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Blood, 15 April 2002, Vol. 99, No. 8, pp. 2794-2800
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Coronary no-reflow is caused by shedding of active tissue factor
from dissected atherosclerotic plaque
Diana Bonderman,
Alexander Teml,
Johannes Jakowitsch,
Christopher Adlbrecht,
Mariann Gyöngyösi,
Wolfgang Sperker,
Harald Lass,
Wilhelm Mosgoeller,
Dietmar H. Glogar,
Peter Probst,
Gerald Maurer,
Yale Nemerson, and
Irene M. Lang
From the Department of Cardiology, University of
Vienna; the Ludwig Boltzmann Institute for Cardiovascular Research; the
Institute for Molecular Oncology, Vienna, Austria; and the Mount Sinai
School of Medicine, New York, NY.
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/cm2 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.
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