Department of Ophthalmology, Medical University of Vienna, Währinger Gürtel 18-20, Vienna, 1090, Austria.
Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria.
Graefes Arch Clin Exp Ophthalmol. 2024 Dec;262(12):3761-3771. doi: 10.1007/s00417-024-06552-4. Epub 2024 Jun 15.
Neurovascular coupling impairment and inner retinal layer thinning are early detectable retinal changes in diabetes, and both worsen during progression of diabetic retinopathy (DR). However, direct interactions between these features have not been investigated so far. Therefore, we aimed to analyze associations between the retinal functional hyperemic response to light stimulation and the thickness of individual neuroretinal layers in eyes with early non-proliferative DR.
Thirty patients with type 1 diabetes featuring mild (n = 15) or moderate (n = 15) non-proliferative DR and 14 healthy subjects were included in this cross-sectional study. Retinal vessel diameters were measured before and during illumination with flickering light using a dynamic vessel analyzer. Individual layer thickness in the macula was analyzed from spectral domain optical coherence tomography.
Flicker light-induced vessel dilation was significantly reduced in patients compared to healthy controls (veins: 3.0% vs. 6.1%, p < 0.001; arteries: 1.3% vs. 5.1%, p = 0.005). Univariately, the response in retinal veins of diabetes patients correlated significantly with ganglion cell layer (GCL) thickness (r = 0.46, p = 0.010), and negatively with hemoglobin A1c (HbA1c) levels (r=-0.41, p = 0.023) and age (r=-0.38, p = 0.037), but not with baseline diameters, glucose levels, or diabetes duration. In a multiple regression model only GCL thickness (p = 0.017, β = 0.42) and HbA1c (p = 0.045, β=-0.35) remained significantly associated with the vascular flicker light response.
The results indicate that thinner GCL and worse glycemic control both contribute to reduced retinal neurovascular coupling in patients with clinical signs of DR. Progression of neurovascular dysfunction in DR might be related to structural degeneration of the neurovascular complex in the inner retina.
神经血管耦合损伤和内视网膜层变薄是糖尿病早期可检测到的视网膜变化，并且在糖尿病视网膜病变（DR）进展过程中都会恶化。然而，到目前为止，还没有研究这些特征之间的直接相互作用。因此，我们旨在分析早期非增生性 DR 眼中光刺激视网膜功能充血反应与单个神经视网膜层厚度之间的相关性。
本横断面研究纳入了 30 名患有 1 型糖尿病的患者，其中轻度（n=15）或中度（n=15）非增生性 DR，以及 14 名健康受试者。使用动态血管分析仪在闪烁光照射前后测量视网膜血管直径。从频域光学相干断层扫描分析黄斑区的各个层厚度。
与健康对照组相比，患者的闪烁光诱导血管扩张明显减少（静脉：3.0%对 6.1%，p<0.001；动脉：1.3%对 5.1%，p=0.005）。在单变量分析中，糖尿病患者视网膜静脉的反应与节细胞层（GCL）厚度显著相关（r=0.46，p=0.010），与血红蛋白 A1c（HbA1c）水平呈负相关（r=-0.41，p=0.023），与年龄呈负相关（r=-0.38，p=0.037），但与基线直径、血糖水平或糖尿病病程无关。在多元回归模型中，只有 GCL 厚度（p=0.017，β=0.42）和 HbA1c（p=0.045，β=-0.35）与血管闪烁光反应显著相关。
结果表明，在有 DR 临床体征的患者中，GCL 变薄和血糖控制恶化均导致视网膜神经血管耦合减少。DR 中神经血管功能障碍的进展可能与内视网膜神经血管复合体的结构退化有关。
