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英文作者:Wei Yuxuan Cheng Wenli
单位:首都医科大学附属北京安贞医院心内高血压中心二区,北京100029
英文单位:Second Ward Hypertension Center Department of Cardiology Beijing Anzhen Hospital Capital Medical University Beijing 100029 China
关键词:高血压;阻塞性睡眠呼吸暂停;淋巴细胞与高密度脂蛋白胆固醇比值
英文关键词:Hypertension;Obstructivesleepapnea;Lymphocytetohigh-densitylipoproteincholesterolratio
目的 探讨淋巴细胞与高密度脂蛋白胆固醇比值(LHR)和高血压患者合并阻塞性睡眠呼吸暂停(OSA)严重程度的相关性。方法 回顾性纳入2018年1月至2019年1月于首都医科大学附属北京安贞医院高血压中心连续住院并接受多导睡眠监测的446例高血压患者。根据呼吸暂停低通气指数(AHI)将患者分为4组:无OSA组(AHI<5次/h,112例)、轻度OSA组(AHI 5~<15次/h,111例)、中度OSA组(AHI 15~<30次/h,112例)及重度OSA组(AHI≥30次/h,111例)。采用多因素有序Logistic回归及限制性立方样条分析LHR与OSA严重程度的关系。采用受试者工作特征曲线评价LHR及高敏C反应蛋白(hs-CRP)对不同OSA严重程度的区分效能,配对DeLong检验比较两者曲线下面积(AUC)。最后进行亚组分析。结果 无、轻度、中度和重度OSA组LHR分别为1.5(1.2,2.0)、1.6(1.2,2.0)、1.6(1.3,2.1)、2.0(1.5,2.5)(P<0.001)。充分调整混杂因素后,LHR仍与OSA严重程度独立相关(比值比=1.439,95%置信区间:1.131~1.747,P=0.021),且呈线性关系。LHR识别任意OSA、中重度OSA和重度OSA的AUC分别为0.594、0.627和0.653,与hs-CRP相比差异均无统计学意义(均P>0.05)。冠心病(冠状动脉粥样硬化性心脏病)史和诊室舒张压对该关联存在交互作用(交互P值分别为<0.01和0.04)。结论 LHR升高与高血压患者OSA严重程度增加独立相关,但该单指标区分效能有限且未优于hs-CRP,可作为OSA严重程度辅助风险分层指标,但仍需前瞻性多中心研究验证。
Objective To explore the correlation between lymphocyte to high-density lipoprotein cholesterol ratio (LHR) and the severity of obstructive sleep apnea (OSA) in hypertensive patients. Methods A total of 446 consecutive hypertensive patients hospitalized and receiving polysomnography at the hypertension center of Beijing Anzhen Hospital, Capital Medical University from January 2018 to January 2019 were retrospectively enrolled. Patients were divided into four groups according to apnea-hypopnea index (AHI): non-OSA group (AHI<5 events/h, 112 cases), mild OSA group (AHI 5-<15 events/h, 111 cases), moderate OSA group (AHI 15-<30 events/h, 112 cases) and severe OSA group (AHI≥30 events/h, 111 cases). Multivariate ordered Logistic regression and restricted cubic spline analysis were used to analyze the relationship between LHR and OSA severity. Receiver operating characteristic curves were adopted to evaluate the discriminatory performance of LHR and high-sensitivity C-reactive protein (hs-CRP) for different OSA severities, and paired DeLong test was applied to compare their area under the curve (AUC). Subgroup analyses were finally conducted. Results The LHR values of the non-OSA, mild OSA, moderate OSA and severe OSA groups were 1.5(1.2, 2.0), 1.6(1.2, 2.0), 1.6(1.3, 2.1) and 2.0(1.5, 2.5), respectively (P<0.001). After full adjustment for confounding factors, LHR remained independently correlated with OSA severity (odds ratio=1.439, 95% confidence interval: 1.131-1.747, P=0.021) with a linear correlation. The AUCs of LHR for identifying any OSA, moderate-to-severe OSA and severe OSA were 0.594, 0.627 and 0.653, respectively, with no statistically significant differences compared with hs-CRP (all P>0.05). History of coronary atherosclerotic heart disease and office diastolic blood pressure had interactive effects on this correlation (P for interaction <0.01 and 0.04, respectively). Conclusion Elevated LHR is independently associated with increased OSA severity in hypertensive patients. However, this single-indicator discriminatory power is limited and not superior to hs-CRP. LHR can serve as an auxiliary risk stratification marker for OSA severity, which still needs verification by prospective multicenter studies.
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