title: Catheter based intracoronary brachytherapy leads to increased platelet activation.
abstract: BACKGROUND
  Vascular brachytherapy (VBT) after percutaneous coronary intervention (PCI) is associated with a higher risk of stent thrombosis than conventional treatment.
  
  
  OBJECTIVE
  To investigate in vivo periprocedural platelet activation with and without VBT, and to assess a possible direct effect of radiation on platelet activation.
  
  
  METHODS
  Of 50 patients with stable angina, 23 received VBT after PCI, while 27 had PCI only. The 23 patients who received VBT after PCI were pretreated for one month with aspirin and clopidogrel. Platelet activation was assessed by flow cytometry.
  
  
  RESULTS
  The two patient groups did not differ in their platelet activation before the intervention. There was a significant increase in activation immediately after VBT, with 21.2% (interquartile range 13.0% to 37.6%) thrombospondin positive and 54.0% (42.3% to 63.6%) CD 63 positive platelets compared with 12.7% (9.8% to 14.9%) thrombospondin positive and 37.9% (33.2% to 45.2%) CD 63 positive platelets before the intervention (p < 0.001 and p < 0.01, respectively). Patients without VBT had no periprocedural difference in platelet activation immediately after PCI. No increase in platelet activation was found after ex vivo irradiation of blood samples obtained from healthy controls.
  
  
  CONCLUSIONS
  Catheter based intracoronary VBT carried out according to current standards is highly thrombogenic. The current antithrombotic treatment with aspirin and clopidogrel is not sufficient to suppress platelet activation during the procedure. From in vitro experiments, it appears that platelet activation during brachytherapy is not caused by irradiation but by the procedure of catheter based VBT.
authors.affiliation: Department of Cardiology, University Hospital Benjamin Franklin, Free University of Berlin, Berlin, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Jaster
authors.forename: V
authors.initials: V
authors.lastname: Fuster
authors.forename: P
authors.initials: P
authors.lastname: Rosenthal
authors.forename: M
authors.initials: M
authors.lastname: Pauschinger
authors.forename: Q-V
authors.initials: QV
authors.lastname: Tran
authors.forename: D
authors.initials: D
authors.lastname: Janssen
authors.forename: W
authors.initials: W
authors.lastname: Hinkelbein
authors.forename: P
authors.initials: P
authors.lastname: Schwimmbeck
authors.forename: H-P
authors.initials: HP
authors.lastname: Schultheiss
authors.forename: U
authors.initials: U
authors.lastname: Rauch
mesh_terms: D000787:Angina Pectoris / Q000532:radiotherapy*; D015906:Angioplasty, Balloon, Coronary; D000925:Anticoagulants / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D001792:Blood Platelets / Q000187:drug effects / Q000528:radiation effects; D001918:Brachytherapy / Q000009:adverse effects*; D000077144:Clopidogrel; D023903:Coronary Restenosis / Q000517:prevention & control; D004868:Equipment Failure; D005260:Female; D005434:Flow Cytometry; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation / Q000528:radiation effects*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D015607:Stents; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D006493:Heparin; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin