Seetho Ian W, Parker Robert J, Craig Sonya, Duffy Nick, Hardy Kevin J, Wilding John P H
Department of Obesity and Endocrinology, University of Liverpool, Clinical Sciences Centre, University Hospital Aintree, Liverpool, UK.
Department of Respiratory Medicine, University Hospital Aintree, Liverpool, UK.
J Sleep Res. 2014 Dec;23(6):700-708. doi: 10.1111/jsr.12156. Epub 2014 Apr 15.
Obstructive sleep apnea is associated with obesity and metabolic syndrome, leading to greater cardiovascular risk. Severely obese patients with obstructive sleep apnea may still be at risk of adverse health outcomes, even without previous cardiovascular disease. Pulse wave analysis non-invasively measures peripheral pulse waveforms and derives measures of haemodynamic status, including arterial stiffness, augmentation pressure and subendocardial viability ratio. We hypothesized that the presence of obstructive sleep apnea in severe obesity, even in the absence of an antecedent history of cardiovascular disease, would affect measurements derived from pulse wave analysis. Seventy-two severely obese adult subjects [obstructive sleep apnea 47 (body mass index 42 ± 7 kg m(-2) ), without obstructive sleep apnea (non-OSA) 25 (body mass index 40 ± 5 kg m(-2) )] were characterised using anthropometric, respiratory and cardio-metabolic parameters. Groups were similar in age, body mass index and gender. More subjects with obstructive sleep apnea had metabolic syndrome [obstructive sleep apnea 60%, without obstructive sleep apnea (non-OSA) 12%]. Those with obstructive sleep apnea had greater arterial stiffness, augmentation pressure and decreased subendocardial viability ratio (all P < 0.001), with significantly higher systolic (P = 0.003), diastolic (P = 0.04) and mean arterial pressures (P = 0.004) than patients without obstructive sleep apnea (non-OSA). Arterial stiffness correlated with mean arterial blood pressure (P = 0.003) and obstructive sleep apnea severity (apnea-hypopnea index; P < 0.001). apnea-hypopnea index significantly predicted arterial stiffness in multiple regression analysis, but components of the metabolic syndrome did not. Thus, patients with obstructive sleep apnea with severe obesity have increased arterial stiffness that may potentially influence cardiovascular risk independently of metabolic abnormalities. The presence of obstructive sleep apnea in severe obesity identifies a group at high cardiovascular risk; clinicians should ensure that risk factors are managed appropriately in this group whether or not treatment of obstructive sleep apnea is offered or accepted by patients.
阻塞性睡眠呼吸暂停与肥胖和代谢综合征相关,会导致更高的心血管风险。即使没有既往心血管疾病,重度肥胖的阻塞性睡眠呼吸暂停患者仍可能面临不良健康结局的风险。脉搏波分析可无创测量外周脉搏波形,并得出血流动力学状态的指标,包括动脉僵硬度、增强压和心内膜下存活比。我们假设,即使没有心血管疾病的既往史,重度肥胖患者中存在阻塞性睡眠呼吸暂停也会影响从脉搏波分析得出的测量结果。使用人体测量、呼吸和心脏代谢参数对72名重度肥胖成年受试者[阻塞性睡眠呼吸暂停47例(体重指数42±7 kg m(-2)),无阻塞性睡眠呼吸暂停(非阻塞性睡眠呼吸暂停)25例(体重指数40±5 kg m(-2))]进行了特征分析。两组在年龄、体重指数和性别方面相似。更多阻塞性睡眠呼吸暂停患者患有代谢综合征[阻塞性睡眠呼吸暂停60%,无阻塞性睡眠呼吸暂停(非阻塞性睡眠呼吸暂停)12%]。阻塞性睡眠呼吸暂停患者的动脉僵硬度更高、增强压更高,心内膜下存活比降低(均P<0.001),收缩压(P=0.003)、舒张压(P=0.04)和平均动脉压(P=0.004)显著高于无阻塞性睡眠呼吸暂停(非阻塞性睡眠呼吸暂停)患者。动脉僵硬度与平均动脉血压(P=0.003)和阻塞性睡眠呼吸暂停严重程度(呼吸暂停低通气指数;P<0.001)相关。在多元回归分析中,呼吸暂停低通气指数显著预测动脉僵硬度,但代谢综合征的组成部分则不然。因此,重度肥胖的阻塞性睡眠呼吸暂停患者动脉僵硬度增加,这可能独立于代谢异常而潜在影响心血管风险。重度肥胖患者中存在阻塞性睡眠呼吸暂停表明这是一组心血管风险高的人群;临床医生应确保无论患者是否接受阻塞性睡眠呼吸暂停的治疗,都要对该组患者的危险因素进行适当管理。