title: Association of periprocedural neurological deficit in carotid stenting with increased anticardiolipin antibodies.
abstract: BACKGROUND
  Carotid stenting (CS) has become a therapeutic alternative to endarterectomy in selected patients. Periinterventional plaque thromboembolism leading to neurological ischemic events remain the major risk of the procedure. We prospectively studied the potential role of thrombophilic conditions including anticardiolipin antibodies (ACA, IgG and IgM isotype), lupus anticoagulants, activated protein C resistance, antithrombin, and protein C and S.
  
  
  METHODS
  The study was approved by the local ethics committee, and written informed consent was obtained from all patients. In total, 236 consecutive patients were included (158 men, 78 woman; median age 73 years). Prothrombotic markers were quantitated on the day of admission. Periprocedural neurological deficits (PND) occurring within 48 hours of the intervention were recorded and classified by an independent neurologist as transient ischemic attack, minor or major stroke. Uni- and multivariable logistic regression analysis were performed to test for the influence of thrombophilic conditions, demographic factors and lesion characteristics on PND.
  
  
  RESULTS
  Neurologic complications occurred in 18 interventions (7.6%). In 4 (36.4%; 3 minor, 1major stroke) out of 11 patients with elevated IgG-ACA neurological events were observed as compared to 14 (6.2%; 6 TIA, 5 minor stroke, 3 major stroke) out of 225 patients with normal IgG-ACA levels. In multivariable analysis, two variables were independently associated with PND: elevated IgG-ACA (OR 6.09, 95% CI 1.49-25.88; P=0.012) and lesion length >10 mm (OR 4.36, 95% CI 1.19 to 16.01; P=0.027).
  
  
  CONCLUSIONS
  A thrombophilic condition due to elevation of anticardiolipin antibodies increases the risk of periinterventional neurological complications during CS.
authors.affiliation: Department of Internal Medicine II, Medical University Vienna, Austria. sabine.steiner-boeker@meduniwien.ac.at
authors.forename: Sabine
authors.initials: S
authors.lastname: Steiner
authors.forename: Roela
authors.initials: R
authors.lastname: Sadushi
authors.forename: Andrea
authors.initials: A
authors.lastname: Bartok
authors.forename: Alexandra
authors.initials: A
authors.lastname: Hammer
authors.forename: Peter
authors.initials: P
authors.lastname: Quehenberger
authors.forename: Christine
authors.initials: C
authors.lastname: Mannhalter
authors.forename: Renate
authors.initials: R
authors.lastname: Koppensteiner
authors.forename: Erich
authors.initials: E
authors.lastname: Minar
authors.forename: Christoph W
authors.initials: CW
authors.lastname: Kopp
mesh_terms: D020016:Activated Protein C Resistance / Q000097:blood / Q000150:complications; D000368:Aged; D000369:Aged, 80 and over; D017153:Antibodies, Anticardiolipin / Q000097:blood*; D000991:Antithrombins / Q000378:metabolism; D016893:Carotid Stenosis / Q000097:blood / Q000276:immunology* / Q000628:therapy*; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D002546:Ischemic Attack, Transient / Q000097:blood / Q000209:etiology / Q000276:immunology; D016682:Lupus Coagulation Inhibitor / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009422:Nervous System Diseases / Q000097:blood / Q000209:etiology* / Q000276:immunology*; D011446:Prospective Studies; D011486:Protein C / Q000378:metabolism; D017293:Protein S / Q000378:metabolism; D012307:Risk Factors; D015607:Stents / Q000009:adverse effects*; D020521:Stroke / Q000097:blood / Q000209:etiology / Q000276:immunology; D019851:Thrombophilia / Q000097:blood / Q000150:complications
chemical_list: D017153:Antibodies, Anticardiolipin; D000991:Antithrombins; D007074:Immunoglobulin G; D016682:Lupus Coagulation Inhibitor; D011486:Protein C; D017293:Protein S