title: Hemostatic markers with bolus versus prolonged heparin after carotid artery stenting.
abstract: BACKGROUND
  The evolving technique of carotid stenting (CS) requires optimal antithrombotic strategies to reduce periinterventional thromboembolic risk. In animal models of balloon injury, tissue factor (TF) was shown to be the major procoagulant of the atherosclerotic plaque mediating prolonged procoagulant activity.
  
  
  METHODS
  We analyzed TF and TF-dependent hemostatic markers before and 2, 6 and 24 h after CS with two antithrombotic drug regimens. Group A (n=20) received prolonged unfractionated heparin (UFH) for 18-20 h starting at intervention next to aspirin and thienopyridine. In group B (n=16), single bolus UFH was administered next to combined antiplatelet therapy. Natural anticoagulants were determined at baseline.
  
  
  RESULTS
  Patients with symptomatic and asymptomatic cerebrovascular disease did not differ in plasma TF levels. Furthermore, no statistically significant difference for TF, TFPI/Xa-complex and prothrombin fragment F1.2 was observed between bolus and prolonged heparin treatment. No significant change was found in time course for these parameters. Two patients (5.5%; one in each treatment group) suffered periinterventional minor stroke associated with increased levels of F1.2 and TFPI/Xa-complex. Both were resistant to activated protein C (APC ratio<1.9) due to heterozygous factor V Leiden mutation.
  
  
  CONCLUSIONS
  No significant activation of the TF pathway was seen with both antithrombotic regimens suggesting that single bolus UFH combined with antiplatelet therapy is generally sufficient to control TF-dependent procoagulant activity after CS. However, patients with resistance to activated protein C may be at increased periinterventional stroke risk.
authors.affiliation: Division of Angiology, 2nd Department of Internal Medicine, General Hospital, University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria. sabine.steiner@univie.ac.at
authors.forename: Sabine
authors.initials: S
authors.lastname: Steiner
authors.forename: Ramazanali
authors.initials: R
authors.lastname: Ahmadi
authors.forename: Andrea
authors.initials: A
authors.lastname: Willfort
authors.forename: Wilfried
authors.initials: W
authors.lastname: Lang
authors.forename: Kurt
authors.initials: K
authors.lastname: Huber
authors.forename: Erich
authors.initials: E
authors.lastname: Minar
authors.forename: Christoph W
authors.initials: CW
authors.lastname: Kopp
mesh_terms: D000368:Aged; D000925:Anticoagulants / Q000008:administration & dosage; D015415:Biomarkers / Q000097:blood; D002340:Carotid Artery Diseases / Q000097:blood / Q000628:therapy*; D004359:Drug Therapy, Combination; D005260:Female; D006487:Hemostasis / Q000187:drug effects*; D006493:Heparin / Q000008:administration & dosage*; D006801:Humans; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage; D011516:Prothrombin; D015607:Stents / Q000009:adverse effects*; D013925:Thromboplastin / Q000032:analysis*; D013997:Time Factors
chemical_list: D000925:Anticoagulants; D015415:Biomarkers; D008074:Lipoproteins; D010446:Peptide Fragments; D010975:Platelet Aggregation Inhibitors; C051928:lipoprotein-associated coagulation inhibitor; C045879:prothrombin fragment 1.2; D011516:Prothrombin; D006493:Heparin; D013925:Thromboplastin