1 guidewires; they include the measurement of
poststenotic absolute coronary flow reserve, the relativ
2 oronary flow velocity and MPR ratios between
poststenotic and angiographically normal vascular beds w
3 l perfusion reserve (MPR) were calculated in
poststenotic and normal reference vascular beds.
4 el of cord compression in combination with a
poststenotic decrease of (18)F-FDG uptake.
5 Poststenotic dilatation (PSD) occurs in a low-pressure r
6 Poststenotic dilatation of greater than 20% was present
7 ical thickness, parenchymal enhancement, and
poststenotic dilatation were measured.
8 rdered flow of the midgraft stenosis yielded
poststenotic dilatation.
9 Poststenotic Doppler average peak flow velocities (APV;
10 Poststenotic flow biases were 1.8% and 31.2%, 5.7% and -
11 Poststenotic flow velocity increased from 6.6 +/- 6.1 to
12 ved from [15O]H2O PET with directly measured
poststenotic intracoronary Doppler flow velocity data ac
13 nal blood flow (RBF) and GFR and accelerates
poststenotic kidney (STK) tissue injury.
14 sized that miR-26a levels are reduced in the
poststenotic kidney and that kidney repair achieved by a
15 factors and tubulointerstitial injury in the
poststenotic kidney are poorly understood.
16 decreased tubular miR-26a expression in the
poststenotic kidney may be responsible for tubular cell
17 stemic hypertension and tissue injury in the
poststenotic kidney, restoring vessel patency alone is i
18 flow, perfusion, and GFR were reduced in the
poststenotic kidney.
19 ith healthy control kidneys, swine and human
poststenotic kidneys had 45.5+/-4.3% and 90.0+/-3.5% low
20 arly correlated (r = .60; P < .001), as were
poststenotic PET MPR and Doppler CFR (r = .76; P < .0002
21 Midgraft stenosis exhibits
poststenotic positive wall remodeling.
22 some of the reported variability from using
poststenotic PSV to detect hemodynamically significant r
23 Poststenotic PSV was mildly dependent on end-organ vascu
24 ip between end-organ vascular resistance and
poststenotic PSV.
25 Arterial rings obtained from the
poststenotic region were more sensitive and responsive t
26 how high levels of phospho-Smad1/5 in ECs at
poststenotic sites, where OSS occurs.
27 inhibited the increased EC uptake of BrdU at
poststenotic sites.
28 d activity of von Willebrand factor (vWF) at
poststenotic sites.
29 The
poststenotic thrombus formation was critically dependent
30 erwent HFR-CEUS measurements of the pre- and
poststenotic vessel segments.