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Effekte der nCPAP-Therapie auf die Prothrombinaktivierung bei Patienten mit obstruktivem Schlafapnoesyndrom

Effects of NCPAP therapy on prothrombin activation in patients with obstructive sleep apnoea syndrome

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Zusammenfassung

Zusammenfassung

Das obstruktive Schlafapnoesyndrom (OSAS) ist mit einem erhöhten Risiko für kardiovaskuläre Erkrankungen vergesellschaftet.

Fragestellung

In Voruntersuchungen konnte eine Prothrombinaktivierung bei unbehandelten Patienten mit OSAS nachgewiesen werden. Da diese Patienten auch andere mögliche Risikofaktoren für eine Prothrombinaktivierung aufweisen (Hypertonie, Adipositas, Diabetes mellitus, koronare Herzkrankheit), sollte geprüft werden, inwieweit allein durch eine adäquate Therapie der obstruktiven Schlafapnoe die Prothrombinaktivierung gemindert werden kann.

Patienten und Methodik

Bei allen Patienten, die mit dem Verdacht auf ein Schlafapnoesyndrom ins Schlaflabor eingewiesen wurden, wurden Prothrombinfragment 1 und 2 (F 1+2). Thrombin-Antithrombin-Komplex (TAT), Fibrinmonomer und D-Dimere nach einer diagnostischen Polysomnographie bestimmt. Es erfolgte die Einstellung auf eine nCPAP-Therapie. Nach einer 4-6wöchigen Therapiephase wurden sowohl die Schlafparameter als auch die Gerinnungswerte erneut ermittelt.

Ergebnisse

23 konsekutive Patienten (21 Männer; Alter 50,3±11,5 Jahre; BMI 31,7±5,5 kg/m2) wurden in die Untersuchung eingeschlossen. Alle Patienten wiesen ein ausgeprägtes OSAS auf (AHI 44,4±26,5/h, Entsättigungsindex 45,3±17,8/h). Die Einstellung auf eine nCPAP-Therapie war bei allen Patienten problemlos möglich und suffizient (mittlerer CPAP-Druck 7,9±0,6 mbar; Nutzung 6,3±2,1 h/Tag; AHI 3,1±2,3/h; Entsättigungsindex 2,3±1,8/h). Die F 1+2 und TAT-Werte waren bei Einschluss deutlich erhöht. Im Verlauf zeigte sich ein signifikanter Abfall (P<0,001) unter nCPAP-Therapie (F 1+2: 6,55±3,57 vs. 1,85±2,59 nmol/L; TAT: 53,1±16,4 vs. 13,6±18,5 μg/L). Fibrinmonomer und D-Dimer waren zu keinem Zeitpunkt nachweisbar.

Schlussfolgerung

OSAS-Patienten haben eine erhöhte Prothrombinaktivierung, diese wird durch eine suffizjente nCPAP-Therapie deutlich gemindert.

Summary

Summary

Obstructive sleep apnoea syndrome (OSAS) is associated with an increased risk for cardiovascular diseases.

Question of the study

Previous investigations demonstrated a prothrombin activation in patients with untreated OSAS. These patients also had additional concurrent risk factors for prothrombin activation such as hypertension, obesity, diabetes, or coronary artery disease. Therefore, this study investigated the effect of adequate therapy of OSAS on prothrombin activation.

Patients and methods

In all patients referred to the sleep laboratory with the diagnosis of OSAS after diagnostic polysomnography, levels of prothrombin fragments 1 and 2 (F 1+2), thrombin-antithrombin complex (TAT), fibrin monomer and D-dimer were measured. Patients were treated with nasal continuous positive airway pressure (nCPAP). After a treatment period of 4–6 weeks, polysomnography and the coagulation tests were repeated.

Results

Twently-three consecutive patients were included in this study (21 male; age: 50.3±11.5 years: BMI: 31.7±5.5 kg/m2). All patients had severe OSAS (AHI: 44.4±26.5/h; desaturation index: 45.3±17.8/h). Sufficient treatment with nCPAP was achieved in all patients (mean CPAP pressure: 7.9±0.6 mbar; daily usage: 6.3±2.1/h; AHI: 3.1±2.3/h: desaturation index: 2.3±1.8/h). On study-inclusion values for F1+2 and TAT were significantly increased. After treatment with nCPAP, a highly significant decrease could be demonstrated (F 1+2: 6.55±3.57 vs. 1.85±2.59; TAT: 53.1±16.4 vs. 13.6±18.5; P<0.001). Fibrin monomer and D-dimers were not detectable at increased levels at any point during the study.

Conclusions

Patients with OSAS have an increased level of prothrombin activation. This can be reduced significantly with nCPAP therapy.

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Literatur

  1. Arnulf I, Merino-Andreu M, Perrier A, Birolleau S, Similowski T, Derenne JP: Obstructive sleep apnea and venous thromboembolism. JAMA 287: 2655–2656, 2002.

    Article  PubMed  Google Scholar 

  2. Bartsch P, Welsch B, Albert M, Friedmann B, Levi M, Kruithof EKO: Balanced activation of coagulation and fibrinolysis after a 2-h triathlon. Med Sci Sports Exere 27: 1465–1470, 1995.

    CAS  Google Scholar 

  3. Bokinsky G, Miller M, Ault K, Husband P, Mitchel J: Spontaneous platelet activation and aggregation during obstructive sleep apnea and its response to therapy with nasal continuous positive airway pressure: a preliminary investigation. Chest 108: 625–630, 1995.

    PubMed  CAS  Google Scholar 

  4. Chin K, Ohi M, Kita H, Noguchi T, Otsuka N, Tsuboi T, Mishima M, Kuno K: Effects of NCPAP therapy on fibrinogen levels in obstructive sleep apnea syndrome. Am J Respir Crit Care Med 153: 1972–1976, 1996.

    PubMed  CAS  Google Scholar 

  5. Donders SHJ, Lustermans FAT, van Wersch JWJ: Prothrombin fragment 1,2 both treated and untreated hypertensive patients. Neth J Med 43: 174–178, 1993.

    PubMed  CAS  Google Scholar 

  6. Feng H, Feng H, Zhang C, Wu K, Yuan Y, Yuan H, Guan J, Wang B: Significance of the changes of platelet activation and fibrinolytic activity in patients with obstructive sleep apneahypopnea syndrome. Zhoughua Jie He He Hu Xi Za Zhi 25: 531–534, 2002.

    Google Scholar 

  7. Geiser T, Buck F, Meyer BJ, Bassetti C, Harberli A, Gugger M: In vivo platelet activation is increased during sleep in patients with obstructive sleep apnea syndrome. Respiration 69: 220–234, 2002.

    Article  Google Scholar 

  8. Hung J, Whitford EG, Parsons RW, Hillman DR: Association of sleep apnoea with myocardial infarction in men. Lancet 336: 261–264, 1990.

    Article  PubMed  CAS  Google Scholar 

  9. Lattimore JL, Celermajer DS, Wilcox I: Obstructive sleep apnea and cardiovascular disease. J Am Coll Cardiol 41: 1429–1437, 2003.

    Article  PubMed  Google Scholar 

  10. Mooe T, Franklin KA, Holmström K, Rabben T, Wiklund U: Sleep-disordered breathing and coronary artery disease. Am J Respir Crit Care Med 164: 1910–1913, 2001.

    PubMed  CAS  Google Scholar 

  11. Rangemark C, Hedner JA, Carlson JT, Gleerup G, Winther K: Platelet function and fibrinolytic activity in hypertensive and normotensive sleep apnea patients. Sleep 18: 188–194, 1995.

    PubMed  CAS  Google Scholar 

  12. Sanner BM, Konermann M, Tepel M, Groetz J, Mummenhoff C, Zidek W: Platelet function in patients with obstructive sleep apnea syndrome. Eur Respir J 16: 648–652, 2000.

    Article  PubMed  CAS  Google Scholar 

  13. Shepard JW: Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. Clin Chest Med 13: 437–458, 1992.

    PubMed  Google Scholar 

  14. Steffens C, Fiedler EA, Pelz J, Bruhn HD: Alteration of the hemostatic system during aerobic and anaerobic exercise by swimming in healthy volunteers. Ann Hematol 72: A24, 1996.

    Google Scholar 

  15. von Känel R, Dimsdale JE: Hemostatic alterations in patients with obstructive sleep apnea and the implications for cardiovascular disease. Chest 124: 1956–1967, 2003.

    Article  Google Scholar 

  16. von Känel R, Le DT, Nelsen RA, Mills PJ, Ancoli-Israel S, Dimsdale JE: The hypercoagulable state in sleep apnea is related to comorbid hypertension. J Hypertens 19: 1445–1451, 2001.

    Article  Google Scholar 

  17. Wada H, Mori Y, Kaneko T, Wakita Y, Nakase T, Minamikawa K, Ohiwa M, Tamaki S, Tanigawa M, Kageyama S, Deguchi K, Nakano T, Shirakawa S, Suzuki K: Elevated plasma levels of vascular endothelial cell markers in patients with hypercholesterolemia. Am J Hematol 44: 112–116, 1993.

    PubMed  CAS  Google Scholar 

  18. Wessendorf TE, Thilmann AF, Wang Y, Schreiber A, Konietzko N, Teschler H: Fibrinogen levels and obstructive sleep apnea in ischemic stroke. Am J Respir Crit Care Med 162: 2039–2042, 2000.

    PubMed  CAS  Google Scholar 

  19. Young T, Peppard PE, Gottlieb DJ: Epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med 165: 1217–1239, 2002.

    Article  PubMed  Google Scholar 

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Authors and Affiliations

  1. Klinik für Innere Medizin II, Städtisches Krankenhaus Martha-Maria Halle-Dölau, Röntgenstr. 1, D-06120, Halle

    Steffen Schädlich, Thomas Arndt, Thomas Blankenburg & Wolfgang Schütte

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  1. Steffen Schädlich
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  2. Thomas Arndt
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  3. Thomas Blankenburg
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  4. Wolfgang Schütte
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Correspondence to Steffen Schädlich.

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Schädlich, S., Arndt, T., Blankenburg, T. et al. Effekte der nCPAP-Therapie auf die Prothrombinaktivierung bei Patienten mit obstruktivem Schlafapnoesyndrom. Somnologie 8, 119–123 (2004). https://doi.org/10.1111/j.1439-054X.2004.00033.x

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