伴有阻塞性睡眠呼吸暂停的高血压患者视网膜微循环评估：基于无症状器官损伤的亚组分析
Evaluation of retinal microcirculation in hypertensive patients with obstructive sleep apnea: a subgroup analysis based on asymptomatic organ damage.
文献信息
| PMID | 42714727 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Güvenç Toprak |
| 作者单位 | Department of Ophthalmology, Faculty of Medicine, Düzce University, Düzce, Turkey. guvenc_toprak@windowslive.com. |
| 期刊 | International ophthalmology |
| SCI 分区 | Q3 |
| IF | 1.8 |
| 研究类型 | 临床研究 · 临床 |
| 所属专科 | 耳科 |
中文摘要
目的： 本研究旨在探讨阻塞性睡眠呼吸暂停综合征（OSAS）严重程度对高血压患者视网膜微血管改变的影响，并确定无症状器官损伤（AOD）的存在是否进一步调节这些眼部变化。
方法： 共纳入102名接受整夜多导睡眠监测的高血压参与者，根据呼吸暂停低通气指数（AHI）分为三组：非OSAS组（n=34）、轻度OSAS组（n=36）和中重度OSAS组（n=32）。所有受试者均接受光学相干断层扫描血管成像（OCTA）以评估中心凹浅层和深层毛细血管密度（FovSupMVD、FovDepMVD）、中心凹无血管区（FAZ）和脉络膜厚度。在OSAS患者中，根据左心室质量指数、颈动脉内膜中层厚度和微量白蛋白尿确定AOD状态。进行比较和相关性分析，以评估OSAS严重程度和AOD存在对视网膜微循环参数的影响。
结果： 随着OSAS严重程度的增加，观察到FovSupMVD和FovDepMVD均显著降低（分别为p = 0.001和p < 0.001），而FAZ大小保持不变。尽管各组间总体视网膜厚度参数大致相似，但RTn在组间差异显著（p = 0.044）。有趣的是，中重度OSAS组的颞侧和鼻侧脉络膜厚度显著增加（分别为p = 0.006和p = 0.005）。尽管AOD与较高的全身血管标志物（如颈动脉厚度、LVMI、微量白蛋白尿）相关，但AOD阳性与AOD阴性患者之间的OCTA参数无显著差异（所有p > 0.05）。未发现OSAS严重程度与AOD对OCTA测量值存在显著交互作用。
结论： 高血压OSAS患者的视网膜微血管损伤与OSAS严重程度密切相关，而AOD的存在似乎并未产生额外影响。这些发现表明，OSAS固有的慢性间歇性缺氧可能在视网膜微血管破坏中起主要作用。视网膜血管密度可能作为高血压OSAS患者微血管功能障碍的无创生物标志物具有潜在价值。
英文摘要
PURPOSE: This study aimed to investigate the impact of obstructive sleep apnea syndrome (OSAS) severity on retinal microvascular alterations in hypertensive individuals and to determine whether the presence of asymptomatic organ damage (AOD) further modulates these ocular changes.
METHODS: A total of 102 hypertensive participants who underwent overnight polysomnography were classified into three groups based on the apnea-hypopnea index (AHI): non-OSAS (n=34), mild OSAS (n=36), and moderate-severe OSAS (n=32). All subjects underwent optical coherence tomography angiography (OCTA) to evaluate foveal superficial and deep capillary densities (FovSupMVD, FovDepMVD), foveal avascular zone (FAZ), and choroidal thickness. Among OSAS patients, AOD status was determined based on left ventricular mass index, carotid intima-media thickness, and microalbuminuria. Comparative and correlation analyses were performed to assess the influence of OSAS severity and AOD presence on retinal microcirculatory parameters.
RESULTS: A significant reduction in both FovSupMVD and FovDepMVD was observed with increasing OSAS severity (p = 0.001 and p < 0.001, respectively), while FAZ size remained unchanged. Although overall retinal thickness parameters were largely similar among groups, RTn differed significantly between groups (p = 0.044). Interestingly, temporal and nasal choroidal thickness increased significantly in the moderate-severe OSAS group (p = 0.006 and p = 0.005). Although AOD was associated with higher systemic vascular markers (e.g., carotid thickness, LVMI, microalbuminuria), OCTA parameters did not differ significantly between AOD-positive and AOD-negative patients (all p > 0.05). No significant interaction was found between OSAS severity and AOD on OCTA measures.
CONCLUSION: Retinal microvascular impairment in hypertensive OSAS patients was found to be strongly associated with OSAS severity, whereas the presence of AOD did not appear to contribute additional effects. These findings suggest that chronic intermittent hypoxia inherent to OSAS may play a primary role in retinal microvascular disruption. Retinal vessel density may have potential as a non-invasive biomarker of microvascular dysfunction in hypertensive patients with OSAS.