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1 ween diastolic pulmonary artery pressure and pulmonary artery wedge pressure.
2 ly greater concentric LVH and estimated mean pulmonary artery wedge pressure (20 mm Hg vs. 16 mm Hg)
3 to 7+/-1 mm Hg, p < 0.01 by ANOVA) and mean pulmonary artery wedge pressure (21+/-3 to 16+/-2 mm Hg,
4 with SCD with RHC-confirmed PH with elevated pulmonary artery wedge pressure and low pulmonary vascul
5 ted the hypothesis that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susc
6 erences in mean pulmonary artery pressure or pulmonary artery wedge pressure between SIPE-susceptible
7 ssure (CHF, 28+/-11; LVAD, 18+/-4 mm Hg) and pulmonary artery wedge pressure (CHF, 16+/-10; LVAD 5+/-
8 pectively), whereas the inverse was true for pulmonary artery wedge pressure (corresponding muPAWP we
9 owing high-risk subgroups: (1) patients with pulmonary artery wedge pressure >15 mm Hg; (2) pulmonary
11 uring the acute stage have revealed a normal pulmonary artery wedge pressure, marked elevation of pul
12 5 cm2 (75 +/- 7% versus 32 +/- 12%) and mean pulmonary artery wedge pressure of < or = 18 versus > 18
13 ree survival by two post-CBC variables: mean pulmonary artery wedge pressure of < or = 18 versus > 18
16 monary vascular disease (PH(PVD), defined as pulmonary artery wedge pressure [PAWP]</=15 mm Hg and PV
17 % and 16 +/- 5% in mean pulmonary artery and pulmonary artery wedge pressures, respectively, but no c
19 le subjects (P=0.004), and the corresponding pulmonary artery wedge pressure was 11.0 mm Hg versus 18
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