title: Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque.
abstract: Defined angiographically, no-reflow (NR) manifests as an acute reduction in coronary flow in the absence of epicardial vessel obstruction. One candidate protein to cause coronary NR is tissue factor (TF), which is abundant in atherosclerotic plaque and a cofactor for activated plasma coagulation factor VII. Scrapings from atherosclerotic carotid arteries contained TF activity (corresponding to 33.03 +/- 13.00 pg/cm(2) luminal plaque surface). Active TF was sedimented, indicating that TF was associated with membranes. Coronary blood was drawn from 6 patients undergoing coronary interventions with the distal protection device PercuSurge GuardWire (Traatek, Miami, FL). Fine particulate material that was recovered from coronary blood showed TF activity (corresponding to 91.1 +/- 62.16 pg/mL authentic TF). To examine the role of TF in acute coronary NR, blood was drawn via a catheter from coronary vessels in 13 patients during NR and after restoration of flow. Mean TF antigen levels were elevated during NR (194.3 +/- 142.8 pg/mL) as compared with levels after flow restoration (73.27 +/- 31.90 pg/mL; P =.02). To dissect the effects of particulate material and purified TF on flow, selective intracoronary injection of atherosclerotic material or purified relipidated TF was performed in a porcine model. TF induced NR in the model, thus strengthening the concept that TF is causal, not just a bystander to atherosclerotic plaque material. The data suggest that active TF is released from dissected coronary atherosclerotic plaque and is one of the factors causing the NR phenomenon. Thus, blood-borne TF in the coronary circulation is a major determinant of flow.
authors.affiliation: Department of Cardiology, University of Vienna, Austria.
authors.forename: Diana
authors.initials: D
authors.lastname: Bonderman
authors.forename: Alexander
authors.initials: A
authors.lastname: Teml
authors.forename: Johannes
authors.initials: J
authors.lastname: Jakowitsch
authors.forename: Christopher
authors.initials: C
authors.lastname: Adlbrecht
authors.forename: Mariann
authors.initials: M
authors.lastname: Gyöngyösi
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Sperker
authors.forename: Harald
authors.initials: H
authors.lastname: Lass
authors.forename: Wilhelm
authors.initials: W
authors.lastname: Mosgoeller
authors.forename: Dietmar H
authors.initials: DH
authors.lastname: Glogar
authors.forename: Peter
authors.initials: P
authors.lastname: Probst
authors.forename: Gerald
authors.initials: G
authors.lastname: Maurer
authors.forename: Yale
authors.initials: Y
authors.lastname: Nemerson
authors.forename: Irene M
authors.initials: IM
authors.lastname: Lang
mesh_terms: D017130:Angioplasty / Q000009:adverse effects; D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology; D016893:Carotid Stenosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D003324:Coronary Artery Disease / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D003326:Coronary Circulation / Q000502:physiology*; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D007150:Immunohistochemistry; D007269:Injections, Intra-Arterial; D023421:Models, Animal; D015607:Stents / Q000009:adverse effects; D013552:Swine; D013925:Thromboplastin / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology*
chemical_list: D013925:Thromboplastin