超越呼吸暂停-低通气指数：伴阻塞性睡眠呼吸暂停的高血压患者的心血管与代谢表型分析——一篇叙述性综述

文献信息

中文摘要

背景： 阻塞性睡眠呼吸暂停（OSA）与高血压密切相关，然而呼吸暂停-低通气指数（AHI）虽可界定呼吸事件的存在与频率，但在个体患者中对心血管风险的预测可靠性不如纳入缺氧暴露深度与持续时间的指标。AHI值相近的患者在夜间低氧血症、交感神经激活、动态血压行为及靶器官损害方面可存在显著差异，暴露出呼吸分类与心血管预后之间持续存在的差距。本综述综合了关于OSA与高血压关联机制的现有证据，包括间歇性缺氧、化学反射介导的交感神经过度活跃、肾素-血管紧张素-醛固酮系统激活、缺氧相关胰岛素抵抗，并审视了新兴指标，包括缺氧负荷、氧减饱和度指数和动态血压监测，这些指标比单独AHI更准确地捕捉心血管风险。我们描述了OSA中高血压的六种心血管表型：难治性、夜间性、非杓型/反杓型、隐匿性及晨峰高血压，以及高血压介导的靶器官损害，每种均具有不同的机制、预后和治疗反应。由于间歇性缺氧和交感神经激活亦涉及胰岛素抵抗和MASLD，这一共享代谢通路贯穿全文整合讨论，而非作为偶然合并症处理。基于这些证据，我们提出一个以表型为导向的临床框架，涵盖心血管筛查、多域表型分析、风险分层和个体化治疗，旨在补充而非替代基于AHI的诊断和当前高血压指南。该框架作为概念性、专家衍生的提议提出，旨在构建临床推理，尚未在独立队列中衍生或验证。我们最后讨论了未来方向，包括数字生物标志物、多模态成像和人工智能辅助表型分析，作为通向伴OSA高血压患者精准心血管医学的路径。

英文摘要

Obstructive sleep apnea (OSA) is strongly associated with hypertension, yet the apnea-hypopnea index (AHI), while it defines the presence and frequency of respiratory events, predicts cardiovascular risk less reliably in the individual patient than metrics that incorporate the depth and duration of hypoxic exposure. Patients with comparable AHI values can differ substantially in nocturnal hypoxemia, sympathetic activation, ambulatory blood pressure behavior, and target-organ damage, exposing a persistent gap between respiratory classification and cardiovascular prognosis. This review synthesizes current evidence on the mechanisms linking OSA to hypertension, intermittent hypoxia, chemoreflex-mediated sympathetic overactivity, renin-angiotensin-aldosterone system activation, hypoxia-associated insulin resistance and examines emerging metrics, including hypoxic burden, oxygen desaturation index, and ambulatory blood pressure monitoring, that capture cardiovascular risk more accurately than AHI alone. We describe six cardiovascular phenotypes of hypertension in OSA: resistant, nocturnal, non-dipping/reverse-dipping, masked, and morning-surge hypertension, alongside hypertension-mediated target-organ damage, each with distinct mechanisms, prognosis, and treatment response. Because intermittent hypoxia and sympathetic activation are also implicated in insulin resistance and MASLD, this shared metabolic pathway is integrated throughout rather than treated as an incidental comorbidity. Building on this evidence, we propose a phenotype-oriented clinical framework spanning cardiovascular screening, multidomain phenotyping, risk stratification, and personalized therapy intended to complement, not replace, AHI-based diagnosis and current hypertension guidelines. This framework is presented as a conceptual, expert-derived proposal intended to structure clinical reasoning, and it has not been derived from or validated in an independent cohort. We conclude with future directions, including digital biomarkers, multimodal imaging, and artificial intelligence-assisted phenotyping, as pathways toward precision cardiovascular medicine in hypertensive patients with OSA.