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目的分析呼吸睡眠暂停低通气综合征(SAHS)对冠心病患者糖脂代谢及血清胆红素水平的影响,以期进一步揭示SAHS促冠心病发病的机制。方法选择2013年12月至2016年12月于宝鸡市中心医院老年心脑血管科就诊的136例冠心病患者作为研究对象,按照是否并发SAHS,分为合并SAHS组(94例)和非SAHS组(42例),进一步根据SAHS的严重程度,分为重度SAHS组(37例)、中度SAHS组(32例)和轻度SAHS组(25例)。比较入组患者的睡眠呼吸指标、糖脂代谢水平及血清胆红素水平。用SPSS 18.0统计软件进行方差分析,两两比较采用SNK-q检验,应用Pearson法进行相关性分析。结果冠心病合并中度、重度SAHS患者空腹血糖(FPG)、餐后2 h血糖(2 hPG)、胰岛素抵抗指数(HOMAIR)、糖化血红蛋白(HbA_(1C))和氧化低密度脂蛋白胆固醇(ox-LDL-C)均明显高于合并轻度SAHS组和非SAHS组患者,合并重度SAHS患者上述指标水平均明显高于合并中度SAHS患者,差异均有统计学意义(P<0.05),与非SAHS组比较,合并轻度SAHS组患者FPG、2 hPG、HOMA-IR、HbA_(1C)和ox-LDL-C水平差异均无统计学意义(P>0.05)。冠心病合并中度、重度SAHS患者血清中总胆红素(TBIL)、间接胆红素(IBIL)水平均明显低于合并轻度SAHS组和非SAHS组患者,合并重度SAHS组患者的上述指标均明显低于合并中度SAHS组患者,差异均有统计学意义(P<0.05),合并轻度SAHS组患者血清中TBIL、IBIL水平与非SAHS组比较,差异均无统计学意义(P>0.05)。相关性分析结果显示,呼吸暂停低通气指数(AHI)与FPG、2 hPG、HbA_(1C)、HOMA-IR和ox-LDL-C均呈明显的正相关(r值分别为0.976、0.986、0.986、0.987和0.960,P<0.01),夜间最低血氧饱和度(LO2)与FPG、2 hPG、HbA_(1C)、HOMA-IR和ox-LDL-C均呈明显的负相关(r值分别为-0.939、-0.976、-0.957、-0.986和-0.913,P<0.01),而AHI和LO2与TBIL、IBIL无明显的相关关系(P>0.05)。结论 SAHS合并冠心病患者普遍存在糖脂代谢及血清胆红素水平异常,这可能是SAHS促冠心病发病的机制。
Objective To analyze the effect of respiration sleep apnea-hypopnea syndrome (SAHS) on glucose and lipid metabolism and serum bilirubin levels in patients with coronary heart disease, in order to further reveal the mechanism of SAHS in promoting coronary heart disease. Methods From Dec 2013 to Dec 2016, 136 patients with coronary heart disease in Baoji Central Hospital were enrolled in this study. Patients were divided into SAHS group (94 cases) and non-SAHS group (42 cases). According to the severity of SAHS, the patients were divided into severe SAHS group (37 cases), moderate SAHS group (32 cases) and mild SAHS group (25 cases). The breathing index, glucose and lipid metabolism and serum bilirubin level were compared between the two groups. ANOVA was performed with SPSS 18.0 statistical software, SNK-q test was used in each comparison, and Pearson’s method was used to analyze the correlation. Results Fasting plasma glucose (FPG), postprandial 2h blood glucose (2hPG), insulin resistance index (HOMAIR), glycosylated hemoglobin (HbA 1c) and ox-LDL were significantly increased in patients with coronary heart disease complicated with moderate- -LDL-C) were significantly higher than those in patients with mild SAHS and non-SAHS. The above indexes in patients with severe SAHS were significantly higher than those with moderate SAHS (P <0.05), and The levels of FPG, 2 hPG, HOMA-IR, HbA 1 C and ox-LDL-C in patients with mild SAHS were not significantly different (all P> 0.05). Serum levels of total bilirubin (TBIL) and indirect bilirubin (IBIL) in patients with coronary heart disease complicated with moderate and severe SAHS were significantly lower than those in patients with mild SAHS and non-SAHS, and those in patients with severe SAHS (P <0.05). The levels of serum TBIL and IBIL in patients with mild SAHS were not significantly different from those in non-SAHS patients (P> 0.05). Correlation analysis showed that the apnea hypopnea index (AHI) was positively correlated with FPG, 2 hPG, HbA 1 C, HOMA-IR and ox-LDL C (r values were 0.976, 0.986 and 0.986 , 0.987 and 0.960, respectively, P <0.01). The nighttime lowest oxygen saturation (LO2) was significantly negatively correlated with FPG, 2 hPG, HbA1C, HOMA-IR and ox-LDL- -0.939, -0.976, -0.957, -0.986 and -0.913, P <0.01). However, there was no significant correlation between AHI and LO2 and TBIL and IBIL (P> 0.05). Conclusions The prevalence of dyslipidemia and serum bilirubin levels in SAHS patients with coronary heart disease may be the mechanism of SAHS in promoting coronary heart disease.