title: Intraprocedural thrombus formation during coil placement in ruptured intracranial aneurysms: treatment with systemic application of the glycoprotein IIb/IIIa antagonist tirofiban.
abstract: OBJECTIVE
  When using detachable coils to treat intracranial aneurysms, thromboembolism is the most feared and frequently reported complication during or after endovascular therapy. The purpose of this study was to document the therapeutic effect of tirofiban on patency of the parent vessel, rate of rebleedings, and outcome of the patients in the setting of acute subarachnoidal hemorrhage.
  
  
  METHODS
  A patient data base was retrospectively reviewed to identify patients in whom thrombus occurred during endovascular treatment of ruptured cerebral aneurysms within a 34-month period and who were treated with tirofiban. All patients underwent anticoagulation with heparin during endovascular treatment procedures. Sixteen patients (age range, 52.9 +/- 10.7 years; 10 women, 6 men) were identified with intraprocedural thrombus formation. The patency of the parent vessel was assessed in a retrospective analysis blinded to outcome. Eight patients received ventriculostomy and had a follow-up CT.
  
  
  RESULTS
  Local nonocclusive thrombus at the coil surface was detected in 5 patients, in all of whom the thrombus was dissolved. In 10 patients, partial or total occlusion of the parent vessel occurred during the intervention; in 8 of these, the vessel was recanalized completely and in 2 drug administration was assisted by mechanical means. In 1 patient, however, the occlusion persisted. No periprocedural rebleedings of the ruptured aneurysm occurred; 3 of 8 ventriculostomies had clinically silent small local bleedings.
  
  
  CONCLUSIONS
  The use of tirofiban in the setting of endovascular treatment of ruptured intracranial aneurysms to dissolve platelet aggregation seems relatively safe and effective.
authors.affiliation: Departments of Neuroradiology, Klinikum Grosshadern, Ludwig-Maximilian University Munich, Munich, Germany.
authors.forename: R
authors.initials: R
authors.lastname: Bruening
authors.forename: S
authors.initials: S
authors.lastname: Mueller-Schunk
authors.forename: D
authors.initials: D
authors.lastname: Morhard
authors.forename: K C
authors.initials: KC
authors.lastname: Seelos
authors.forename: H
authors.initials: H
authors.lastname: Brueckmann
authors.forename: R
authors.initials: R
authors.lastname: Schmid-Elsaesser
authors.forename: A
authors.initials: A
authors.lastname: Straube
authors.forename: T E
authors.initials: TE
authors.lastname: Mayer
mesh_terms: D000328:Adult; D000368:Aged; D017542:Aneurysm, Ruptured / Q000150:complications / Q000000981:diagnostic imaging / Q000601:surgery*; D015901:Angiography, Digital Subtraction; D002533:Cerebral Angiography; D004621:Embolization, Therapeutic / Q000009:adverse effects*; D005260:Female; D005343:Fibrinolytic Agents / Q000008:administration & dosage*; D006801:Humans; D007262:Infusions, Intravenous; D002532:Intracranial Aneurysm / Q000000981:diagnostic imaging / Q000601:surgery*; D020767:Intracranial Thrombosis / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000209:etiology; D007431:Intraoperative Complications / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D013345:Subarachnoid Hemorrhage / Q000209:etiology; D000077466:Tirofiban; D014443:Tyrosine / Q000008:administration & dosage / Q000031:analogs & derivatives*
chemical_list: D005343:Fibrinolytic Agents; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014443:Tyrosine; D000077466:Tirofiban