Healthy Brain Aging and Sleep Center Department of Psychiatry New York University Langone Medical Center New York City NY.
Division of Brain Aging Department of Psychiatry New York University Grossman School of Medicine New York City NY.
J Am Heart Assoc. 2024 Aug 6;13(15):e034079. doi: 10.1161/JAHA.123.034079. Epub 2024 Jul 26.
Although related, the precise mechanisms linking obstructive sleep apnea (OSA) and cardiovascular disease (CVD) are unclear. Platelets are mediators of CVD risk and thrombosis and prior studies suggested associations of OSA and platelet activity. The aim of this study is to assess the link between OSA, platelet activity, and CVD-related risk factors.
We studied the association of OSA-measures and platelet aggregation in participants dually enrolled in the SHHS (Sleep Heart and Health Study) and FHS (Framingham Heart Study). We applied linear regression models with adjustment for demographic and clinical covariates and explored interactions with OSA and CVD-related factors, including age, sex, body mass index, hypertension, OSA diagnosis (apnea-hypopnea index 4%≥5), and aspirin use. Our final sample was of 482 participants (60 years [14.00], 50.4% female). No associations were observed between apnea-hypopnea index 4% and platelet aggregation in the main sample. Stratified analysis revealed an association in aspirin users (n=65) for our primary exposure (apnea-hypopnea index 4%, β=0.523; <0.001; n=65), and secondary exposures: hypoxic burden (β=0.358; <0.001), minimum saturation (β=-0.519; =0.026), and oxygen desaturation index 3% (β=74.672; =0.002). No associations were detected in nonaspirin users (n=417).
No associations were detected between OSA and platelet aggregation in a community sample. Our finding that OSA associates with increased platelet aggregation in the aspirin group, most of whom use it for primary prevention of CVD, suggests that platelet aggregation may mediate the adverse impact of OSA on vascular health in individuals with existing CVD risk, supporting further investigation.
阻塞性睡眠呼吸暂停（OSA）和心血管疾病（CVD）虽有关联，但两者之间的确切机制尚不清楚。血小板是 CVD 风险和血栓形成的介质，先前的研究表明 OSA 与血小板活性之间存在关联。本研究旨在评估 OSA、血小板活性与 CVD 相关危险因素之间的联系。
我们研究了同时参加 SHHS（睡眠心脏和健康研究）和 FHS（弗雷明汉心脏研究）的参与者中 OSA 测量值与血小板聚集之间的关系。我们应用线性回归模型，对人口统计学和临床协变量进行了调整，并探讨了与 OSA 和 CVD 相关因素（包括年龄、性别、体重指数、高血压、OSA 诊断（呼吸暂停低通气指数 4%≥5）和使用阿司匹林）的交互作用。我们的最终样本为 482 名参与者（60 岁[14.00]，50.4%为女性）。在主要样本中，呼吸暂停低通气指数 4%与血小板聚集之间未观察到相关性。分层分析显示，在阿司匹林使用者（n=65）中，我们的主要暴露因素（呼吸暂停低通气指数 4%，β=0.523；<0.001；n=65）和次要暴露因素（缺氧负担，β=0.358；<0.001；最低饱和度，β=-0.519；=0.026；和 3%氧减饱和指数，β=74.672；=0.002）之间存在相关性。在非阿司匹林使用者（n=417）中未检测到相关性。
在社区样本中，未发现 OSA 与血小板聚集之间存在相关性。我们的研究结果表明，在阿司匹林组中，OSA 与血小板聚集增加相关，其中大多数人使用阿司匹林预防 CVD，这表明血小板聚集可能介导 OSA 对存在 CVD 风险个体血管健康的不良影响，支持进一步研究。
