Clinical Research Studies
Platelet activation is increased in peripheral arterial disease
K. Cassar, MD, FRCS(Ed)a
P. Bachoo, FRCS(Gen Surg)
I. Ford, PhDc
M. Greaves, MD, FRCP, FRCPath
J. Brittenden, MD, FRCS(Gen Surg)
Abstract
Objective: Platelet activation was assessed in patients with peripheral arterial disease compared with healthy control subjects.
Methods
This prospective comparative study included 100 subjects: 40 consecutive patients with intermittent claudication, 20 consecutive patients with critical ischemia and tissue loss, and 40 healthy control subjects. Whole blood flow cytometric analysis was performed to determine resting and stimulated platelet P-selectin expression and resting and stimulated platelet fibrinogen binding. Results are presented as platelet percentage and also as mean fluorescence intensity.
Results
P-selectin expression was significantly increased in patients with intermittent claudication (median, 0.85%; range, 0.31%-4.77%; P = .023) and critical ischemia (median, 1.11%; range, 0.2%-3.26%; P = .028) compared with control subjects (median, 0.59%; range, 0.16%-4.58%). The percentage of platelets binding fibrinogen was also significantly higher in patients with intermittent claudication (median, 2.89%; range, 1.08%-9.59%; P < .001) compared with control subjects (median, 1.57%; range, 0.17%-10.7%). There was no significant difference in percentage of platelet fibrinogen binding between control subjects and patients with critical ischemia. Fibrinogen binding by stimulated platelets was significantly diminished in patients with critical limb ischemia compared with control subjects (67.2% vs 77.9%; P = .006).
Conclusions
Platelet activation is increased in patients with peripheral arterial disease, suggesting an underlying prothrombotic state. Platelets from patients with critical limb ischemia are less responsive to in vitro stimulation.
Publishing and Reprint Information
Department of Vascular SurgeryAberdeen, Scotland, United Kingdom
Department of Medicine and Therapeutics, University of Aberdeen, Aberdeen, Scotland, United Kingdom
Vascular Unit, United Kingdom
Competition of interest: none.
*Reprint requests: K. Cassar, MD, Ward 36, Vascular Unit, Aberdeen Royal Infirmary, Foresterhill, Aberdeen AB25 2ZN, Scotland, United Kingdom.; Email:
k.cassar@abdn.ac.uk
Submitted October 29, 2002.
Accepted on December 19, 2002.
Copyright © 2003 by The Society for Vascular Surgery and The American Association for Vascular Surgery
doi:10.1016/S0741-5214(03)00129-0
You are currently accessing this Site as a guest. Please login or register by clicking Here
Linear Mode
