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1.
Eur J Vasc Endovasc Surg ; 32(6): 668-74, 2006 Dec.
Article in English | MEDLINE | ID: mdl-16968668

ABSTRACT

BACKGROUND: Because subintimal angioplasty (SA) is a technique that can achieve recanalization of long arterial occlusions, it is considered an alternative to lower limb bypass operations. The aim of this prospective study was to identify the risk factors that affect patency of SA in patients suffering from critical limb ischemia (CLI). METHODS AND RESULTS: 51 consecutive infrainguinal SA were done in 46 patients suffered from CLI. The patients were followed-up with regular duplex scans up to 12 months post-intervention. Sex, atherosclerosis risk factors, and some technical details of the procedure (number of patent run-off vessels after the procedure, length and re-entry point of angioplasty) were examined as potential risk factors of patency, using survival analysis statistical techniques. The overall patency rate at 12 months post-intervention was 50%. According to Cox-regression analysis, the factors that affect patency were the number of run-off vessels and the length of occlusion. Patients with two or three run-off vessels had a hazard of occlusion of 0.30 (P = .027) compared to those who had one run-off vessel. The 12-months patency in patients with more than one run-off vessels was 81% vs. 25% in patients with one run-off vessel. Regarding the length of angioplasty, the hazard of reocclusion was 1.02 for every centimeter of occlusion (P = .049). CONCLUSIONS: The number of patent run-off crural vessels after the angioplasty and the length of occlusion are significant risk factors for reocclusion of infrainguinal SA in patients with CLI. Trying to recanalize more than one run-off vessels could raise the SA patency.


Subject(s)
Angioplasty/methods , Arterial Occlusive Diseases/surgery , Ischemia/surgery , Lower Extremity/blood supply , Vascular Patency , Adult , Aged , Aged, 80 and over , Amputation, Surgical , Arterial Occlusive Diseases/mortality , Arterial Occlusive Diseases/physiopathology , Female , Femoral Artery/surgery , Follow-Up Studies , Humans , Ischemia/mortality , Kaplan-Meier Estimate , Limb Salvage , Male , Middle Aged , Popliteal Artery/surgery , Prospective Studies , Regression Analysis , Reoperation , Risk Factors , Time Factors , Treatment Outcome , Tunica Intima/surgery
2.
J Vasc Res ; 37(6): 437-42, 2000.
Article in English | MEDLINE | ID: mdl-11146396

ABSTRACT

The receptor tyrosine kinase Tie-1 is expressed predominantly on endothelial cells where it has an essential role in blood vessel formation. Targeted disruption of the Tie-1 gene results in a lethal phenotype with severe disruption to the normal integrity of the vasculature. In an examination of Tie-1 in vivo, we observed a significant pool of the receptor present in the circulation associated with the platelet fraction. Western blotting reveals the platelet form of Tie-1 to be a protein of approximately 110 kDa, this contrasts with the 135/125-kDa doublet found in endothelial cells. Platelet activation results in increased surface expression of Tie-1. The closely related receptor tyrosine kinase Tie-2/Tek is not present in platelets. Endothelial Tie-1 undergoes metalloprotease-mediated ectodomain cleavage in response to phorbol ester and other agonists. Tie-1 cleavage leads to release of the extracellular domain and generation of a cell-associated intracellular domain with signalling capacity. The potential for cleavage was investigated in platelets. In contrast to endothelial Tie-1, phorbol ester does not stimulate truncation of the platelet receptor, suggesting these cells lack one or more components of the regulated metalloprotease system controlling Tie-1. These data demonstrate the Tie-1 receptor tyrosine kinase is present on platelets and its surface expression is regulated. Furthermore, platelet Tie-1 differs significantly from the endothelial receptor. Platelet Tie-1 has the potential to modulate endothelial function by competing for any Tie ligands and may have signalling roles important in controlling aspects of platelet behaviour.


Subject(s)
Blood Platelets/enzymology , Receptor Protein-Tyrosine Kinases/physiology , Receptors, Cell Surface/physiology , Adenosine Diphosphate/pharmacology , Adult , Blotting, Western , Cells, Cultured , Endothelium, Vascular/enzymology , Humans , Molecular Weight , Neovascularization, Physiologic , Organ Specificity , Platelet Activation , Protease Inhibitors/pharmacology , Protein Structure, Tertiary , Receptor Protein-Tyrosine Kinases/blood , Receptor Protein-Tyrosine Kinases/chemistry , Receptor Protein-Tyrosine Kinases/genetics , Receptor, TIE-1 , Receptor, TIE-2 , Receptors, Cell Surface/agonists , Receptors, Cell Surface/chemistry , Receptors, Cell Surface/genetics , Receptors, TIE , Tetradecanoylphorbol Acetate/pharmacology , Thrombin/pharmacology , Umbilical Veins
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