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Objective To observe the elderly with obstructive sleep apnea hypopnea syndrome (Obstructive Sleep Apnea-Hypopnea Syndrome OSAHS) platelet function in patients with the situation, as well as blood pressure, electrocardiogram, and carotid intima-media thickness, to explore the relationship between OSAHS and cardiovascular disease. To October 2008 to September 2010 in our hospital south tower hospitalized the night snoring elderly patients 101 people, aged 50-94 (73.88 ± 12.32) years of age as the research object, using polysomnography breathing apparatus (PSG) sleep monitoring, divided into three groups based on the results (sleep apnea hypopnea index AHI ≤ 5 times / h) in 26 cases, mild OSAHS (AHI 5-20 / h) 30 cases, moderate OSAHS group (AHI 20 - 40 / h), 23 cases of severe OSAHS group (AHI ≥ 40 times / h) 22 cases. Test the next morning fasting repose comprehensive biochemical tests, venous blood line, automated blood cell analysis instrument line blood tests, blood coagulation analyzer meter line coagulation indicators check, the Bank of the Thromboelastography 53 blood samples Bank detection, 36 blood samples flow cytometry. Of which 67 underwent 24-hour ambulatory blood pressure and Holter. 79 routine ultrasound carotid intima-media thickness. Results with increasing age, the incidence and severity of with OSAHS increases, the difference was statistically significant. Control group with varying degrees OSAHS group were not statistically different in the body mass index, total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol and other indicators. Control group with different degrees the OSAHS group in platelet count, platelet distribution width and platelet than plot differences were not statistically different. Varying degrees OSAHS group mean platelet volume was significantly higher than the control group (10.97 ± 1.22,10.91 ± 1.37,11.34 ± 1.44vs10.05 ± 1.07, P = 0.014). Mean platelet volume after controlling for age and AHI positively correlated (r = 0.2673) (P = 0.007). With the increase in the severity of OSAHS, thrombin time (TT), plasma prothrombin time (PT), activated partial thromboplastin time (APTT) indicators shortened, but only severe OSAHS group in TT (15.71 ± 1.35 vs16.59 ± 1.27 P lt; 0.05) and APTT (33.95 ± 3.33vs37.07 ± 4.67P lt; 0.05) was significantly shorter than that in the control group. Varying degrees OSAHS group and the control group (0.40 ± 0.18,0.78 ± 0.56,0.93 ± 0.76vs0.28 ± 0.14P lt; 0.05) and fibrinogen D-dimer (3.14 ± 0.65,3.34 ± 0.69,3.51 ± 0.76vs2.83 ± 0.62 P lt; 0.05) relatively significantly increased. In varying degrees OSAHS group and the control group, platelet chart parameters, R, reaction time, severe OSAHS group than in the control group and reduce mild OSAHS group (4.91 ± 1.67,5.02 ± 2.17vs7.39 ± 1.96,6.72 ± 1.34P lt; 0.05), mild OSAHS group than in the control group, although reducing, but the difference was not significant. R time end-to-tracings rate of 20mm required the K groups OSAHS significantly lower than the control group (2.09 ± 0.78,2.01 ± 0.60,1.33 ± 0.44vs2.91 ± 0.97P lt; 0.05). MA maximum amplitude in the severe OSAHS group increased compared with the control group and the mild OSAHS group (62.46 ± 5.48,64.60 ± 4.75 vs55.23 ± 8.04,59.15 ± 5.10 P lt; 0.05), mild OSAHS group than in the control group increased, but the difference was not significant. Flow cytometry platelet surface glycoprotein found that the the OSAHS group with the control group in the PAC-1 (57.42 ± 19.80,54.72 ± 21.14,57.86 ± 24.49vs24.46 ± 6.33 P lt; 0.05) and CD62P (23.30 ± 10.30,39.51 ± 17.65,44.00 ± 20.37vs8.19 ± 3.77 P lt; 0.05) expression was significantly increased, while there was no significant difference in CD148. Control group with varying degrees OSAHS group at 24h average diastolic blood pressure, mean diastolic blood pressure of day and night as well as daytime mean arterial pressure differences were not statistically significant. The average systolic blood pressure of severe OSAHS group 24h, daytime and nighttime systolic blood pressure, and 24h pulse pressure, daytime and nighttime pulse pressure compared with the control group, mild, moderate OSAHS group was significantly higher (P lt; 0.05). The OSAHS group of varying degrees of non-dipper-shaped blood pressure increased incidence compared with the control group, a statistically significant difference. Non-dipper-shaped blood pressure group than in the scoop-shaped blood pressure group CD62P (32.20 ± 19.94vs16.59 ± 14.94 P lt; 0.05) and PAC-1 (53.37 ± 22.48vs35.30 ± 20.89 P lt; 0.05) expression was significantly higher. The OSAHS group of various arrhythmias and ST-T changes occurred compared with the control group significantly increased. Mean carotid intima-media thickness with OSAHS severity, AHI positive correlation, negative correlation with the lowest SaO2, a statistically significant difference. Conclusions Elderly patients with OSAHS platelets on physical characteristics, functional status has changed, and with sleep apnea hypopnea severity, platelet activation and secretion of inflammatory cytokines capacity energizing mouth. Increased the OSAHS influence arterial blood pressure of elderly patients, in systolic blood pressure and pulse pressure affect more significantly, caused by the change of the circadian rhythm of blood at the same time, more emphasis on platelet activation. The OSAHS lead to a variety of arrhythmias and ST-T changes, but also caused an increase in the carotid intima-media thickness, are prompted OSAHS may be risk factors for vascular disease.
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