title: Triple antiplatelet therapy does not increase femoral access bleeding with vascular closure devices.
abstract: BACKGROUND
  The use of arteriotomy closure devices (CDs) to achieve hemostasis after femoral artery access in percutaneous coronary intervention is steadily increasing. However, the safety information with these devices in the era of triple antiplatelet therapy is limited.
  
  
  METHODS
  We reviewed prospectively collected data from the Do Tirofiban and ReoPro Give Similar Efficacy Outcomes Trial (TARGET), where all patients received aspirin, clopidogrel, and glycoprotein IIb/IIIa inhibitor therapy. At the treating physician's discretion, manual compression (MC) or a vascular hemostasis device was selected following femoral angiography. Patients receiving MC were to have sheaths removed 2 to 6 hours postprocedure when the activated clotting time was < or = 175 seconds.
  
  
  RESULTS
  Of 4809 patients, 4736 had femoral access, and 985 of these had a CD (Perclose 47%, Angio-Seal 43%, VasoSeal 5%, and other 5%). The MC and CD groups were similar regarding most demographic characteristics, including age, systolic blood pressure, and weight, but those with MC were more often female, diabetic, and had history of peripheral vascular disease. Patients with a CD had a lower ischemic event rate suggesting they were a lower risk cohort overall. There were no differences in major bleeding at the access site (0.4% vs 0.5%, P =.588), minor bleeding at the access site (1.9% vs. 3.1%, P =.142) or transfusions (0.8% vs 1.0%, P =.513) between the MC and CD groups, respectively.
  
  
  CONCLUSIONS
  In contemporary percutaneous coronary intervention practice, with appropriate patient selection, a CD can be safely utilized despite aggressive polypharmacy for procedural anticoagulation.
authors.affiliation: Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio, USA.
authors.forename: Jose E
authors.initials: JE
authors.lastname: Exaire
authors.forename: Harold L
authors.initials: HL
authors.lastname: Dauerman
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Topol
authors.forename: James C
authors.initials: JC
authors.lastname: Blankenship
authors.forename: Kathy
authors.initials: K
authors.lastname: Wolski
authors.forename: Russell E
authors.initials: RE
authors.lastname: Raymond
authors.forename: Eric A
authors.initials: EA
authors.lastname: Cohen
authors.forename: David J
authors.initials: DJ
authors.lastname: Moliterno
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D001241:Aspirin / Q000009:adverse effects / Q000627:therapeutic use; D000077144:Clopidogrel; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D005260:Female; D005263:Femoral Artery; D006470:Hemorrhage / Q000517:prevention & control*; D006488:Hemostasis, Surgical / Q000295:instrumentation*; D006493:Heparin / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D018579:Patient Selection; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects* / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D011446:Prospective Studies; D013536:Suture Techniques; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D006493:Heparin; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin