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Blood, 1 November 2001, Vol. 98, No. 9, pp. 2726-2729
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Thrombogenic potential of human coronary atherosclerotic
plaques
Diego Ardissino,
Piera
Angelica Merlini,
Kenneth A. Bauer,
Ezio Bramucci,
Maurizio Ferrario,
Raffaella Coppola,
Raffaela Fetiveau,
Stefano Lucreziotti,
Robert D. Rosenberg, and
Pier Mannuccio Mannucci
From the Division of Cardiology, Ospedale Maggiore and
University of Parma, Italy; Angelo Bianchi Bonomi Hemophilia and
Thrombosis Center, IRCCS, Maggiore Hospital, University of Milan,
Italy; Division of Cardiology, Ospedale Niguarda, Milan; Division of
Cardiology, IRCCS, Policlinico San Matteo, Pavia, Italy; Division of
Cardiology, Ospedale Legnano, Italy; Charles A. Dana Research
Institute, Department of Medicine, Beth Israel Deaconess Medical Center
and Harvard Medical School; and Department of Biology, Massachusetts
Institute of Technology, Cambridge, MA.
Higher levels of tissue factor (the initiator of blood coagulation)
have been found in coronary atherosclerotic plaques of patients with
unstable coronary artery disease, but it is not established whether
they are associated with a different thrombotic response to in vivo
plaque rupture. In 40 patients undergoing directional coronary
atherectomy, prothrombin fragment 1 + 2, a marker of thrombin
generation, was measured in intracoronary blood samples obtained
proximally and distally to the coronary atherosclerotic plaque before
and after the procedure. Before the procedure, plasma prothrombin
fragment 1 + 2 levels were significantly increased across the lesion
in patients with unstable, but not in those with stable, coronary
disease (unstable, median increase, 0.37 nM; range,  0.35-1.16 nM)
(stable, median increase, 0.065 nM; range, 0.58-1.06 nM)
(P = .0021). After plaque removal, an increase in
prothrombin fragment 1 + 2 across the lesion was observed only in patients with unstable coronary disease (unstable, median increase, 0.25 nM; range, 1.04-4.9 nM) (stable, 0.01 nM; range, 0.48-3.59 nM) (P = .036)]. There was a correlation
between the tissue factor content of the plaque and the increase in
thrombin generation across the lesion ( = 0.33;
P = .038). The higher tissue factor content found in
plaques obtained from patients with unstable coronary disease was
associated with a local increase in thrombin generation, thus
suggesting a link with the in vivo thrombogenicity of the plaque.
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