Effects of NCPAP therapy on fibrinogen levels in obstructive sleep apnea syndrome

被引:193
作者
Chin, K
Ohi, M
Kita, H
Noguchi, T
Otsuka, N
Tsuboi, T
Mishima, M
Kuno, K
机构
[1] Department of Clinical Physiology, Chest Disease Research Institute, Kyoto University
[2] Department of Clinical Physiology, Chest Disease Research Institute, Kyoto University, Sakyo-Ku, Kyoto 606
关键词
D O I
10.1164/ajrccm.153.6.8665063
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
In patients with obstructive sleep apnea syndrome (OSAS), the blood coagulation system may contribute to an increased risk of cardiovascular events, which occur most frequently in the morning. Nasal continuous positive airway pressure (NCPAP) treatment can improve the mortality of patients with OSAS. We measured the plasma fibrinogen concentration, which is an independent risk factor for cardiovascular events, in the afternoon (3:30 P.M.) and the next morning upon awakening (8:30 A.M.) in 11 patients with OSAS (apnea and hypopnea index > 20) before and after NCPAP therapy. We also measured the hematocrit, the C-reactive protein, and the total plasma protein at the same time. The plasma fibrinogen and hematocrit levels in the morning (298 +/- 16 mg/dl and 48.5 +/- 1.5%, mean +/- SEM) were significantly higher than on the previous afternoon (275 +/- 14 mg/dl and 46.6 +/- 1.3%) (fibrinogen, p < 0.02; hematocrit, p < 0.005). The whole blood viscosity (WBV) at a shear rate of 208 inverse seconds, which can be predicted based on the hematocrit and total plasma protein, was also significantly higher in the morning (4.98 +/- 0.20/s) than in the afternoon (4.73 +/- 0.17/s) (p < 0.005). These increases in the plasma fibrinogen concentration and the WBV in the morning disappeared after NCPAP treatment. The attenuation of morning increases in the plasma fibrinogen concentration and WBV induced by NCPAP treatment may contribute to an overall improvement in the mortality from cardiovascular events in patients with OSAS.
引用
收藏
页码:1972 / 1976
页数:5
相关论文
共 30 条
  • [1] Carlson J, 1993, BLOOD PRESSURE, V2, P166
  • [2] EHRLY A M, 1973, Biorheology, V10, P577
  • [3] ELLIS BC, 1961, J LAB CLIN MED, V58, P477
  • [4] THE SLEEP HYPOPNEA SYNDROME
    GOULD, GA
    WHYTE, KF
    RHIND, GB
    AIRLIE, MAA
    CATTERALL, JR
    SHAPIRO, CM
    DOUGLAS, NJ
    [J]. AMERICAN REVIEW OF RESPIRATORY DISEASE, 1988, 137 (04): : 895 - 898
  • [5] SLEEP APNEA SYNDROMES
    GUILLEMINAULT, C
    TILKIAN, A
    DEMENT, WC
    [J]. ANNUAL REVIEW OF MEDICINE, 1976, 27 : 465 - 484
  • [6] MORTALITY AND APNEA INDEX IN OBSTRUCTIVE SLEEP-APNEA - EXPERIENCE IN 385 MALE-PATIENTS
    HE, J
    KRYGER, MH
    ZORICK, FJ
    CONWAY, W
    ROTH, T
    [J]. CHEST, 1988, 94 (01) : 9 - 14
  • [7] OBSERVATIONS ON BLOOD-VISCOSITY CHANGES AFTER ACUTE MYOCARDIAL-INFARCTION
    JAN, KM
    CHIEN, S
    BIGGER, JT
    [J]. CIRCULATION, 1975, 51 (06) : 1079 - 1084
  • [8] FIBRINOGEN AND RISK OF CARDIOVASCULAR-DISEASE - THE FRAMINGHAM-STUDY
    KANNEL, WB
    WOLF, PA
    CASTELLI, WP
    DAGOSTINO, RB
    [J]. JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1987, 258 (09): : 1183 - 1186
  • [9] SNORING AS A RISK FACTOR FOR ISCHEMIC-HEART-DISEASE AND STROKE IN MEN
    KOSKENVUO, M
    KAPRIO, J
    TELAKIVI, T
    PARTINEN, M
    HEIKKILA, K
    SARNA, S
    [J]. BRITISH MEDICAL JOURNAL, 1987, 294 (6563) : 16 - 19
  • [10] EFFECTS OF TREATMENT WITH NASAL CONTINUOUS POSITIVE AIRWAY PRESSURE ON ATRIAL-NATRIURETIC-PEPTIDE AND ARGININE VASOPRESSIN RELEASE DURING SLEEP IN PATIENTS WITH OBSTRUCTIVE SLEEP-APNEA
    KRIEGER, J
    FOLLENIUS, M
    SFORZA, E
    BRANDENBERGER, G
    PETER, JD
    [J]. CLINICAL SCIENCE, 1991, 80 (05) : 443 - 449