

150 ed with raised pulmonary artery pressure and right ventricular hypertrophy.

151 ressures, pulmonary vascular remodeling, and right ventricular hypertrophy.

152 PE + SU produced right ventricular hypokinesis, dilation, and hypertrophy

153 nscript, abolished Hand2 expression, causing right ventricular hypoplasia and embryonic lethality in

154 astic left heart syndrome and related single right ventricular lesions has drastically improved the o

155 % subendocardial, 71% transmural), including right ventricular LGE (96%).

156 Pulmonary arterial compliance and right ventricular load improve over time in acute respir

157 ith nonsurvivors, suggesting improvements in right ventricular load.

158 Despite the fact that assessment of right ventricular longitudinal strain (RVLS) carries imp

159 strain, strain rates, emptying fraction, and right ventricular longitudinal strain were measured.

160 e of adverse events than left ventricular or right ventricular longitudinal strain.

161 Indexed left ventricular mass and right ventricular mass (left ventricular mass/body surfa

162 Right ventricular mass and function also improved.

163 e area, 96+/-13 and 62+/-10 g/m(2); P<0.001; right ventricular mass/body surface area, 36+/-7 and 24+

164 used to create a three-dimensional model of right ventricular motion.

165 le overestimation resulted from inclusion of right ventricular myocardium (n=37; 38.1%), LV trabecula

166 ss of myocytes and fibrofatty replacement of right ventricular myocardium; biventricular involvement

167 t comorbidity in patients with postoperative right ventricular outflow tract (RVOT) obstruction or pu

168 There was no difference in E12 in the right ventricular outflow tract compared with the right-

169 Surgical right ventricular outflow tract cryoablation was perform

170 A conduit prestent and lower discharge right ventricular outflow tract gradient were associated

171 ars restricted to the anterior subepicardial right ventricular outflow tract in 11 patients (group B)

172 abnormal electric activity in the epicardial right ventricular outflow tract may be beneficial in pat

173 increase in the risk of Ebstein's anomaly (a right ventricular outflow tract obstruction defect) in i

174 The prevalence of right ventricular outflow tract obstruction defects was

175 persion of repolarization are present in the right ventricular outflow tract of BrS patients.

176 activity were then evaluated in response to right ventricular outflow tract PVCs with fixed short, f

177 ngenital heart defects in children requiring right ventricular outflow tract reconstruction typically

178 ocytes, as well as conduction slowing in the right ventricular outflow tract region.

179 (range, 0.4-7 years), 32 patients underwent right ventricular outflow tract reintervention for obstr

180 clinical entity of an isolated subepicardial right ventricular outflow tract scar serving as a substr

181 ith risk factors for early primary repair by right ventricular outflow tract stenting (stent).

182 Right ventricular outflow tract stenting of symptomatic

183 of a significant delay in the anterolateral right ventricular outflow tract.

184 gical pulmonary valve replacement in dilated right ventricular outflow tracts, permitting lower risk,

185 Right ventricular pacing (RVP) increases risk of atrial

186 high risk of developing HF in the setting of right ventricular pacing and to determine whether these

187 Although right ventricular pacing can contribute to cardiomyopath

188 (Biventricular Versus Right Ventricular Pacing in Heart Failure Patients With

189 The BLOCK HF (Biventricular Versus Right Ventricular Pacing in Heart Failure Patients With

190 The Biventricular versus Right Ventricular Pacing in Heart Failure Patients with

191 and thus presumed to have a higher burden of right ventricular pacing, experienced an increased risk

192 h current leadless pacemakers are limited to right ventricular pacing, future advanced, communicating

193 ejection fraction </=50% to biventricular or right ventricular pacing.

194 Three devices (0.3%) were replaced for right ventricular pacing.

195 endurance training has been associated with right ventricular pathological remodeling and ventricula

196 F) and serves as an important determinant of right ventricular performance and exercise capacity.

197 Left ventricular PGD, right ventricular PGD, or both, were observed in 99 pati

198 ning arrhythmogenic cardiomyopathy, often of right ventricular predominance.

199 de B is up-regulated in both ventricles with right ventricular preference.

200 ame amount of particulate intake, changes in right ventricular pressure and intimal thickening of pul

201 /kg), pulmonary vascular obstruction induced right ventricular pressure increase and dilatation, but

202 ease in PA diameter; and 2) 25% reduction in right ventricular pressure or 50% decrease in PA gradien

203 ventricular circulation: 1) 20% reduction in right ventricular pressure or 50% increase in PA diamete

204 from Schistosoma-induced PH, with decreased right ventricular pressures, pulmonary vascular remodeli

205 as not responsible for observed increases in right ventricular pressures.

206 Future studies should assess the impact of right ventricular protective acute respiratory distress

207 Right ventricular-pulmonary arterial coupling was decrea

208 rofiling could identify plasma signatures of right ventricular-pulmonary vascular (RV-PV) dysfunction

209 Right ventricular-pulmonary vascular coupling was worse

210 We performed left ventricular (LV) and right ventricular quantitative analysis and late gadolin

211 ilatation and leaflet tethering from adverse right ventricular remodelling in response to any of seve

212 Right ventricular (RV) and left ventricular (LV) functio

213 nce (CMR) imaging is recommended to quantify right ventricular (RV) and left ventricular (LV) functio

214 ly measurable, differential associations for right ventricular (RV) and left ventricular (LV) mass ma

215 Sustained right ventricular (RV) apical pacing may lead to deterio

216 Beginning with atrial synchronous right ventricular (RV) apical pacing, the search has con

217 ith an impaired rest-to-exercise response in right ventricular (RV) contractility.

218 Right ventricular (RV) dysfunction (RVD) is a poor progn

219 Tricuspid regurgitation (TR) and right ventricular (RV) dysfunction adversely affect outc

220 Pulmonary hypertension and associated right ventricular (RV) dysfunction are important determi

221 Pulmonary hypertension (PH) and right ventricular (RV) dysfunction are strong predictors

222 nation may contribute to long-term pulmonary right ventricular (RV) dysfunction in patients after sur

223 cebo in normotensive patients with acute PE, right ventricular (RV) dysfunction on imaging, and a pos

224 iated stiffness in rats with mild and severe right ventricular (RV) dysfunction.

225 ed with pulmonary disease, which can lead to right ventricular (RV) dysfunction.

226 (MR) imaging in patients with arrhythmogenic right ventricular (RV) dysplasia/cardiomyopathy (ARVD/C)

227 s, aged 13.0+/-2.9 years, had higher indexed right ventricular (RV) end-diastolic (range 85-326 mL/m(

228 e evaluated and those with PA:A>1 had higher right ventricular (RV) end-diastolic and end-systolic vo

229 Right ventricular (RV) end-systolic dimensions provide i

230 The mechanisms of right ventricular (RV) failure in pulmonary arterial hyp

231 Right ventricular (RV) failure remains a major cause of

232 in increased pulmonary vascular resistance, right ventricular (RV) failure, and premature death.

233 We report right ventricular (RV) filling and ejection abnormalitie

234 ss, the relationship between CMR findings of right ventricular (RV) function and outcomes after trans

235 ionship between parasympathetic activity and right ventricular (RV) function in patients with PAH, an

236 Although it is known that right ventricular (RV) function is dependent on LV healt

237 ffect of angiotensin II receptor blockers on right ventricular (RV) function is still unknown.

238 Right ventricular (RV) functional reserve affects functi

239 Right ventricular (RV) impairment is postulated to be re

240 ), symptomatic pulmonary embolism (PE) (1C), right ventricular (RV) infarct (1C), the efficacy of flu

241 een pulmonary artery (PA) stiffness and both right ventricular (RV) mass and function with cardiac ma

242 Right ventricular (RV) morphology has been associated wi

243 is an established therapy for dysfunctional right ventricular (RV) outflow tract conduits.

244 or the congenital heart disease patient with right ventricular (RV) outflow tract dysfunction.

245 hogenetic protein receptor 2 (BMPR2) gene on right ventricular (RV) pressure overload in patients wit

246 Adverse right ventricular (RV) remodeling has significant progno

247 We hypothesized that baseline right ventricular (RV) size and function are associated

248 Right ventricular (RV) size and systolic function betwee

249 confidence interval [CI]: 1.20 to 1.83) and right ventricular (RV) systolic dysfunction (HR: 1.68; C

250 Indexed left ventricular (LV) and right ventricular (RV) volume (LV, 77.1+/-8.5-83.9+/-8.6

251 y of Fallot provides symptomatic benefit and right ventricular (RV) volume reduction.

252 ues and to identify the main determinants of right ventricular (RV) volumes and systolic function usi

253 inded quantification of left ventricular and right ventricular (RV) volumes was performed from standa

254 For identification of epicardial right ventricular scar, an endocardial UV cutoff value o

255 ar electroanatomical mapping and ablation of right ventricular scar-related ventricular tachycardia w

256 e of septal intramural circuits or extensive right ventricular scarring.

257 vian vein and, after positioning against the right ventricular septum (RVS) using a preshaped guiding

258 These leadless devices are self-contained right ventricular single-chamber pacemakers implanted by

259 ventricular size (96% versus 83%; P<0.001), right ventricular size (94% versus 80%; P=0.001), and ri

260 ted echocardiogram as normal or abnormal for right ventricular size and function in patients with acu

261 ventricular strain, left atrial strain, and right ventricular strain) are also discussed.

262 In post hoc analysis, right ventricular stroke volume increased by 4.87 ml/m(2

263 pnea, paroxysmal nocturnal dyspnea, left and right ventricular structure and function, natriuretic pe

264 MRI measurements reflecting right ventricular structure and stiffness of the proxima

265 tion and to analyze their clinical value for right ventricular substrate delineation.

266 nstrated leftward septal shift and prolonged right ventricular systole, both known to affect LV diast

267 namics, leftward septal shift, and prolonged right ventricular systole.

268 namics, leftward septal shift, and prolonged right ventricular systole.

269 verity, leftward septal shift, and prolonged right ventricular systole.

270 PE was not associated with overt left or right ventricular systolic dysfunction (ejection fractio

271 SAVR patients experienced significant right ventricular systolic dysfunction at discharge and

272 g, more paravalvular regurgitation, and less right ventricular systolic dysfunction compared with SAV

273 t ventricular (LV) hypertrophy, worse LV and right ventricular systolic function, and worse LV diasto

274 s score (hazard ratio 1.55), higher baseline right ventricular systolic pressure (hazard ratio 1.11),

275 The rise in right ventricular systolic pressure (RVSP) normally obse

276 ndexed LV end-systolic diameter (LVESD), and right ventricular systolic pressure (RVSP) were 62 +/- 2

277 itral effective regurgitant orifice, resting right ventricular systolic pressure (RVSP), exercise met

278 asurements indicated modest increases in the right ventricular systolic pressure and right ventricle

279 atment significantly attenuated elevation of right ventricular systolic pressure and right ventricula

280 of echocardiogram data, pHTN was defined as right ventricular systolic pressure greater than or equa

281 Society of Thoracic Surgeons score and right ventricular systolic pressure were 2+/-3 and 15+/-

282 The Society of Thoracic Surgeons score and right ventricular systolic pressure were 3.3+/-3 and 31+

283 rifice, indexed LV end-diastolic volume, and right ventricular systolic pressure were 4+/-1%, 62+/-3%

284 n fraction, mean aortic valve gradients, and right ventricular systolic pressure were 7+/-6, 58+/-6%,

285 ypertension ( approximately 118% increase in right ventricular systolic pressure) but not polycythemi

286 iety of Thoracic Surgeons score and baseline right ventricular systolic pressure) provided incrementa

287 s score, degree of aortic regurgitation, and right ventricular systolic pressure) was 0.64 (95% confi

288 emia, medications, aortic regurgitation, and right ventricular systolic pressure), increased the c-st

289 ia-treated rats with established PH improved right ventricular systolic pressures, right ventricular

290 UBc-LacZ; n=12), followed by 3 to 4 weeks of right ventricular tachypacing (240 bpm).

291 PR, but it is unknown whether relief of the right ventricular volume and/or pressure overload by TPV

292 pulmonary regurgitant fraction, facilitates right ventricular volume improvements, and preserves biv

293 e disease, when progressive dilation begins, right ventricular volume is the essential parameter to m

294 ss (beta=0.23; P<0.0001) and elevated LV and right ventricular volumes (LV: beta=0.26, P<0.0001; righ

295 elations were found for left ventricular and right ventricular volumes and ejection fraction with N-t

296 s, patients with PH had a 2-fold increase in right ventricular volumes, 62% increase in annular area,

297 ndergoing catheter ablation for scar-related right ventricular VT, 2 distinct scar distributions were

298 atria, and in discrete puncta throughout the right ventricular wall and septum, as well.

299 tial distributions for anterior and inferior right ventricular walls were 3.4% and 4.5%, respectively

300 aximally involved, whereas inferolateral and right ventricular were usually spared.