title: Vascular closure devices in patients treated with anticoagulation and IIb/IIIa receptor inhibitors during percutaneous revascularization.
abstract: OBJECTIVE
  The study assessed clinical outcomes of closure device use following percutaneous coronary revascularization using current standards of anticoagulation and antiplatelet therapy.
  
  
  BACKGROUND
  Evaluation of the outcomes of patients by use of vascular closure devices during coronary interventions employing current standards of anticoagulation and glycoprotein (GP) IIb/IIIa inhibitor therapy is limited.
  
  
  METHODS
  We evaluated outcomes of 4,525 consecutive patients who underwent percutaneous coronary intervention between July 1997 and April 2000. All patients received anticoagulation with heparin and GP IIb/IIIa inhibitor therapy with abciximab. The closure method was manual in 1,824 patients, Angioseal in 524 patients and Perclose in 2,177 patients. Procedural and hospital vascular outcomes were evaluated.
  
  
  RESULTS
  Closure device success was 97.1% Angioseal and 94.1% Perclose (p < 0.05). Minor vascular complications occurred in 1.8% of manual patients, 1.1% of Angioseal patients and 1.2% of Perclose patients (p = NS); major complications occurred in 1.3% of manual patients, 1.1% of Angioseal patients and 1.0% of Perclose patients (p = NS). Multivariate logistic regression identified only closure device failure as an independent predictor of a vascular complication. In patients with successful closure with a device, minor complications (0.8% vs. 1.8%, p < 0.05) and any complication (1.5% vs. 2.5%, p < 0.05) were reduced compared to manual compression.
  
  
  CONCLUSIONS
  Arterial closure following coronary interventions using anticoagulation and GP IIb/IIIa inhibitor therapy can be safely and effectively performed, with vascular complication rates similar to or lower than with manual pressure. Additionally, vascular complication rates using GP IIb/IIIa inhibitor therapy regardless of the method of arterial closure are equivalent to or lower than previously published rates of vascular complications.
authors.affiliation: Section of Cardiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1045, USA. bapplega@wfubmc.edu
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Applegate
authors.forename: Mark A
authors.initials: MA
authors.lastname: Grabarczyk
authors.forename: William C
authors.initials: WC
authors.lastname: Little
authors.forename: Timothy
authors.initials: T
authors.lastname: Craven
authors.forename: Michael
authors.initials: M
authors.lastname: Walkup
authors.forename: Frederic R
authors.initials: FR
authors.lastname: Kahl
authors.forename: Gregory A
authors.initials: GA
authors.lastname: Braden
authors.forename: Kevin M
authors.initials: KM
authors.lastname: Rankin
authors.forename: Michael A
authors.initials: MA
authors.lastname: Kutcher
mesh_terms: D000077284:Abciximab; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D000925:Anticoagulants / Q000627:therapeutic use*; D005260:Female; D006489:Hemostatic Techniques / Q000295:instrumentation*; D006493:Heparin / Q000627:therapeutic use*; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009204:Myocardial Revascularization; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D007140:Immunoglobulin Fab Fragments; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D006493:Heparin; D000077284:Abciximab