ライフサイエンスコーパス: pulmonary artery

1 had occlusion of hTPV with aneurysm of main pulmonary artery.

2 permanent MEMS-based pressure sensor in the pulmonary artery.

3 tional phase-contrast MR imaging of the main pulmonary artery.

4 and sex, and the relative area change of the pulmonary artery.

5 lly between the subclavian artery and either pulmonary artery.

6 s an obstructive disease of the precapillary pulmonary arteries.

7 -regulated in the endothelium of distal iPAH pulmonary arteries.

8 l distribution of nerves around the proximal pulmonary arteries.

9 perpolarization in mitochondria from IDD rat pulmonary arteries.

10 lated immunity and adverse remodeling in the pulmonary arteries.

11 the mean flows+/-2 SD were as follows: main pulmonary artery, 56 (44, 68); ascending aorta, 41 (29,

12 7, 30%), and abnormal branching of the right pulmonary artery (ABRPA) (14/47, 30%) were most commonly

13 Pulsed-wave Doppler determination of the pulmonary artery acceleration time (PAAT) as a surrogate

14 ect link between a structural abnormality of pulmonary arteries and a response to targeted treatment

15 Image quality of pulmonary arteries and lung parenchyma was scored on a f

16 The apparent signal-to-noise ratio in pulmonary arteries and lung parenchyma was significantly

17 Histologically, lungs showed ectatic pulmonary arteries and pulmonary veins.

18 with abnormal muscularization of peripheral pulmonary arteries and right ventricular hypertrophy.

19 veloping heart septates into the base of the pulmonary artery and aorta to guide deoxygenated right v

20 y hypoxic mouse and rat lungs, as well as in pulmonary artery and pulmonary artery smooth muscle cell

21 This study tested the hypothesis that pulmonary artery and pulmonary artery wedge pressures ar

22 tetralogy of Fallot with poor anatomy (small pulmonary arteries) and adverse factors (multiple comorb

23 ed smooth muscle-specific apoptosis in small pulmonary arteries, and reversed hypoxia-induced pulmona

24 ac output and pressures in the right atrium, pulmonary artery, and pulmonary capillary wedge position

25 The diameters of the pulmonary artery, aorta, and right and left ventricles a

26 nts of the common carotid artery, aorta, and pulmonary artery appears to reflect a transition between

27 The donor aorta and pulmonary artery are anastomosed peripherally to the fem

28 receptor stimulation, as well as hypoxia in pulmonary artery, are shown to be dependent on both ROS

29 Considering the dilation of the pulmonary arteries as a paramount sign of PAH, we hypoth

30 eter z score, the right/left ventricular and pulmonary artery/ascending aorta diameter ratios were hi

31 89] versus 0.77 [95% CI, 0.75-0.8]; P=0.008] pulmonary arteries at the time of subsequent surgical re

32 ction, and to demonstrate denervation of the pulmonary artery at a histological level.

33 atrial switch operation) or 2-stage repairs (pulmonary artery band followed by arterial switch operat

34 control mice underwent the same stress using pulmonary artery banding (Low-PAB).

35 By performing pulmonary artery banding of different diameters for 7 we

36 rapy, tricuspid valve repair or replacement, pulmonary artery banding, and implantation of an assist

37 measured the PA:A ratio at the level of the pulmonary artery bifurcation on CT scans.

38 ct of the pulmonary arterial wall beyond the pulmonary artery bifurcation.

39 of the aortic arch in mice as well as human pulmonary artery branches.

40 ies have observed an increase in the rate of pulmonary artery catheter (PAC) use in heart failure adm

41 tent pulmonary artery thermodilution using a pulmonary artery catheter (PAC-CO) with regard to accura

42 ardiac output was measured simultaneously by pulmonary artery catheter and aortic transpulmonary ther

43 ivered into the right atrium via a multiport pulmonary artery catheter during continuous hemodynamic

44 atheter for blood pressure measurement and a pulmonary artery catheter for bolus thermodilution.

45 by transducing a peripheral intravenous and pulmonary artery catheter, respectively, after zeroing a

46 icenter population of HF patients undergoing pulmonary artery catheterization (PAC).

47 uation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE)

48 uation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness) trial we

49 uation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness], CHARM [

50 Pulmonary artery catheterization was performed before an

51 rs) were instrumented with radial artery and pulmonary artery catheters and performed moderate cycle

52 r to have similar accuracy as thermodilution pulmonary artery catheters.

53 zed by fibrothrombotic obstructions of large pulmonary arteries combined with small-vessel arteriopat

54 ially increased (up to 2-fold) in distal PAH pulmonary arteries compared with controls.

55 +/-3 versus -1+/-2 mm Hg; P=0.002), improved pulmonary artery compliance (+1.5+/-1.1 versus +0.6+/-0.

56 Recent studies have shown that pulmonary artery denervation improves pulmonary hemodyna

57 Pulmonary artery denervation offers the possibility of a

58 y, to determine the effect of radiofrequency pulmonary artery denervation on acute pulmonary hyperten

59 Pulmonary artery denervation resulted in reduced mean pu

60 Animals were assigned to either pulmonary artery denervation, using a prototype radiofre

61 th clinical-, Doppler echocardiography-, and pulmonary artery-derived hemodynamic variables and also

62 Patient-related variables included main pulmonary artery diameter (mPAD) at computed tomography

63 ater than or equal to 106 cm(3) (OR = 3.59), pulmonary artery diameter greater than or equal to 28 mm

64 eater than or equal to 28 mm (OR = 2.52) and pulmonary artery diameter to aorta diameter ratio of gre

65 een pulmonary artery enlargement (defined as pulmonary artery diameter to ascending aorta diameter [P

66 The CPI40, main pulmonary artery diameter to ascending aorta diameter ra

67 Conversely, the mean pulmonary artery diameter z score, the right/left ventri

68 modynamic monitor-derived baseline estimated pulmonary artery diastolic pressure (ePAD) and change fr

69 cultured human umbilical vein ECs and human pulmonary artery ECs, depletion of Galpha12 and soluble

70 estigated the mechanical properties of human pulmonary artery endothelial cells (ECs) using atomic fo

71 e was significantly elevated in PAH, both in pulmonary artery endothelial cells (P < 0.05) and periph

72 Exposing primary porcine pulmonary artery endothelial cells (PAECs) to VEGF for 1

73 lature in vivo and the functional effects on pulmonary artery endothelial cells (PAECs) undergoing En

74 n of PPARgamma target genes in primary human pulmonary artery endothelial cells (PAECs) was suppresse

75 eas current data support the notion that, in pulmonary artery endothelial cells (PAECs), expression o

76 rmine if elafin amplifies BMPR2 signaling in pulmonary artery endothelial cells and to elucidate the

77 Human pulmonary artery endothelial cells cultured with serum f

78 ated the metabolic abnormalities observed in pulmonary artery endothelial cells from patients with id

79 In normal and patient pulmonary artery endothelial cells, elafin promoted angi

80 of pulmonary artery smooth muscle cells and pulmonary artery endothelial cells, leading to pulmonary

81 al PAH, and decreased the migration of human pulmonary artery endothelial cells, providing the proof

82 were related to exaggerated proliferation of pulmonary artery endothelial cells, pulmonary artery smo

83 ed) pulmonary artery smooth muscle cells and pulmonary artery endothelial cells, we found that KCNK3

84 o analyses of human PAH and control cultured pulmonary artery endothelial cells.

85 y abnormal growth and enhanced glycolysis of pulmonary artery endothelial cells.

86 We aimed to assess the association between pulmonary artery enlargement (defined as pulmonary arter

87 Pulmonary artery enlargement is prevalent in adult patie

88 Pulmonary artery enlargement was associated with exacerb

89 At baseline, patients with pulmonary artery enlargement were younger than those wit

90 Doppler interrogation of pulmonary artery flow may provide an insight into the se

91 ure and flow sensors were placed at the main pulmonary artery for measuring pulmonary artery resistan

92 g right ventricle dysfunction or failure and pulmonary artery hypertension by using pressure or volum

93 transcription factor FRA2 was restricted to pulmonary artery hypertension.

94 ary arteries than in those with normal-sized pulmonary arteries in the validation cohort (hazard rati

95 Restoration of miRNA-96 expression in pulmonary arteries in vivo via administration of an miRN

96 essure and flow velocity measurements in the pulmonary artery in control subjects and patients with p

97 nsporter (5-HTT) play important roles in the pulmonary artery in pulmonary hypertension.

98 excess pressure analyses were applied in the pulmonary artery in subjects with and without pulmonary

99 acterized by severe remodeling of the distal pulmonary arteries, increased pulmonary vascular resista

100 ures performed were fenestration closure and pulmonary artery intervention.

101 mechanical interaction with the dilated main pulmonary artery (MPA).

102 exposed to chronic hypoxia, with less distal pulmonary artery muscularization and fewer Ki67-stained

103 he accuracy of E/e' ratio as a surrogate for pulmonary artery occlusion pressure in patients with dec

104 The validity of E/e' for predicting pulmonary artery occlusion pressure in patients with dec

105 al and mean E/e' were poorly correlated with pulmonary artery occlusion pressure, if at all, in both

106 icular systolic pressure and hypertrophy and pulmonary artery occlusive changes.

107 ted to the common carotid artery, aorta, and pulmonary artery of turtles.

108 tients in the validation cohort had enlarged pulmonary arteries (PA:A>1).

109 There has been an increase in the use of pulmonary artery (PA) catheters in heart failure (HF) in

110 Computed tomography-detected relative pulmonary artery (PA) enlargement defined as a PA to asc

111 of LMCA extrinsic compression from a dilated pulmonary artery (PA) in patients with PAH and angina or

112 Elevated pulmonary artery (PA) pressures in patients with heart f

113 Remote monitoring of pulmonary artery (PA) pressures provides clinicians with

114 is a vasculopathy characterized by enhanced pulmonary artery (PA) smooth muscle cell (PASMC) prolife

115 Although exposed to stressful conditions, pulmonary artery (PA) smooth muscle cells (PASMCs) exhib

116 Risk factors associated with outcomes for pulmonary artery (PA) stenting remain poorly defined.

117 nts between a cohort of patients with branch pulmonary artery (PA) stents who underwent stent fractur

118 urpose To determine the relationship between pulmonary artery (PA) stiffness and both right ventricul

119 Purpose To investigate whether the pulmonary artery (PA)-to-ascending aorta (Ao) ratio is a

120 e-vessel anastomosis (superior vena cava and pulmonary artery [PA] or bidirectional Glenn operation e

121 1 (LATS1) is inactivated in small remodeled pulmonary arteries (PAs) and distal PAVSMCs in idiopathi

122 s in lung tissues from patients with PAH and pulmonary arteries (PAs) from rodent models of HPH were

123 mooth muscle cells (PASMCs) and human distal pulmonary arteries (PAs) in response to hypoxia.

124 tures of calcified lesions within the distal pulmonary arteries (PAs).

125 arallels the growth in tumor volume, whereas pulmonary artery perfusion remained unchanged.

126 e Contegra conduit in the right ventricle to pulmonary artery position.

127 Patients with systolic pulmonary artery pressure >35 mm Hg on echocardiogram un

128 ain of EPAS1 in Angus cattle with HAPH, mean pulmonary artery pressure >50 mm Hg in two independent h

129 vs 0.22 +/- 0.03, p < 0.001) and lower mean pulmonary artery pressure (26 +/- 3 vs 34 +/- 7 mm Hg; p

130 a lower 6-min walking distance, whereas mean pulmonary artery pressure (46.9 +/- 13.3 mm Hg vs. 43.9

131 , including the following mean 24H measures: pulmonary artery pressure (6.8 vs 9.0 mm Hg), reservoir

132 .8] vs 42.0 [17.8] years), had a higher mean pulmonary artery pressure (60.5 [13.8] vs 56.4 [15.3] mm

133 ed surrogate, the rest-to-exercise change in pulmonary artery pressure (DeltaPAP).

134 t consensus opinion, PH is defined by a mean pulmonary artery pressure (mPAP) >/=25 mm Hg.

135 Mean pulmonary artery pressure (mPAP) and 6-minute walking di

136 Pulmonary hypertension (PH) exists when mean pulmonary artery pressure (mPAP) is 25 mm Hg or greater.

137 At baseline, mean pulmonary artery pressure (mPAP) was 44 +/- 10 mm Hg (ra

138 Despite a similar mean pulmonary artery pressure (noncarriers 54+/-15 versus mu

139 y of late filling (p = 0.031), and diastolic pulmonary artery pressure (p < 0.001) were independently

140 lowed by the invasive measurements of a mean pulmonary artery pressure (PAP) >/=25 mm Hg and mean wed

141 arterioles, leading to chronic elevation of pulmonary artery pressure (pulmonary hypertension) and r

142 01) and pressure (r=-0.37, P=0.002), but not pulmonary artery pressure (r=-0.07, P=0.58).

143 pe I procollagen values also had higher mean pulmonary artery pressure (r=0.553; P=0.014), transpulmo

144 s and analyzed as follows: group 1, systolic pulmonary artery pressure (sPAP) <40 mm Hg (346 patients

145 sure (RAP) (r = 0.863; p < 0.0001), systolic pulmonary artery pressure (sPAP) (r = 0.880; p < 0.0001)

146 vivo antagonized hypoxia-induced increase in pulmonary artery pressure and distal arteriole musculari

147 Diastolic pulmonary artery pressure and mean PAWP were measured to

148 nts in the treatment group were managed with pulmonary artery pressure and patients in the control gr

149 es (LVADs) has decoupling of their diastolic pulmonary artery pressure and pulmonary capillary wedge

150 d as a >5 mm Hg difference between diastolic pulmonary artery pressure and pulmonary capillary wedge

151 artery denervation resulted in reduced mean pulmonary artery pressure and pulmonary vascular resista

152 tely correlated with absolute change in mean pulmonary artery pressure and pulmonary vascular resista

153 ry cell infiltration, associated with raised pulmonary artery pressure and right ventricular hypertro

154 There was a strong correlation between mean pulmonary artery pressure and SCmin at baseline and duri

155 ences in cardiac output between groups, mean pulmonary artery pressure at cardiac output=13.8 L.min(-

156 n left atrial enlargement and lower systolic pulmonary artery pressure compared with left-sided heart

157 in GUCY1A3 in 3 subjects with a normal mean pulmonary artery pressure encodes an alpha1-A680T solubl

158 ndomised access, investigators had access to pulmonary artery pressure for all patients (open access

159 or heart failure were seen after 6 months of pulmonary artery pressure guided management compared wit

160 Compared with baseline, systolic pulmonary artery pressure immediately improved after TAV

161 sGC as a pharmacological target for reducing pulmonary artery pressure in humans at altitude.

162 Although the pulmonary artery pressure in SCD patients with pulmonary

163 diac determinants are the excessive systolic pulmonary artery pressure increase and the reduced peak

164 After pulmonary artery pressure information became available t

165 Interdependence was enhanced as pulmonary artery pressure load increased (P for interact

166 At reassessment, a mean pulmonary artery pressure of >/=30 mm Hg correlated with

167 A mean pulmonary artery pressure of >/=38 mm Hg and pulmonary v

168 men; mean age, 66.6 +/- 9.2 yr), with a mean pulmonary artery pressure of 36.0 (+/- 8.9) mm Hg, PVRi

169 oman with acute respiratory failure and mean pulmonary artery pressure of 65 mm Hg.

170 tatistically significant differences in mean pulmonary artery pressure or pulmonary artery wedge pres

171 annular plane systolic excursion to systolic pulmonary artery pressure ratio (P = 0.015) predicted Cp

172 annular plane systolic excursion to systolic pulmonary artery pressure ratio predicted Cpc-PH in DHF

173 ts managed with guidance from an implantable pulmonary artery pressure sensor compared with usual car

174 edicare claims data from patients undergoing pulmonary artery pressure sensor implantation between Ju

175 acceleration time (PAAT) as a surrogate for pulmonary artery pressure was found to be of clinical va

176 heart failure based on home transmission of pulmonary artery pressure with an implanted pressure sen

177 Pulmonary hypertension (mean pulmonary artery pressure, >/=25 mm Hg) was present in 8

178 ed according to whether PH was present (mean pulmonary artery pressure, >/=25 mm Hg; n=325) or not (n

179 or precapillary pulmonary hypertension (mean pulmonary artery pressure, >/=25 mm Hg; pulmonary vascul

180 g 29 (18%) regarded as moderate-severe (mean pulmonary artery pressure, >/=35 mm Hg) and 28 (34%) als

181 plane systolic excursion, exercise systolic pulmonary artery pressure, and exercise cardiac output w

182 Cardiac index, pulmonary artery pressure, and pulmonary capillary wedge

183 Mean pulmonary artery pressure, estimated by transthoracic ec

184 Invasive hemodynamic data including pulmonary artery pressure, pulmonary vascular resistance

185 ted disease progression as evaluated by mean pulmonary artery pressure, vascular resistance, and limi

186 Nitrite improved pulmonary artery pressure-flow relationships in HFpEF an

187 This study examines the impact of pulmonary artery pressure-guided heart failure (HF) care

188 otal trial proved the safety and efficacy of pulmonary artery pressure-guided heart failure managemen

189 Pulmonary artery pressure-guided HF management in Medica

190 Intracardiac and pulmonary artery pressure-guided management has become a

191 the diastolic pressure difference (diastolic pulmonary artery pressure-left ventricular end-diastolic

192 ate the DPD as per usual practice (diastolic pulmonary artery pressure-mean PAWP).

193 ex to calculate the QRS-gated DPD (diastolic pulmonary artery pressure-QRS-gated PAWP).

194 enta growth factor (PlGF) and high estimated pulmonary artery pressure.

195 of LV function, fixed perfusion defects, and pulmonary artery pressure.

196 ystemic arterial pressure was higher and the pulmonary artery pressure/systemic arterial pressure rat

197 cting right ventricular afterload (diastolic pulmonary artery pressure; p < 0.001).

198 nce, left ventricular filling pressures, and pulmonary artery pressures and improved compliance (p <

199 diameter (mPAD) at computed tomography (CT), pulmonary artery pressures at echocardiography and right

200 sus +0.6+/-0.9 mL/mm Hg), and decreased mean pulmonary artery pressures at rest (-7+/-4 versus -3+/-4

201 reduces biventricular filling pressures and pulmonary artery pressures at rest and during exercise i

202 as required for the development of increased pulmonary artery pressures in a model of pulmonary hyper

203 when left ventricular filling pressures and pulmonary artery pressures increase.

204 the treatment group, in which daily uploaded pulmonary artery pressures were used to guide medical th

205 ght and left ventricular function and higher pulmonary artery pressures, and were more likely to have

206 ar end-diastolic pressure, and elevated main pulmonary artery pressures.

207 e procedures, 671 aortic procedures, and 245 pulmonary artery procedures.

208 Pulmonary artery pulsatility increased in two of three l

209 uded elevated right atrial pressure, reduced pulmonary artery pulse pressure, and reduced stroke volu

210 g segments and extensive lobar and segmental pulmonary artery reconstruction.

211 lmonary artery endothelial cells, leading to pulmonary artery remodeling: consequently, restoring KCN

212 the decellularized grafts are implanted as a pulmonary artery replacement in three young lambs and ev

213 d at the main pulmonary artery for measuring pulmonary artery resistance (Z0), effective arterial ela

214 rtery trunk allowed continuous assessment of pulmonary artery resistance, effective elastance, compli

215 ized by progressive remodeling of the distal pulmonary arteries, resulting in elevated pulmonary vasc

216 ction and vascular remodeling obstruct small pulmonary arteries, resulting in increased pulmonary vas

217 Quantitative evaluation of the central pulmonary arteries revealed higher arterial volume and g

218 voir-excess pressure analysis applied to the pulmonary artery revealed distinctive differences betwee

219 a renewed interest in the right ventricle-to-pulmonary artery shunt as the source of pulmonary blood

220 with a significantly greater number of small pulmonary artery side branches <300 mum per cm vessel (3

221 Clamping of the pulmonary artery significantly increased afterload (Delt

222 f obliterative and plexiform-like lesions in pulmonary arteries, similar to PAH patients.

223 However, other markers of morbidity and pulmonary artery size favored the PDA stent group, suppo

224 lar anomalies, and surgical outcomes of left pulmonary artery sling (LPAS) using cardiovascular compu

225 ptamine 1B receptor (5-HT1BR) mediates human pulmonary artery smooth muscle cell (hPASMC) proliferati

226 ypertension (PH) and its role in controlling pulmonary artery smooth muscle cell (PA-SMC) proliferati

227 iRNAs) play important roles in regulation of pulmonary artery smooth muscle cell (PASMC) phenotype an

228 tive vasculopathy characterized by excessive pulmonary artery smooth muscle cell (PASMC) proliferatio

229 ldosterone-Raptor signaling induces abnormal pulmonary artery smooth muscle cell (PASMC) survival pat

230 ed platelets released serotonin and promoted pulmonary artery smooth muscle cell proliferation in a s

231 bunit Raptor by aldosterone induces abnormal pulmonary artery smooth muscle cell survival patterns to

232 ation of pulmonary artery endothelial cells, pulmonary artery smooth muscle cell, adventitial fibrobl

233 lly reduced basal BMPR-II signaling in human pulmonary artery smooth muscle cells (hPASMCs).

234 at lungs, as well as in pulmonary artery and pulmonary artery smooth muscle cells (PASMC) exposed to

235 lphide, hereafter sulphide) concentration in pulmonary artery smooth muscle cells (PASMCs) has been p

236 pha) is increased, the role of HIF-1alpha in pulmonary artery smooth muscle cells (PASMCs) remains co

237 an IPAH and control patient lung tissues and pulmonary artery smooth muscle cells (PASMCs) were used

238 found to contribute to the proliferation of pulmonary artery smooth muscle cells (PASMCs), and inhib

239 characterized by excessive proliferation of pulmonary artery smooth muscle cells (PASMCs).

240 regulates miR-143/145 microRNA expression in pulmonary artery smooth muscle cells (PASMCs).

241 vage via the sheddases, ADAM10 and ADAM17 in pulmonary artery smooth muscle cells (PASMCs).

242 ression and activity are strongly reduced in pulmonary artery smooth muscle cells and endothelial cel

243 technique in freshly isolated (not cultured) pulmonary artery smooth muscle cells and pulmonary arter

244 itable PAH and contributes to dysfunction of pulmonary artery smooth muscle cells and pulmonary arter

245 expression was also detected in female human pulmonary artery smooth muscle cells compared with male.

246 Pulmonary artery smooth muscle cells derived from Bmpr2

247 Similarly, pulmonary artery smooth muscle cells from Bmpr2(+/-) mic

248 We used pulmonary artery smooth muscle cells from Bmpr2(+/-) mic

249 m ion (Ca(2+)) homeostasis and transition of pulmonary artery smooth muscle cells to a proliferative

250 BMPR-II deficiency in mouse and human pulmonary artery smooth muscle cells was associated with

251 )]i signals in diacylglycerol-stimulated rat pulmonary artery smooth muscle cells.

252 Signaling studies used cultured human pulmonary artery smooth muscle cells.

253 ve for the treatment of right ventricular to pulmonary artery stenosis or pulmonary regurgitation.

254 lmonary hypertension (defined as an elevated pulmonary artery systolic pressure >40 mm Hg on echocard

255 ion </=40%, lower mean transaortic gradient, pulmonary artery systolic pressure >60 mm Hg; p < 0.05 f

256 PH was defined as the presence of estimated pulmonary artery systolic pressure (PASP) >35 mmHg and/o

257 Measurements of ventilation and pulmonary artery systolic pressure (PASP) assessed by Do

258 0 mg/g) and available echocardiogram-derived pulmonary artery systolic pressure (PASP) from the Jacks

259 Although elevated pulmonary artery systolic pressure (PASP) is associated

260 Pulmonary artery systolic pressure (PASP) was serially a

261 5 reduced ejection fraction) with PH (HF-PH; pulmonary artery systolic pressure [PASP] >/=40 mm Hg) w

262 vels, especially associated with an elevated pulmonary artery systolic pressure on echocardiogram, ma

263 PAVA is not simply increased cardiac output, pulmonary artery systolic pressure or sympathetic nervou

264 were more closely associated with the TAPSE/pulmonary artery systolic pressure ratio.

265 rding to impairment in RV-PA coupling (TAPSE/pulmonary artery systolic pressure) ratio.

266 An increase in pulmonary artery systolic pressure, estimated noninvasiv

267 ance (Ea) and right ventricular afterload by pulmonary artery systolic pressure.

268 Sildenafil had no effect on pulmonary artery systolic pressure.

269 bation was shorter in patients with enlarged pulmonary arteries than in those with normal-sized pulmo

270 c cells located at the base of the aorta and pulmonary artery that are likely involved in efferent re

271 Duration of vortical blood flow in the main pulmonary artery that is determined by using phase-contr

272 ils to achieve sufficient enhancement in the pulmonary arteries, the study investigates an alternativ

273 sion of agreement compared with intermittent pulmonary artery thermodilution measurements in a clinic

274 with cardiac output measured by intermittent pulmonary artery thermodilution using a pulmonary artery

275 ts in the 30 mg group died during the study (pulmonary artery thrombosis and cardiorespiratory failur

276 Unexpected evidence of pulmonary artery thrombus formation was found in 19% of

277 excess pressure analyses were applied in the pulmonary artery to characterize changes in wave propaga

278 o evaluate the nerve distribution around the pulmonary artery, to determine the effect of radiofreque

279 Pressure and flow sensors placed at the pulmonary artery trunk allowed continuous assessment of

280 duration of vortical blood flow in the main pulmonary artery (tvortex, the percentage of cardiac pha

281 LT (0 [H0], 6, 12, 24, 48 and 72 hours after pulmonary artery unclamping).

282 The realization that in addition to pulmonary artery vascular cells, other tissues and cells

283 lling pressures with exercise, and depressed pulmonary artery vasodilator reserve.

284 logy, increase in RV filling time (P=0.002), pulmonary artery velocity time integral (P=0.006), and R

285 Elafin reverses obliterative changes in pulmonary arteries via elastase inhibition and caveolin-

286 lar remodeling of donor, PH-COPD, and PH-IPF pulmonary arteries was assessed.

287 Airway-based delivery of AAV vectors to the pulmonary arteries was feasible, efficient, and safe in

288 normal in most patients, whereas the neomain pulmonary artery was typically oval shaped with decrease

289 ced by temporary, unilateral clamping of the pulmonary artery, was tested before and after induction

290 eous respiration and dynamic stress tests on pulmonary artery wave propagation and reservoir function

291 owing high-risk subgroups: (1) patients with pulmonary artery wedge pressure >15 mm Hg; (2) pulmonary

292 ated, potentially related to the use of mean pulmonary artery wedge pressure (PAWP).

293 erences in mean pulmonary artery pressure or pulmonary artery wedge pressure between SIPE-susceptible

294 The pulmonary artery wedge pressure was </=15 mm Hg in 54%,

295 le subjects (P=0.004), and the corresponding pulmonary artery wedge pressure was 11.0 mm Hg versus 18

296 Hg; pulmonary vascular resistance, >3.0 WU; pulmonary artery wedge pressure, </=15 mm Hg).

297 ted the hypothesis that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susc

298 f tetralogy of Fallot with confluent central pulmonary arteries were studied: stent group (n=42), pri

299 lation lesions on the luminal surface of the pulmonary artery were accompanied by histological and bi

300 Stent patients had the smallest pulmonary arteries with a median (95% credible intervals