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Stroke Research and Treatment
Volume 2012 (2012), Article ID 945849, 7 pages
http://dx.doi.org/10.1155/2012/945849
Research Article

Fibrinolytic Activity and Platelet Function in Subjects with Obstructive Sleep Apnoea and a Patent Foramen Ovale: Is There an Option for Prevention of Ischaemic Stroke?

1Department of Neurology, University of Oulu and Oulu University Hospital, P.O. Box 25, 900029 OYS, Finland
2Department of Neurology, “A. Avogadro” University, Novara, Italy
3Department of Clinical Chemistry, Laboratory of Hematology, University of Helsinki and Helsinki University Hospital, Finland
4Department of Pharmacological Sciences, University of Tampere and Tampere University Hospital, Tampere, Finland
5Department of Neurology, Tokyo Women’s Medical University, Tokyo, Japan

Received 13 July 2012; Revised 28 September 2012; Accepted 28 September 2012

Academic Editor: Luis Castilla-Guerra

Copyright © 2012 Monica Reggiani et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Obstructive sleep apnoea (OSA) carries an increased risk of ischaemic stroke, but the underlying mechanism is not clear. As right-to-left shunting can occur through a patent foramen ovale (PFO) during periods of apnoea, we investigated nocturnal changes in fibrinolytic activity and platelet function in subjects who had OSA with or without PFO and in controls. We determined plasminogen activator inhibitor 1 (PAI-1) activity and antigen and platelet activation parameters. The severity of OSA was verified by polygraphy and PFO was detected by ear oximetry. We found a higher PAI-1 activity and antigen and a lower ratio of 2,3-dinor- to 2,3-dinor-TXB2 in the subjects with OSA than in the controls. Linear regression analysis showed the apnoea-hypopnoea index (β-coefficient, 0.499; ) and PFO (β-coefficient, 0.594; ) to be associated independently with PAI-1 activity in the morning, while the increment in PAI-1:Ag from evening to morning was significantly associated with the presence of PFO ( , ). Both OSA and PFO reduce fibrinolytic activity during nocturnal sleep. We hypothesize that subjects having both OSA and PFO may develop a more severe prothrombotic state during sleep than those having either OSA or PFO alone.