scholarly journals Histopathological reaction of the abdominal aorta wall to non-covered stents]]>

Author(s):  
Rubio Bombonato ◽  
Jos� H. Palma ◽  
Jos� A. Marcondes ◽  
Aury N. Moraes ◽  
Jo�o L. Rocha ◽  
...  
2013 ◽  
Vol 42 (s1) ◽  
pp. 145-145
Author(s):  
S. Visentin ◽  
R. Salmaso ◽  
K. Ludwig ◽  
F. Gobbo ◽  
E. Cosmi

2011 ◽  
Author(s):  
Takaya Hayashi ◽  
Yusuke Fujita ◽  
Yoshihiro Mitani ◽  
Yoshihiko Hamamoto ◽  
Makoto Segawa ◽  
...  

1997 ◽  
Vol 17 (7) ◽  
pp. 1346-1355 ◽  
Author(s):  
Pierre Boutouyrie ◽  
Yvonnick Bézie ◽  
Patrick Lacolley ◽  
Pascal Challande ◽  
Philippe Chamiot-Clerc ◽  
...  

VASA ◽  
2009 ◽  
Vol 38 (1) ◽  
pp. 66-71 ◽  
Author(s):  
Schubert

We describe a case of aortic coarctation at the level of the infrarenal abdominal aorta which is encountered in less than six individuals in one million. In contrast to aortic narrowing above or including the renal arteries, this seems to be a relatively benign anomaly without systemic hypertension or impaired renal function. For the first time in this type of anomaly, contrast-enhanced MR angiography (ce-MRA) on a multi-receiver channel MR system, with an 8-channel phased array coil and parallel imaging was used. Ce-MRA displayed a tortuous, narrowed aortic segment that was found to be associated with mesenteric artery stenosis and compression of the orthotopic left renal vein, also known as the nutcracker phenomenon. All major aortic branches could be depicted using 3D surface-shaded displays and subvolume maximum intensity projections (MIPs). Collateral vessels of the abdominal wall were identified using whole-volume MIPs. Since the majority of aortic malformations are diagnosed at a younger age, and many suffer from renal insufficiency, we conclude that ce-MRA will eventually place conventional DSA as the modality of choice in malformations of the abdominal aorta.


1987 ◽  
Vol 26 (05) ◽  
pp. 224-228 ◽  
Author(s):  
Y. Isaka ◽  
H. Etani ◽  
K. Kimura ◽  
S. Yoneda ◽  
T. Kamada ◽  
...  

Tissue-type plasminogen activator (t-PA) which has a high affinity for fibrin in the clot, was labeled with 131I by the iodogen method, and its binding to de-endothelialized lesions in the rabbit was measured to assess the detectability of thrombi. The de-endothelialized lesion was induced in the abdominal aorta with a Fogarty 4F balloon catheter. Two hours after the de-endothelialization, 131I-labeled t-PA (125 ± 46 μCi) was injected intravenously. The initial half-life of the agent in blood (n = 12) was 2.9 ± 0.4 min. The degree of binding of 131I-labeled t-PA to the de-endothelialized lesion was evaluated at 15 min (n = 6) or at 30 min (n = 6) after injection of the agent. In spite of the retention of the biochemical properties of 131I-labeled t-PA and the presence of fibrin deposition at the de-endothelialized lesion, the binding of t-PA to the lesion was not sufficiently strong. Lesion-to-control ratios (cpm/g/cpm/g) were 1.65 ± 0.40 (at 15 min) and 1.39 ± 1.31 (at 30 min), and lesion-to-blood ratios were 1.39 ± 0.32 (at 15 min) and 1.36 ± 0.23 (at 30 min). These results suggest that radiolabeled t-PA may be inappropriate as a radiopharmaceutical for the scintigraphic detection of a pre-existing thrombotic lesion.


1994 ◽  
Vol 71 (04) ◽  
pp. 499-506 ◽  
Author(s):  
Mark W C Hatton ◽  
Bonnie Ross-Ouellet

SummaryThe behavior of 125I-labeled recombinant hirudin towards the uninjured and de-endothelialized rabbit aorta wall has been studied in vitro and in vivo to determine its usefulness as an indicator of thrombin activity associated with the aorta wall. Thrombin adsorbed to either sulfopropyl-Sephadex or heparin-Sepharose bound >95% of 125I-r-hirudin and the complex remained bound to the matrix. Binding of 125I-r-hirudin to the exposed aorta subendothelium (intima-media) in vitro was increased substantially if the tissue was pre-treated with thrombin; the quantity of l25I-r-hirudin bound to the de-endothelialized intima-media (i.e. balloon-injured in vitro) correlated positively with the quantity of bound 131I-thrombin (p <0.01). Aortas balloon-injured in vivo were measured for thrombin release from, and binding of 125I-r-hirudin to, the de-endothelialized intimal surface in vitro; 125I-r-hirudin binding correlated with the amount of active thrombin released (p <0.001). Uptake of 125I-r-hirudin by the aorta wall in vivo was proportional to the uptake of 131I-fibrinogen (as an indicator of thrombin activity) before and after balloon injury. After 30 min in the circulation, specific 125I-r-hirudin binding to the uninjured and de-endo- thelialized (at 1.5 h after injury) aorta wall was equivalent to 3.4 (± 2.5) and 25.6 (±18.1) fmol of thrombin/cm2 of intima-media, respectively. Possibly, only hirudin-accessible, glycosaminoglycan-bound thrombin is measured in this way.


1980 ◽  
Vol 16 (1) ◽  
pp. 135
Author(s):  
KW Kim ◽  
CY Park ◽  
JH Suh
Keyword(s):  

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