阻塞性睡眠呼吸暂停相关高血压:文献回顾与临床管理策略。

Obstructive sleep apnea -related hypertension: a review of the literature and clinical management strategy.

机构信息

Department of Cardiology, Tokyo Medical University, Tokyo, Japan.

出版信息

Hypertens Res. 2024 Nov;47(11):3085-3098. doi: 10.1038/s41440-024-01852-y. Epub 2024 Aug 29.

Abstract

Obstructive Sleep Apnea (OSA) and hypertension have a high rate of co-occurrence, with OSA being a causative factor for hypertension. Sympathetic activity due to intermittent hypoxia and/or fragmented sleep is the most important mechanisms triggering the elevation in blood pressure in OSA. OSA-related hypertension is characterized by resistant hypertension, nocturnal hypertension, abnormal blood pressure variability, and vascular remodeling. In particular, the prevalence of OSA is high in patients with resistant hypertension, and the mechanism proposed includes vascular remodeling due to the exacerbation of arterial stiffness by OSA. Continuous positive airway pressure therapy is effective at lowering blood pressure, however, the magnitude of the decrease in blood pressure is relatively modest, therefore, patients often need to also take antihypertensive medications to achieve optimal blood pressure control. Antihypertensive medications targeting sympathetic pathways or the renin-angiotensin-aldosterone system have theoretical potential in OSA-related hypertension, Therefore, beta-blockers and renin-angiotensin system inhibitors may be effective in the management of OSA-related hypertension, but current evidence is limited. The characteristics of OSA-related hypertension, such as nocturnal hypertension and obesity-related hypertension, suggests potential for angiotensin receptor-neprilysin inhibitor (ARNI), sodium-glucose cotransporter 2 inhibitors (SGLT2i) and glucose-dependent insulinotropic polypeptide receptor/ glucagon-like peptide-1 receptor agonist (GIP/GLP-1 RA). Recently, OSA has been considered to be caused not only by upper airway anatomy but also by several non-anatomic mechanisms, such as responsiveness of the upper airway response, ventilatory control instability, and reduced sleep arousal threshold. Elucidating the phenotypic mechanisms of OSA may potentially advance more personalized hypertension treatment strategies in the future. Clinical characteristics and management strategy of OSA-related hypertension. OSA obstructive sleep apnea, BP blood pressure, ABPM ambulatory blood pressure monitoring, CPAP continuous positive airway pressure, LVH left ventricular hypertrophy, ARB: angiotensin II receptor blocker, SGLT2i Sodium-glucose cotransporter 2 inhibitors, ARNI angiotensin receptor-neprilysin inhibitor, CCB calcium channel blocker, GIP/GLP-1 RA glucose-dependent insulinotropic polypeptide receptor and glucagon-like peptide-1 receptor agonist.

摘要

阻塞性睡眠呼吸暂停(OSA)和高血压的发生率很高,OSA 是高血压的一个致病因素。间歇性低氧和/或睡眠片段化引起的交感神经活动是触发 OSA 血压升高的最重要机制。与 OSA 相关的高血压的特点是难治性高血压、夜间高血压、血压变异性异常和血管重塑。特别是,在难治性高血压患者中,OSA 的患病率很高,提出的机制包括 OSA 加重动脉僵硬引起的血管重塑。持续气道正压通气治疗对降低血压有效,然而,血压下降的幅度相对较小,因此,患者通常还需要服用降压药物以达到最佳血压控制。针对交感神经通路或肾素-血管紧张素-醛固酮系统的降压药物在与 OSA 相关的高血压中具有理论潜力,因此,β受体阻滞剂和肾素-血管紧张素系统抑制剂可能对 OSA 相关高血压的治疗有效,但目前的证据有限。与 OSA 相关的高血压的特征,如夜间高血压和肥胖相关的高血压,提示血管紧张素受体-脑啡肽酶抑制剂(ARNI)、钠-葡萄糖共转运蛋白 2 抑制剂(SGLT2i)和葡萄糖依赖性胰岛素促分泌肽/胰高血糖素样肽-1 受体激动剂(GIP/GLP-1RA)有潜在作用。最近,人们认为 OSA 的发生不仅与上呼吸道解剖结构有关,还与几个非解剖机制有关,如上呼吸道反应的反应性、通气控制不稳定和睡眠觉醒阈值降低。阐明 OSA 的表型机制可能在未来为更个性化的高血压治疗策略提供依据。与 OSA 相关的高血压的临床特征和管理策略。OSA 阻塞性睡眠呼吸暂停,BP 血压,ABPM 动态血压监测,CPAP 持续气道正压通气,LVH 左心室肥厚,ARB:血管紧张素 II 受体阻滞剂,SGLT2i 钠-葡萄糖共转运蛋白 2 抑制剂,ARNI 血管紧张素受体-脑啡肽酶抑制剂,CCB 钙通道阻滞剂,GIP/GLP-1RA 葡萄糖依赖性胰岛素促分泌肽/胰高血糖素样肽-1 受体激动剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b8f/11534699/84dfbba714cc/41440_2024_1852_Figa_HTML.jpg

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