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From the Department of Neurology (Drs. Eisensehr and Noachtar), University of Munich, Germany; the Department of Neurology (Dr. Ehrenberg and K. Korbett), the Clinical Study Unit (A. McAuley), the Pediatric Hematology Research Laboratory (A. Byrne), and the Department of Cardiology (Dr. Palabrica), Tufts University, Boston, MA.
Address correspondence and reprint requests to Dr. Ilonka Eisensehr, Department of Neurology, Klinikum Grosshadern, University of Munich, Marchioninistrasse 15, 81377 Munich, Germany.
Objective: There is an increased risk of patients with obstructive sleep apnea syndrome (OSAS) to have stroke or cardiac infarcts. Besides hypertension, epinephrine-induced platelet activation could be a further reason for the increased cardiovascular morbidity and mortality in OSAS.
Methods: During a 4-month period (August 1994 to December 1994) we recruited prospectively 76 patients referred for polysomnograms because of a suspected sleep disorder such as OSAS.
Results: Fifty patients had no respiratory events during sleep (non-OSAS), 19 patients had more than five but less than 50 obstructive apneas or hypopneas per hour of total sleep time (mild-to-moderate OSAS group), and seven patients had an apnea hypopnea index of more than 50 per hour of total sleep time (severe OSAS group). Blood pressure, plasma epinephrine levels, and P-selectin expression (as a marker for platelet activation) were measured in every patient at 9 PM and 6 AM (before and after the polysomnogram). There was a significant correlation of the apnea hypopnea index with 9 PM and 6 AM systolic and diastolic blood pressure, with 9 PM platelet activation, and with 6 AM epinephrine levels mainly due to high values in the severe OSAS group.
Conclusions: Our results suggest that platelet activation, epinephrine, and high blood pressure play a role in the high prevalence of cerebrovascular and cardiovascular events in patients with OSAS.
Supported by grants from the General Clinical Research Center, New England Medical Center, and Tufts University at Boston.
Received September 3, 1997. Accepted in final form March 8, 1998.
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