Sleep Heart Health Study (SHHS-BioLINCC)

<u style="">Accessing Data </u><br>Please refer to the "Authorized Access" section below regarding accessing data through the BioData Catalyst ecosystem. The data from this accession is not available for download through dbGaP.

<u>Related Studies</u><br>Parent cohort phenotype data can be accessed through ARIC-BioLINCC, Framingham-BioLINCC, and CHS-BioLINCC.

<u>Objectives </u><br>To determine the cardiovascular and other consequences of sleep-disordered breathing and to test whether sleep-disordered breathing is associated with an increased risk of coronary heart disease, stroke, all-cause mortality and hypertension by examining subjects from well-characterized and established epidemiologic cohorts.

<u>Background </u><br>Obstructive sleep apnea syndrome (OSA) is a potentially debilitating condition characterized by repetitive episodes of apnea while asleep, nocturnal oxygen desaturation, excessive daytime sleepiness, and loud disruptive snoring. Epidemiologic data from middle-aged adults indicate that OSA is common, with prevalence rates of 4% in men and 2% in women. Prior studies implicated OSA as a risk factor for the development of hypertension, ischemic heart disease, congestive heart failure, stroke and consequently premature death. Questions arose as to whether an increased propensity for cardiovascular and cerebrovascular diseases was limited to only those with frank OSA or whether more subtle forms of sleep-disordered breathing (SDB) would also confer elevated risk. Further evidence was also needed to clarify whether, SDB, including OSA, is an independent risk factor for the development of cardiovascular or cerebrovascular disease. Known cardiovascular and cerebrovascular disease risk factors such as obesity and smoking are commonly present in those with SDB; therefore, apparent associations between SDB and cardiovascular and cerebrovascular diseases may have resulted from the effects of these concomitant risk factors. Moreover, there was no understanding as to whether such factors as race, age, gender, and prevalent cardiovascular or cerebrovascular disease might interact with SDB to alter future cardiovascular and cerebrovascular disease risk. Mechanisms underlying any propensity to develop cardiovascular or cerebrovascular disease with SDB had not been firmly established (Quan, et al., 1997, PMID: [9493915](https://pubmed.ncbi.nlm.nih.gov/9493915/)).

<u>Participants </u><br>Participants in SHHS were recruited from nine existing NHLBI epidemiological studies in which data on cardiovascular risk factors had been collected previously. The &#8220;parent&#8221; cohorts included:
- Two sites of the Atherosclerosis Risk in Communities Study (ARIC) - Three sites of the Cardiovascular Health Study (CHS) - The Framingham Offspring Cohort - The Strong Heart Study (SHS) sites in South Dakota, Oklahoma, and Arizona - The New York Hypertension Cohorts - The Tucson Epidemiologic Study of Airways Obstructive Diseases and the Health and Environment Study
From these parent cohorts, a sample of participants who met the inclusion criteria (age 40 years or older; no history of treatment of sleep apnea; no tracheostomy; no current home oxygen therapy) was invited to participate in the baseline examination of the SHHS, which included an initial polysomnogram (SHHS-1). Several cohorts over-sampled snorers in order to increase the study-wide prevalence of sleep-disordered breathing. In all, 6441 individuals were enrolled between November 1, 1995 and January 31, 1998.

During exam cycle 3 (January 2001-June 2003), a second polysomnogram (SHHS-2) was obtained in 3295 of the participants.

Due to sovereignty issues, Strong Heart Study participants are not included in the shared SHHS data. Data from a total of 5839 participants (1920 ARIC, 1249 CHS, 997 Framingham Offspring and OMNI 1, and 1673 from other studies), consenting to share data are available.

<u>Design </u><br>The Sleep Heart Health Study added in-home polysomnography to the data collected in each of the parent studies at a baseline SHHS exam and a follow-up approximately 4 years later. Using the Compumedics PS polysomnograph, sleep studies were obtained in an unattended setting, usually in the homes of the participants, by trained and certified technicians. The recording montage consisted of:
- C3/A2 and C4/A1 EEGs, sampled at 125 Hz - right and left electrooculograms (EOGs), sampled at 50 Hz - a bipolar submental electromyogram (EMG), sampled at 125 Hz - thoracic and abdominal excursions (THOR and ABDO), recorded by inductive plethysmography bands and sampled at 10 Hz - "airflow" detected by a nasal-oral thermocouple (Protec, Woodinville, WA), sampled at 10 Hz - finger-tip pulse oximetry (Nonin, Minneapolis, MN) sampled at 1 Hz - ECG from a bipolar lead, sampled at 125 Hz for most SHHS-1 studies and 250 Hz for SHHS-2 studies - Heart rate (PR) derived from the ECG and sampled at 1 Hz - body position (using a mercury gauge sensor) - ambient light (on/off, by a light sensor secured to the recording garment)
This montage provides data on the occurrence of sleep-disordered breathing, sleep stages, heart rate, oximetry and on arousals. Each participant in the parent studies was also asked to complete the Sleep Habits Questionnaire which covers usual sleep pattern, snoring, and sleepiness.

数据获取
请参阅下文的「授权访问」章节，了解如何通过BioData Catalyst生态系统（BioData Catalyst ecosystem）获取本数据集的数据。本入组数据无法通过基因型表型数据库（database of Genotypes and Phenotypes, dbGaP）下载。

相关研究
亲本队列的表型数据可通过ARIC-BioLINCC、Framingham-BioLINCC以及CHS-BioLINCC获取。

研究目标
本研究旨在明确睡眠呼吸紊乱（sleep-disordered breathing, SDB）对心血管系统及其他器官系统的影响，并通过对特征明确的成熟流行病学队列对象开展研究，验证睡眠呼吸紊乱是否与冠心病、脑卒中、全因死亡率及高血压的发病风险升高存在关联。

研究背景
阻塞性睡眠呼吸暂停综合征（Obstructive sleep apnea syndrome, OSA）是一种可能导致机体衰弱的疾病，其特征为睡眠期间反复出现呼吸暂停、夜间血氧饱和度下降、日间过度嗜睡以及响亮且干扰他人的打鼾声。针对中年成年人的流行病学数据显示，阻塞性睡眠呼吸暂停综合征患病率较高，男性患病率为4%，女性为2%。既往研究已证实，阻塞性睡眠呼吸暂停综合征是高血压、缺血性心脏病、充血性心力衰竭、脑卒中乃至过早死亡的危险因素。然而目前仍存在若干疑问：心血管及脑血管疾病的发病风险升高是否仅局限于确诊的阻塞性睡眠呼吸暂停综合征患者？更为隐匿的睡眠呼吸紊乱是否也会增加发病风险？此外，仍需更多证据明确包括阻塞性睡眠呼吸暂停综合征在内的睡眠呼吸紊乱是否为心血管及脑血管疾病的独立危险因素。睡眠呼吸紊乱患者常合并肥胖、吸烟等已知的心血管及脑血管疾病危险因素，因此睡眠呼吸紊乱与心血管、脑血管疾病之间的表观关联可能源于这些共存危险因素的影响。此外，目前尚不清楚种族、年龄、性别以及已存在的心血管或脑血管疾病是否会与睡眠呼吸紊乱相互作用，进而改变未来心血管及脑血管疾病的发病风险。睡眠呼吸紊乱引发心血管及脑血管疾病的潜在机制尚未明确（Quan等人，1997年，PubMed唯一标识符（PubMed ID, PMID）：[9493915](https://pubmed.ncbi.nlm.nih.gov/9493915/)）。

研究对象
睡眠心脏健康研究（Sleep Heart Health Study, SHHS）的研究对象招募自9项已有的美国国家心肺血液研究所（National Heart, Lung, and Blood Institute, NHLBI）流行病学研究，上述研究此前已收集了心血管危险因素相关数据。本次研究的「亲本」队列包括：
- 社区动脉粥样硬化风险研究（Atherosclerosis Risk in Communities Study, ARIC）的2个研究中心
- 心血管健康研究（Cardiovascular Health Study, CHS）的3个研究中心
- 弗雷明汉后代队列（Framingham Offspring Cohort）
- 南达科他州、俄克拉荷马州及亚利桑那州的强心脏研究（Strong Heart Study, SHS）研究中心
- 纽约高血压队列
- 图森气道阻塞性疾病流行病学研究及健康与环境研究

从上述亲本队列中，我们邀请符合纳入标准的研究对象参与睡眠心脏健康研究的基线检查：年龄≥40岁；无睡眠呼吸暂停治疗史；未接受气管造口术；当前未进行家庭氧疗。本次基线检查包含首次多导睡眠图（polysomnogram, SHHS-1）检测。部分队列对打鼾者进行了过度抽样，以提高全研究范围内睡眠呼吸紊乱的患病率。最终，共有6441名研究对象于1995年11月1日至1998年1月31日期间入组。

在第3次检查周期（2001年1月-2003年6月）中，3295名研究对象接受了第二次多导睡眠图检测（SHHS-2）。

由于主权问题，强心脏研究的研究对象未被纳入共享的睡眠心脏健康研究数据中。目前共有5839名同意共享数据的研究对象的可用数据，其中包括1920名社区动脉粥样硬化风险研究对象、1249名心血管健康研究对象、997名弗雷明汉后代及OMNI 1队列研究对象，以及来自其他研究的1673名研究对象。

研究设计
睡眠心脏健康研究在基线检查及约4年后的随访检查中，为每项亲本研究收集的数据增加了家庭多导睡眠图检测。研究采用Compumedics PS多导睡眠记录仪，由经过培训并获得资质的技术人员在无人值守的环境中（通常为研究对象家中）完成睡眠监测。监测导联包括：
- C3/A2及C4/A1脑电图（electroencephalogram, EEG），采样频率为125 Hz
- 右眼及左眼眼电图（electrooculogram, EOG），采样频率为50 Hz
- 双极颏下肌电图（electromyogram, EMG），采样频率为125 Hz
- 胸部及腹部运动幅度（THOR及ABDO），通过感应体积描记法导联带记录，采样频率为10 Hz
- 经鼻-口腔热电偶（Protec，美国华盛顿州伍丁维尔市）检测的「气流」信号，采样频率为10 Hz
- 指尖脉搏血氧饱和度监测（Nonin，美国明尼阿波利斯市），采样频率为1 Hz
- 双极导联心电图（electrocardiogram, ECG），SHHS-1检测的采样频率多为125 Hz，SHHS-2检测的采样频率为250 Hz
- 由心电图衍生的心率（PR），采样频率为1 Hz
- 体位监测（采用水银应变计传感器）
- 环境光线监测（通过固定于记录服装上的光线传感器检测光线通断）

上述监测导联可采集睡眠呼吸紊乱、睡眠分期、心率、血氧饱和度及觉醒相关的数据。所有亲本队列的研究对象均需填写《睡眠习惯问卷》，问卷内容涵盖日常睡眠模式、打鼾情况及嗜睡程度。