title: Thrombin generation and platelet activation related to subintimal percutaneous transluminal angioplasty.
abstract: OBJECTIVE
  The purpose of this study was to measure the in vivo platelet activation and thrombin generation in arterial blood after passing a subintimal conduit.
  
  
  METHODS
  Subintimal percutaneous transluminal angioplasty (SPTA) is a technique where a subintimal channel is created, allowing recanalization of long peripheral arterial occlusion. From 10 patients with intermittent claudication, undergoing successful SPTA for femoropopliteal occlusive disease, we collected antecubital venous blood samples immediately before treatment, preprocedural arterial blood samples taken at the entry level proximal to the vessel occlusion, and subsequently at the reentry level after successful recanalization. Venous follow-up blood samples were taken after 24 hours. Plasma concentrations of β-thromboglobulin (β-TG), RANTES, and Prothrombin fragment (F1 + 2), were determined by immunoassay. Fibrinogen binding to platelets, leukocyte-platelet adhesion, and P-selectin were determined by flow cytometry.
  
  
  RESULTS
  We found a statistically significant transluminal increase in the plasma concentrations of RANTES, β-TG and F1 + 2 (p = 0.002, 0.001 and 0.001 respectively), which all normalized within 24 hours. Platelet-leukocyte aggregates significantly decreased after 24 hours compared with preprocedural and preentry levels (3.26% versus 5.26 %, p = 0.017). P-selectin expression on circulating platelets was statistically significantly increased in the blood sample taken at the re-entry level compared with the pre-procedural and pre-entry level (p = 0.007). After 24 hours there was no statistically significant difference to pre-procedural levels. There was no significant change in platelet fibrinogen binding at any levels.
  
  
  CONCLUSIONS
  When passing a subintimal conduit, in vivo sampled blood demonstrated an extremely rapid and substantial uniform platelet activation and thrombin generation.
authors.affiliation: Department of Vascular Surgery, Oslo University Hospital, Oslo, Norway. erik.krag.jenssen@unn.no
authors.forename: Erik Krag
authors.initials: EK
authors.lastname: Jenssen
authors.forename: Frank
authors.initials: F
authors.lastname: Brosstad
authors.forename: Turid
authors.initials: T
authors.lastname: Pedersen
authors.forename: Stine
authors.initials: S
authors.lastname: Bjørnsen
authors.forename: Jørgen J
authors.initials: JJ
authors.lastname: Jørgensen
authors.forename: Gunnar
authors.initials: G
authors.lastname: Sandbæk
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D017130:Angioplasty; D050197:Atherosclerosis / Q000097:blood* / Q000628:therapy; D001792:Blood Platelets / Q000378:metabolism / Q000473:pathology; D018946:Chemokine CCL5 / Q000097:blood; D005260:Female; D005263:Femoral Artery / Q000473:pathology; D006801:Humans; D007383:Intermittent Claudication / Q000097:blood / Q000628:therapy; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000473:pathology; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation; D011150:Popliteal Artery / Q000473:pathology; D013917:Thrombin / Q000378:metabolism*; D001620:beta-Thromboglobulin / Q000378:metabolism
chemical_list: C483024:CCL5 protein, human; D018946:Chemokine CCL5; D019007:P-Selectin; D001620:beta-Thromboglobulin; D013917:Thrombin