Platelet activation in patients with obstructive sleep apnea syndrome and effects of nasal-continuous positive airway pressure

被引用文献3件
  • SHIMIZU M
    Department of Laboratory Medicine, Tokai University School of Medicine
  • KAMIO Kazutaka
    Department of Pulmonary Medicine, Tokai University School of Medicine
  • HAIDA Munetaka
    Department of Physiology, Tokai University School of Medicine
  • ONO Yoshiaki
    Department of Pulmonary Medicine, Tokai University School of Medicine
  • MIYACHI Hayato
    Department of Laboratory Medicine, Tokai University School of Medicine
  • YAMAMOTO Masahiro
    Department of Neurology,Tokai University School of Medicine Yokohama Stroke and Brain Center
  • SHINOHARA Yukito
    Department of Neurology, Tokai University School of Medicine
  • ANDO Yasuhiko
    Department of Laboratory Medicine, Tokai University School of Medicine

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Objective: Our study was undertaken to determine whether increased platelet activation occurs in patients with obstructive sleep apnea syndrome (OSAS) and whether a therapy with nasal-continuous positive airway pressure (N-CPAP) alters this activation. Methods: We measured the positive rate of activated platelets using activation-dependent monoclonal antibodies (MoAb) and flow cytometry in whole blood from 94 patients with OSAS, and from 31 age-matched controls. Thrombotic vascular diseases were surveyed as a background of alternative of platelet activation. Results: The positive rate for activated platelets was significantly higher in patients with OSAS (PAC1 52.6±22.9%, CD62P 6.8±7.1%, mean±SD), as compared with healthy control subjects (PAC1 16.7±8.6%, CD62P 0.7±0.5%, p<0.001). The activation indexes were significantly reduced after 1 month with N-CPAP treatment as a whole (PAC1; from 52.6±22.9 to 44.2±22.4, p<0.05, CD62P; from 6.8±7.1 to 5.3±5.5, p<0.05). In nearly 60% of patients, platelets activation remained high despite significant improvement of sleep apnea-episodes after N-CPAP. These patients had significantly higher incidence of previous myocardial infarction and/or cerebral infarction and abnormalities of head MRI and carotid sonograpy; indicating that the platelet activation appears to be induced by existing atheroma plaque and not by sympathetic activity in OSAS. Conclusion: In conclusion, patients with OSAS have increased percentages of activated platelets as assessed by flow cytometrical analysis of activation dependent surface markers, and were divided into two groups, one group with response to N-CPAP treatment in the reduction of platelet activation and the other without. One possible reason of no response to N-CPAP treatment in the reduction of platelet activation was suggested to be thrombotic diseases.

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