Abstract：
BACKGROUND: 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.
RESULTS: 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; P<0.001; n=65), and secondary exposures: hypoxic burden (β=0.358; P<0.001), minimum saturation (β=-0.519; P=0.026), and oxygen desaturation index 3% (β=74.672; P=0.002). No associations were detected in nonaspirin users (n=417).
CONCLUSIONS: 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.
RESULTS: 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; P<0.001; n=65), and secondary exposures: hypoxic burden (β=0.358; P<0.001), minimum saturation (β=-0.519; P=0.026), and oxygen desaturation index 3% (β=74.672; P=0.002). No associations were detected in nonaspirin users (n=417).
CONCLUSIONS: 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.
摘要：
背景：尽管相关，阻塞性睡眠呼吸暂停(OSA)与心血管疾病(CVD)的确切关联机制尚不清楚.血小板是CVD风险和血栓形成的介质，先前的研究表明OSA和血小板活性相关。这项研究的目的是评估OSA之间的联系，血小板活性，和CVD相关危险因素。
结果：我们研究了参与SHHS（睡眠心脏与健康研究）和FHS（弗雷明汉心脏研究）的参与者的OSA测量值与血小板聚集的关系。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相关因素的相互作用，包括年龄,性别,身体质量指数,高血压,OSA诊断（呼吸暂停低通气指数4%≥5），使用阿司匹林。我们的最终样本是482名参与者(60岁[14.00]，50.4%女性）。在主要样本中未观察到呼吸暂停低通气指数4%与血小板聚集之间的关联。分层分析显示，阿司匹林使用者（n=65）与我们的主要暴露有关（呼吸暂停低通气指数4％，β=0.523；P<0.001；n=65），和继发性暴露：低氧负荷(β=0.358；P<0.001)，最小饱和度(β=-0.519；P=0.026)，氧饱和度指数为3%(β=74.672;P=0.002)。在非阿司匹林使用者中未检测到关联（n=417）。
结论：在社区样本中未检测到OSA与血小板聚集之间的关联。我们发现OSA与阿司匹林组血小板聚集增加相关，大多数人将其用于CVD的一级预防，提示血小板聚集可能介导OSA对存在CVD风险的个体血管健康的不利影响,支持进一步调查。
结果：我们研究了参与SHHS（睡眠心脏与健康研究）和FHS（弗雷明汉心脏研究）的参与者的OSA测量值与血小板聚集的关系。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相关因素的相互作用，包括年龄,性别,身体质量指数,高血压,OSA诊断（呼吸暂停低通气指数4%≥5），使用阿司匹林。我们的最终样本是482名参与者(60岁[14.00]，50.4%女性）。在主要样本中未观察到呼吸暂停低通气指数4%与血小板聚集之间的关联。分层分析显示，阿司匹林使用者（n=65）与我们的主要暴露有关（呼吸暂停低通气指数4％，β=0.523；P<0.001；n=65），和继发性暴露：低氧负荷(β=0.358；P<0.001)，最小饱和度(β=-0.519；P=0.026)，氧饱和度指数为3%(β=74.672;P=0.002)。在非阿司匹林使用者中未检测到关联（n=417）。
结论：在社区样本中未检测到OSA与血小板聚集之间的关联。我们发现OSA与阿司匹林组血小板聚集增加相关，大多数人将其用于CVD的一级预防，提示血小板聚集可能介导OSA对存在CVD风险的个体血管健康的不利影响,支持进一步调查。
