与睡眠呼吸障碍相关的肺动脉高压。

文献信息

中文摘要

目的综述： 睡眠呼吸障碍（SDB）日益被认为是WHO第3组肺动脉高压（PH）的一个促成因素。本综述探讨了将SDB与PH联系起来的流行病学和病理生理学，评估了针对睡眠的治疗在改变肺血流动力学方面的证据基础，并重点介绍了可能改变疾病进程的新兴治疗方式。
近期发现： SDB相关PH的机制是多因素的，包括反复夜间低氧血症、胸腔内压力改变以及肥胖驱动的代谢和炎症失调。气道正压治疗仍然是SDB相关PH治疗的基石，尽管下颌前移装置和舌下神经刺激提供了可行的替代方案。低氧负荷，而非仅凭呼吸暂停低通气指数，日益被认为是SDB中心血管和肺血管结局的更好预测指标。长期氧疗对静息性低氧血症患者提供血流动力学获益，但在仅有夜间血氧饱和度下降的患者中证据有限。
总结： SDB是PH一个诊断不足且具有临床重要性的促成因素。早期识别和治疗，特别是在有指征时采用气道正压治疗，可以有意义地降低肺动脉压。未来研究应优先开展前瞻性试验，考察胰高血糖素样肽-1受体激动剂和减重手术对肺血流动力学的直接影响，并将低氧负荷作为临床终点的使用标准化。

英文摘要

PURPOSE OF REVIEW: Sleep-disordered breathing (SDB) is an increasingly recognized contributor to WHO Group 3 pulmonary hypertension (PH). This review examines the epidemiology and pathophysiology linking SDB to PH, evaluates the evidence base for sleep-directed therapies in modifying pulmonary hemodynamics, and highlights emerging treatment modalities that may be able to alter disease course.
RECENT FINDINGS: The mechanisms underlying SDB-related PH are multifactorial, including recurrent nocturnal hypoxemia, altered intrathoracic pressures, and obesity-driven metabolic and inflammatory dysregulation. Positive airway pressure therapy remains the cornerstone of treatment of SDB-related PH, though mandibular advancement devices and hypoglossal nerve stimulation offer viable alternatives. Hypoxic burden, rather than apnea-hypopnea index alone, is increasingly recognized as a better predictor for cardiovascular and pulmonary vascular outcomes in SDB. Long-term oxygen therapy provides hemodynamic benefit in patients with resting hypoxemia, though evidence is limited in those with isolated nocturnal desaturation.
SUMMARY: SDB is an underdiagnosed and clinically important contributor to PH. Early identification and treatment, particularly with positive airway pressure therapy when indicated, can meaningfully reduce pulmonary arterial pressures. Future research should prioritize prospective trials examining the direct impact of glucagon-like peptide-1 receptor agonists and bariatric surgery on pulmonary hemodynamics and standardize the use of hypoxic burden as a clinical endpoint.