The study aimed to evaluate the retinal vessel density to explore potentially novel insights into the mechanisms underlying refractive error development in patients with myopic anisometropia using optical coherence tomography angiography. The anterior segment parameters of patients with myopic anisometropia were highly symmetrical in both groups (Table 1). This is in accordance with previous research, which found that asymmetric axial elongation of the vitreous cavity was the leading cause of myopic anisometropia [15].
This study demonstrated that the vessel density in the superficial macular layer in the LAG was significantly increased in all regions, with the exception of the foveal region, compared to that in the CLG. Yang et al. [16] demonstrated that varying degrees of myopia did not affect macular vessel density in healthy young adults. However, Al-Sheikh et al. [17] concluded that severe myopia was associated with decreased macular vessel density, in accordance with another previous study [18]. The superficial macular vascular plexus primarily supplies blood to the IPL, ganglion cell layer, and retinal nerve fibre layer (RNFL), and is not uniformly distributed from the margin of the FAZ to the parafoveal region [19]. Therefore, we believe that a compensatory increase in the oxygen and nutrient demands of the superficial macular vessel density occurs to ensure normal visual function, accompanied by axial elongation. We also noticed that the fovea is primarily an avascular region; therefore, it is less sensitive to certain differences in foveal vessel density.
Moreover, the RPC density was significantly decreased in the LAG compared to the CLG. The RPC is primarily responsible for supplying the nutritional requirements of the retinal ganglion cells. Previous studies have noted that the RPC density was remarkably increased in the capillary networks of the arcuate fibre region, which may play a crucial role in neuronal function [20]. Shimada et al. [21] reported that individuals with severe myopia had reduced peripapillary retinal perfusion compared to that in emmetropic eyes. In the present study, the decrease in the RPC density could have been caused by the loss of the RNFL in the corresponding area, which may have affected the demand for regional oxygen or vascular supply in the peripapillary area, thereby triggering the retinal vascular adjustment via autoregulatory mechanisms [22]. With the progression of myopia in the longer axial eyes, the eyeball is being elongated and stretched, resulting in decreased blood flow. However, the blood flow was not significantly decreased in the nasal region in the current study. This could have been associated with peripapillary atrophy, which often occurs from the side of the optic disk. Further research with a larger sample size is needed to clarify the exact underlying mechanism.
We did not find any changes in the deep macular vessel density in any regions. The deep macular plexus regions receive a portion of nutrients from the choroidal blood flow, which was not sufficiently sensitive to perceive the differences. There were no significant differences in the FAZ area measurements between groups. Indeed, the FAZ area was found to vary considerably among healthy participants based on age and other factors [23]. Our study also found no significant difference in the CCP area. Although Mo et al. observed decreased vessel density in myopic compared to emmetropic eyes [24], the chorioretinal atrophy areas may have confounded the results because of the shadowing effect caused by the lesions in their study [13]. We specifically eliminated pathological retinal changes and eyes with myopia of > 6.00 D in our research.
Furthermore, we noted that the SE negatively correlated with the superficial macular vessel density and superficial parafoveal vessel density, but was not associated with the deep macular vessel density or RPC density. Our study did not identify any association between the AL and the macular vessel density or the RPC density. In contrast, Spina et al. [25] reported that the ocular blood flow appeared to be negatively related to the AL. Yang et al. [16] demonstrated that the SE did not affect the macular vessel density in young patients (26.0 ± 1.7 years) with myopia without pathological retinal changes. We speculated that the refractive error alone might imply a diverse mechanism in the alteration of retinal vessel density.
The potential limitations of our study should be considered. First, we focused on non-amblyopic myopic anisometropia eyes of patients aged 20–59 years and excluded the eyes with myopia of > 6.00D and myopia-related retinopathies. Further longitudinal studies may help to address the question of whether retinal vessel density is altered with age. Second, even subtle ocular movements during imaging can cause significant artifacts that may confound the analysis of the results; appropriate interpretation is needed to acquire a high-quality retinal vascular network image [26]. Thirdly, the sample size was relatively small. Thus, further long-term studies with a greater age spectrum and larger samples might reveal greater detail regarding the changes in vessel density in myopic anisometropia.