(Circulation. 1999;100:e86-e87.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Hemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK
| Introduction |
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Inappropriate platelet activation and thrombus formation are
frequent findings in many cardiovascular disorders and
are believed to have an important pathogenic role. P-selectin, the
membrane of the component of
-granule and membrane of the
Weibel-Palade body, aids the adhesion of leukocytes bearing its ligand.
Increased expression of P-selectin at the surface of the platelet,
as defined by flow cytometry, is therefore a likely marker of the
activation of these cells.1
The recent article by Minamino and colleagues2 reporting increased expression of P-selectin by platelets in subjects with atrial fibrillation (AF) is therefore in keeping with platelet activation and a prothrombotic state in AF, leading to the high risk of stroke and thromboembolism in this common condition. Nevertheless, a soluble form of P-selectin (sP-selectin) is also present in the plasma, and increasing evidence points toward elevated plasma levels among patients with thrombotic disorders, stroke, and atherosclerosis, thus providing an additional tool to study platelet activation.3 4 Similar to Minamino and colleagues,2 we hypothesised that patients with AF would have raised levels of sP-selectin.
To investigate this further, we recruited 52 consecutive patients (45
males, mean age 66 years) with chronic AF who were not taking any
antithrombotic therapy and 60 age- and sex-matched healthy controls.
sP-selectin was measured in citrated plasma by commercial ELISA (R&D
Systems). Mean±SD levels in the patients with AF were 232±181 ng/mL
compared with 161±82 ng/mL in the controls (unpaired t test
P=0.015). Like Minamino and colleagues,2
we would interpret our preliminary data showing
Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Japan
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