Quantitative Analysis of Choroidal Vascular Structures and Anatomical Changes in Pachychoroid Spectrum Diseases Using ultra-widefield SS-OCTA

doi:10.21203/rs.3.rs-4962371/v1

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Quantitative Analysis of Choroidal Vascular Structures and Anatomical Changes in Pachychoroid Spectrum Diseases Using ultra-widefield SS-OCTA

https://doi.org/10.21203/rs.3.rs-4962371/v1

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This study utilized ultra-widefield swept-source optical coherence tomography angiography (UWF SS-OCTA) to quantitatively assess and compare choroidal blood flow structures and anatomical changes in eyes affected by central serous chorioretinopathy (CSC), pachychoroidal neovasculopathy (PNV), and uncomplicated pachychoroid (UCP). Additionally, we examined the distribution patterns of vortex veins across the three patient groups and conducted a preliminary investigation into the origin of choroidal neovascularization (CNV) in PNV. A total of 44 patients with CSC, 38 with PNV, and 46 with UCP were included in the analysis. Three-dimensional data were obtained from scans with dimensions of 20 mm vertically by 24 mm horizontally and a scan depth of 6 mm, covering nine subfields. The results demonstrated higher choroidal vessel volume per unit area (mCVV/a), choroidal vascularity index (CVI), and choroidal thickness (CT) in CSC eyes, while the PNV group exhibited similarities with the UCP group. Notably, PNV eyes showed the lowest foveal choriocapillaris density, suggesting that PNV and CSC may represent a continuous pathological spectrum, whereas UCP could be considered either a precursor to CSC or a remission stage following CSC resolution. CNV in PNV may result from choriocapillaris occlusion and ischemia due to mechanical compression by hypertrophic choroidal vessels. These findings provide valuable insights into choroidal structure analysis, hemodynamics within the pachychoroid spectrum disease (PSD), and the pathogenesis of CNV in PNV, thereby contributing to the understanding of shared etiologies within the PSD spectrum.

Health sciences/Anatomy

Health sciences/Medical research

pachychoroid spectrum diseases (PSD)

Choroid

Swept-source optical coherence tomography angiography (SS-OCTA)

vortex veins

choroidal neovascularization

The pachychoroid spectrum disease (PSD) encompasses a continuum of pathological processes, driven by a sequence of structural and functional modifications within the choroidal architecture¹. The main features observed in this spectrum of diseases are diffusely thickened choroid and enlarged blood vessels known as pachyvessels. In 2019, Siedlecki et al² proposed a classification system that categorizes pachychoroid spectrum diseases into five types: type 0/UCP (uncomplicated pachychoroid); type I/PPE(Pachychoroid pigment epitheliopathy); type II/CSC(Central serous chorioretinopathy); Type III/PNV (Pachychoroid neovasculopathy) can be categorized into two subtypes: type IIIa, characterized by neurosensory detachment (overlapping with central serous chorioretinopathy), and type IIIb, lacking neurosensory detachment. Lastly, Type IV/AT1, now termed pachychoroid aneurysmal type 1 choroidal neovascularization, was formerly referred to as polypoidal choroidal vasculopathy (PCV).

Choroidal thickening and vortex vein dilation are critical factors contributing to abnormal choroidal blood flow in PSD^1,3. Studies have confirmed vortex vein remodeling in PSD, including the formation of collateral connections linking the upper and lower vortex veins— a commonly observed phenomenon.^3,4. Several studies have suggested that the anatomical positioning and functional alterations of vortex veins may be significantly linked to the onset and progression of CSC⁵. However, the correlation between vortex veins and PSD remains inadequately explored.

Ultra-widefield swept-source optical coherence tomography angiography (UWF SS-OCTA) is a sophisticated imaging method utilized for assessing choroidal blood flow and anatomical alterations in individuals with choroidal disease. It offers crucial data and structural details for quantitative analysis of various pachychoroidal diseases. When compared to traditional OCT, UWF SS-OCTA demonstrates notable benefits in the visualization of choroidal blood flow images⁶.Therefore the purpose of the this study was to evaluate and compare the choroid vascular changes affecting vortex veins in eyes with UCP, CSC and PNV using UWF-OCTA in order to elucidate the underlying pathophysiology. We also investigated the relationship between choroidal neovascularization (CNV) and vortex veins in PNV.

The demographic and clinical profiles of patients with PSD are detailed in Table 1 and Fig. 1. Our cohort comprised 44 eyes with CSC, 38 eyes with PNV, and 46 eyes with UCP. Among the eyes with CSC, there were 34 males (77.3%) and 10 females (22.7%), with a mean age of 45.45 ± 6.94 years. The BCVA (logMAR) was 0.29 ± 0.26 and the central choroidal thickness was 432.11 ± 103.29 µm. The PNV eyes consisted of 25 men (73.3%) and 13 women (26.7%) with an average age of 51.55 ± 10.19 years. The BCVA (logMAR) was 0.34 ± 0.20 and the central choroidal thickness was 374.37 ± 102.59 µm. The UCP eyes had 30 men (65.5%) and 16 women (34.5%) with an average age of 48.87 ± 7.52 years. The BCVA (logMAR) was 0.04 ± 0.05 and the central choroidal thickness was 416.96 ± 61.72 µm.

Significant differences in ages were observed between patients with CSC and PNV, as well as between CSC and UCP (P < 0.05) (Fig. 1a). However, there were no significant differences between PNV and UCP. Patients with CSC and PNV eyes exhibited significantly worse BCVA compared to UCP eyes (P < 0.0001). Furthermore, BCVA was statistically worse in PNV eyes compared to CSC eyes (P < 0.05) (Fig. 1b). CT measurements also indicated significant differences between patients with CSC and PNV (P < 0.05) (Fig. 1c), while no significant differences were observed between PNV and UCP, as well as CSC and UCP.

Significant differences were observed in the proportion of eyes exhibiting anastomosis between the CSC eyes and UCP eyes (P < 0.01). However, no significant differences were found in the proportion of eyes showing anastomosis between the CSC eyes and PNV eyes, nor between PNV and CSC.

In the group of 44 CSC eyes, the superior and inferior vortex veins exhibited a symmetrical distribution in 26 cases (59.1%) (Fig. 1). Among these, 12 eyes (27.3%) exhibited upper-dominant while 6 eyes (13.6%) exhibited a lower-dominant.

Among the 38 PNV eyes, 11 eyes (28.9%) exhibited a symmetrical distribution of the superior and inferior vortex veins (Fig. 1). Of these, 18 eyes (47.4%) exhibited an upper-dominant pattern, while 6 eyes (15.8%) demonstrated a lower-dominant. Additionally, a horizontal watershed was noted in 3 eyes (7.9%). In the group of 46 eyes with UCP, the superior and inferior vortex veins were symmetrically distribution in 14 eyes (30.4%). Among these, 10 eyes (21.7%) displayed an upper-dominant and 13 eyes (28.3%) showing lower-dominant. Moreover, a horizontal watershed was found in 9 eyes (19.6%).

Table 2 summarizes the differences in choroidal features among various conditions within the PSD We also evaluated choroidal parameters in nine subfields in the CSC eyes, the PNV eye, and UCP eyes.The choroidal vessel volume per unit area (mCVV/a), in the CSC eyes was elevated compared to the PNV eyes in most regions except the superotemporal, nasal and inferonasal (P < 0.05).The mCVV/a in the CSC eyes was elevated compared to the UCP eyes in most regions except the nasal and Inferonasal(P < 0.05).The density of the Choriocapillaris (VD-cc) in the PNV eyes was lower compared to the CSC and UCP eyes in central regions (P < 0.05) and the VD-cc in the UCP eyes exhibited higher compared to the PNV and CSC eyes in nasal regions .In comparison to the PNV eyes, significant differences in choroidal vascularity index (CVI) were evident in the CSC eyes for nasal, Inferotemporal, lower, Inferonasal subfields and average .Additionally, CVI in CSC eyes surpassed values in UCP eyes in various directions, except for the temporal,nasal, and central areas.The CT in the CSC eyes was elevated compared to the PNV eyes in most regions except the nasal and superonasal (P < 0.05).The Choroidal thickness (CT) in CSC eyes was significantly higher than in UCP eyes in most regions, except for the superotemporal, upper, temporal, central, and inferotemporal areas (P < 0.05). However, no significant differences were observed in mCVV/a, CVI, and CT across all subfields when comparing the PNV eyes to the UCP eyes (P > 0.05) (Fig. 2).

UWF-OCTA detected CNV network vessels situated between the detached retinal pigment epithelium (RPE) and Bruch's membrane. These vessels consistently originated at the temporal of the optic disc or in close proximity to it in 35 eyes with PNV. Upon detailed examination of the figures, it is evident that the network vessels of CNV are present either at the site of symmetric vortex vein dilatation anastomosis or at the endpoint of the dominant vortex vein dilatation (Figs. 3–4).

This study investigates the relationship between choroidal blood flow and anatomical variations in PSD through the use of UWF SS-OCTA. The findings highlight the significant role of the choroidal vortex venous drainage system in PSD. Additionally, the study suggests that PNV and CSC may represent a continuous process, while UCP may be considered as either a pre-CSC stage or a period of remission following the healing of CSC.

The removal of choriocapillaris projection artifacts in healthy eyes using UWF SS-OCTA significantly enhances the visibility of large choroidal blood flow patterns. This advancement highlights the capability of SS-OCTA to offer clearer images, a crucial factor for choroidal structural and functional analysis^7,8.The study observed vortex vein anastomosis in over 90% of eyes with CSC and PNV, indicating that congestion in the vortex vein anastomosis can occur at any stage of PSD development. This finding reinforces the hypothesis that vortex vein anastomosis plays a role in the pathogenesis of PSD. Matsumoto³ similarly observed that over 90% of patients with pachychoroid disease had anastomoses linking the superior and inferior vortex veins, with rates of 90.2% in CSC and 95.1% in PNV. Notably, our study revealed a higher rate of vortex vein anastomosis in CSC compared to PNV, which may be influenced by racial disparities and variations in inclusion/exclusion criteria. Previous research by Mori et al. ⁹suggested that 38–50% of healthy eyes exhibit vortex vein anastomoses, but our results demonstrated a higher rate of 80.4% in eyes with underlying pachychoroid, indicating a potential association between choroidal thickening and vortex vein anastomoses leading to congestion^2,6,10–12.

Analysis of vortex vein expansion patterns indicated that symmetry was present in 59.1% of CSC eyes, with an upper-dominant pattern observed in 47.4% of PNV eyes. However, the distribution of these expansion forms was relatively uniform in vortex vein anastomosis in UCP eyes. These findings suggest that the upper-dominant vortex vein drainage system may serve as the primary route for choroidal drainage in PNV eyes. A comparison of vortex vein expansion patterns on En-face ultra-wide-angle OCTA shows a correlation with CVI. In CSC eyes, thickening of CVI is observed in 9 directions, while PNV predominantly an increase in CVI is noted in the upper, superonasal, and central regions, aligning with the upper-dominant vortex venous drainage system. Previous research by Matsumoto et al. ¹³ indicated that the average diameter of the CSC vortex vein was significantly larger than that of PCV and PNV, suggesting potential vascular connections and anastomoses in cases of vortex vein congestion. This finding supports the results of our study, which indirectly suggests abnormal vortex veins in CSC eyes through an increase in mCVV/a and CVI, reflecting elevated blood vessel volume and density due to hyperemia throughout the choroid.

Recent literature emphasizes that asymmetric drainage of the choroidal vortex veins is a characteristic feature of CSC, with the dominant drainage branch frequently localized in the temporal quadrant^5,12,13. Although this may initially appear to contradict our study findings, our research actually supports this notion. Our results indicate that the majority of choroidal blood flow and choroidal thickening in CSC eyes is predominantly concentrated in the the temporal region, particularly within the drainage area of the temporal segment. This aligns with the outcomes of our own study. The analysis of choroidal vascular parameters revealed that CVI was generally elevated in most drainage quadrants of CSC eyes compared to PNV and UCP eyes, except in the temporal region, where choroidal blood flow was markedly greater than in the nasal region. Moreover, mCVV/a, CT values in the upper temporal, superotemporal, and central regions of CSC were found to be higher than those in the inferotemporal, temporal, and lower regions. Interestingly, Compared to CSC eyes, the area of choroidal blood flow change in PNV and UCP eyes is more limited. This observation leads us to hypothesize that during the progression or self-healing phase of CSC, compensatory drainage in the vortex vein drainage area above CSC may increase. Additionally, choroidal blood flow on the temporal region consistently surpasses that on the nasal region across different vortex vein dilation modes. This phenomenon is thought to be linked to the vascular watershed that separates the choroidal vascular circulatory system in the optic disc area and the anatomical position of the optic nerve¹⁴. Regardless of the pattern of vortex vein dilation, the drainage of vortex veins in all quadrants will ultimately impact the blood perfusion of the foveal choroid. The elevated choroidal blood flow observed in CSC eyes, relative to PNV eyes, may be attributed to symmetrical venous drainage, which potentially leads to vortex vein congestion and subsequent choroidal thickening. However, with time, the formation of venous-venous anastomosis between veins in different levels of vortex vein congestion may lead to asymmetric choroidal vortex venous drainage and reduced choroidal congestion. The varying durations and stages of PSD in these studies may have led to heterogeneity in the results. To further confirm our findings and explore the association of different vortex vein distributions with PSD, a large longitudinal cohort study comparing vortex vein dilatation between PNV and CSC should be conducted in the future.

Our study revealed that UCP and PNV were largely similar, with the exception of a significantly lower VD-cc in the central region of PNV compared to UCP. While the proportion and degree of vortex vein anastomosis in UCP eyes were not as severe as in PNV eyes, they still indicate that UCP has the anatomical structural basis for the development of CSC and PNV. However, this may not necessarily lead to pathological consequences. Matsumoto et al.³ found that CSC patients were the youngest, followed by those with PNV, and then PCV. Correspondingly, CSC eyes had the greatest CT values, followed by PNV and PCV eyes. The study suggests a potential continuum from CSC to PNV, with our findings indicating that CSC patients were younger than UCP and PNV. This suggests that PNV and CSC may represent a continuum or different stages of the same disease process, with UCP potentially serving as a pre-CSC phase or a period of remission following CSC resolution.

Comparing the VD-cc of CSC, PNV, and UCP reveals that while VD-cc did not change significantly in most directions, the central area warrants particular attention. Notably, the PNV eye exhibits the smallest VD-cc, while the UCP eye displays the largest VD-cc. Interestingly, the VD-cc of the CSC eye falls somewhere in between. These observations suggest that VD-cc may experience dynamic changes during the progression of PSD¹⁵. Studies have shown that patients with CSC have a significantly higher choroidal blood flow area compared to healthy individuals (53.4 ± 5.8% vs. 49.45 ± 8.16%)¹⁶. Moreover, the choriocapillaris (CC) layer exhibited a significantly reduced blood flow area compared to the deep choroidal layer¹⁶. Another study demonstrated that patients with acute CSC had markedly decreased perfusion in the choriocapillaris compared to healthy eyes¹⁷. Cennamo et al.¹⁵ studied changes in Choriocapillaris density in CSC patients with CNV before and after intravitreal ranibizumab injection. They observed a notably reduced baseline choriocapillaris density in CSC compared to control eyes, with no improvement after treatment. This implies that CNV may develop in regions with reduced choriocapillaris blood flow, potentially linked to choroidal hypoperfusion as a contributing factor to disease onset and CNV progression.

Our study similarly shows that the CVI and mCVV/a of PNV are notably smaller than those of CSC, with PNV's foveal VD-cc significantly lower than that of CSC and UCP eyes. While the exact pathogenic mechanism underlying these choroidal changes requires further investigation, it is possible to propose a plausible hypothesis based on existing research findings. Initially, certain factors may trigger choroidal overperfusion, leading to changes in UCP. In response to congestion, CSC-affected eyes may form vascular connections between the upper and lower vortex veins to enhance drainage and alleviate venous pressure. If this drainage system becomes overwhelmed, manifestations such as subretinal fluid accumulation can occur, leading to the onset of CSC. A structurally uneven drainage system may lead to an unequal distribution of venous blood flow, resulting in varying degrees of choroidal thickening across different regions. Vortex vein anastomoses occurring in various regions may represent a compensatory mechanism within the choroid. A predominant drainage pathway in the superior temporal region may facilitate greater blood flow out of the sclera via the vortex veins, thereby alleviating venous congestion. This observation may offer insights into the diverse clinical outcomes observed in patients with CSC. Some patients with CSC experience spontaneous healing as collateral anastomoses compensate for chronic congestion. However, in other patients with CSC, abnormal choroidal arteriovenous anastomosis may contribute to the progression of CSC, leading to venous overload, chronic congestion, and the formation of thick choroidal vessels that compress the choriocapillaris. This ischemic state in the outer retinal layer can trigger CNV. Notably, in eyes affected by PNV, dilation of the upper-dominant vortex veins seems to constitute the principal channel for choroidal drainage, highlighting an anatomical predisposition to PNV development. Additionally, there may be developmental abnormalities in the spatial arrangement of venous drainage pathways in PNV eyes, particularly in the asymmetric distribution of superior and inferior vortex veins, suggesting congenital anatomic variations^18,19. Additional research is required to determine whether varying distribution patterns of vortex veins in PNV might act as risk factors for the progression of CSC to PNV. Prolonged observation of eyes transitioning from CSC to PNV is crucial to substantiate these findings.

Additionally, En face OCT and OCTA analysis can provide a more precise localization of CNV network vessels, aiding in a better comprehension of the pathophysiology of PNV. CNV network vessels in PNV eyes have been observed to form either at the locations of symmetric vortex vein dilation and anastomosis or at the terminal points of dominant vortex vein dilation (Figs. 3–4). These results support prior research highlighting the strong connection between vortex vein and PSD Findings on En-face imaging that contribute to our evolving understanding of the choroidal neovascular in PNV. We utilized the UWF SS-OCTA En-face model to explore peripheral choroidal regions, focusing on the relationship between vortex veins and CNV. The network vessels of CNV occur either at the site of symmetric vortex vein dilatation anastomosis or at the endpoint of the dominant vortex vein dilatation in PNV eyes (Figs. 3–4). These findings align with Matsumoto et al, who similarly discovered CNV originating from anastomotic vessels²⁰. They propose that the enlargement of outer choroidal vessels, associated with chronic choriocapillaris ischemia, may play a role in CNV development in PNV-affected eyes. However, the mechanisms of neovascularization in PNV remain unclear. The pathogenesis of PNV remains incompletely understood, but our findings suggest that the mechanical compression of dilated pachyvessels may ultimately result in ischemic necrosis of the choriocapillaris and subsequent development of CNV. Several studies have consistently found no correlation between cytokine levels and the response to anti-vascular endothelial growth factor (anti-VEGF) therapy in patients with PNV^21,22. In our study, we observed that dilated vortex veins were consistently positioned below the CNV in PNV eyes, which suggests that the dilation of outer choroidal vessels, associated with chronic choriocapillaris ischemia, might contribute to CNV formation in these eyes. Therefore, we propose that CNV in PNV arises from choriocapillaris occlusion and ischemia caused by mechanical pressure exerted by hypertrophic choroidal vessels. This observation led to the hypothesis of a potential mechanism for the origin of CNV. However, we did not provide direct evidence to support the idea that the mechanism of CNV is necessarily linked to the dilation of the vortex veins. Moving forward, our future studies should delve deeper into the molecular mechanisms underlying these hypotheses and validate their clinical significance.

The study’s cross-sectional design and small sample size limit our ability to establish a causal link between the choroidal vortex venous drainage system and PSD. To advance the understanding of vortex vein distribution, future studies with a larger sample size are imperative. Additionally, The inability to fully observe vortex vein branches from the macula to the ampulla limits the correlation analysis between dilated macular branches and ampulla condition. Future prospective and longitudinal studies should track changes in vortex vein distribution across different disease stages to potentially trigger neovasculopathy development. Additional research, incorporating detailed subgroup analyses, is necessary to explore this further.

In conclusion, our findings offer valuable insights of choroidal structure, hemodynamics in PSD, and the origin of CNV in PNV. UWF SS-OCTA is highly valuable for comparing choroidal blood flow and structural alterations in patients with various choroidal diseases, This in-depth analysis of subdomain characteristics may deepen our understanding of the diverse manifestations of PSD, thereby facilitating a more comprehensive exploration of potential common etiologies among disorders within the PSD.

Subjects

This cross-sectional research was conducted at the Ophthalmology Department of the General Hospital under the Central Theater Command from April 2023 to February 2024The study enrolled 44 CSC patients, 38 with PNV, and 46 with UCP. Ethical approval was granted by the Ethics Review Board of the General Hospital under the Central Theater Command, in accordance with the Declaration of Helsinki. Written informed consent was obtained from all participants before

The diagnosis of CSC is established based on specific criteria, including (1) the presence of subretinal fluid (SRF) and/or pigment epithelial detachment (PED) visible on SS-OCT; (2) Fundus fluorescein angiography (FFA) shows RPE dye leakage; (3) Enhanced local choroidal vascular permeability is detectable in the late phase of indocyanine green angiography (ICGA). PNV¹ is diagnosed when CNV associated with a thick choroid is detected by FFA, ICGA, OCTA, or a combination of these imaging techniques. It is important to note that CNV associated with polypoidal lesions, known as PCV, does not fall under the PNV category .UCP²³ is identified by increased choroidal thickness (subfoveal CT > 300 µm or an extrafoveal region at least 50 µm thicker), dilated choroidal vessels, inner choroidal thinning, and the absence of abnormalities such as PPE, CSC, PNV, or PCV on FAA, ICGA, or OCTA.Exclusion criteria for participants included the following factors:(1) Patients with macular neuroepithelial detachment and PED resulting from age-related macular degeneration (AMD), AT1 and other basic diseases; (2) High myopia or refractive stromal opacity and inability to cooperate Examining the patient. (3) Patients undergoing intraocular surgery other than cataract surgery. (4) Conditions leading to poor image quality (OCT or OCTA score below 8);(5) Patients with severe systemic diseases.

Ultra-widefield SS-OCT analysis

Participants were imaged using a 400 kHz SS-OCTA device (BM-400K BMizar, TowardPi Medical Technology, Beijing, China) with settings including a 400 kHz scan rate, 6 mm axial scan depth, 24 mm B-scan length, and a 24 × 20 mm OCTA area centered on the fovea. Additionally, structural OCT was employed to assess the macular lateral structure. Data were collected from nine subfields: superotemporal, superior, superonasal, temporal, central, nasal, inferotemporal, inferior, and inferonasal regions. Measurements included choroid thickness (CT), choroidal vascularity index (CVI), choroidal vessel volume per unit area (mCVV/a), and choriocapillaris density (VD-cc). CVI, representing proportion of vessel volume to choroidal volume, was calculated, while mCVV/a provided a quantification of choroidal vessel volume. CT is defined as the distance from Bruch's membrane (BM) to the choroid-scleral interface (CSI).The software automatically detects BM and CSI, with accuracy confirmed by manual verification of B-scans We ensured measurement consistency by standardizing for axial length (AL) magnification through the modified Littmann formula (Bennett method).Measurements were consistently centered on the fovea without rotation, and data from the left eyes were mirrored horizontally for analysis (Fig. 5).

The evaluation of vortex veins dilation patterns (VVDP) was carried out by two retina specialists (SYP and YM) using en face OCTA images. The VVDP was categorized into three primary groups: upper-dominant, lower-dominant, and symmetry. In cases where there were conflicting viewpoints, a third specialist in retinal imaging was consulted to address the inconsistency (Fig. 6).

Statistical Analysis

Data analysis was conducted using IBM SPSS software (version 27.0). Normally distributed data were reported as mean ± standard deviation (SD) and assessed for normality with the Kolmogorov-Smirnov test. Patient characteristics were summarized using standard descriptive statistics, including mean (SD), median, interquartile range (IQR), and proportions. Comparative analysis between CSC, PNV, and UCP eyes was performed using ANOVA for normally distributed variables and the Kruskal-Wallis test for non-normally distributed variables. A p-value below 0.05 was deemed to indicate statistical significance.

Table 1

Demographic and clinical characteristics of patients with pachychoroid spectrum diseases. CSC = central serous chorioretinopathy, PNV = pachychoroid neovasculopathy UCP = uncomplicated pachychoroid.
Characteristic	CSC Eyes	PNV Eyes	UCP Eyes
No. of eyes	44	38	46
Age (years)	45.45 ± 6.94	51.55 ± 10.19	48.87 ± 7.52
Male,gender,n(%)	34(77.3%)	25(65.8%)	30(65.5%)
BCVA(logMAR)	0.29 ± 0.26	0.34 ± 0.20	0.04 ± 0.05
Central choroidal thickness (µm)	432.11 ± 103.29	374.37 ± 102.59	416.96 ± 61.72
Vortex vein anastomosis (+)	44(100%)	35(92.1%)	37(80.4%)
Vortex veins dilation patterns(VVDP)
upper-dominant	12(27.3%)	18(47.4%)	10(21.7%)
symmetry	26(59.1%)	11(28.9%)	14(30.4%)
lower-dominant	6(13.6%)	6(15.8%)	13(28.3%)

Table 2

Choroidal vasculature comparisons across nine regions were conducted among CSC, PNV, and UCP eyes. ¹ CSC VS PNV. ² CSC VS UCP. ³ PNV VS UCP. These analyses were performed using one-way ANOVA for normally distributed parameters and the Kruskal–Wallis test for non-normally distributed parameters.
	CSC Eyes	PNV Eyes	UCP Eyes		P-value ²	P-value ³
mCVV/a, µm, mean ± SD
Superotemporal	129.75 ± 39.2	110.82 ± 32.69	98.28 ± 20.1	0.057	< 0.001	0.125
Upper	136.02 ± 42.23	114.47 ± 30.66	105.48 ± 22.68	0.028	< 0.001	0.360
Superonasal	118.95 ± 43.36	98.63 ± 29.12	96.43 ± 26.37	0.041	0.012	0.978
Temporal	107.39 ± 35.11	89.18 ± 22.71	82.93 ± 19.3	0.018	< 0.001	0.456
Central	142.61 ± 35.66	123.21 ± 27.67	126.41 ± 19.5	0.021	0.029	0.909
Nasal	104.8 ± 36.3	86.89 ± 31.69	89.59 ± 22.1	0.057	0.058	0.961
Inferotemporal	105.34 ± 47.04	77.24 ± 26.55	83.87 ± 27.35	0.003	0.031	0.602
Lower	106.52 ± 35.32	85.68 ± 29.85	88.07 ± 22.3	0.015	0.013	0.969
Inferonasal	66.39 ± 25.84	53.95 ± 20.96	55.39 ± 17.49	0.054	0.062	0.982
Average	113.09 ± 32.52	93.37 ± 21.17	91.74 ± 16.69	0.005	< 0.001	0.973
Choriocapillaris density, %,mean ± SD
Superotemporal	47.68 ± 5.59	48.03 ± 4.42	48.04 ± 6.14	0.777	0.755	0.989
Upper	48.07 ± 1.89	47.84 ± 2.34	48.48 ± 1.79	0.61	0.332	0.149
Superonasal	47.43 ± 4.76	47.24 ± 5.54	48.13 ± 6.3	0.875	0.554	0.467
Temporal	45.89 ± 3.98	46.03 ± 3.64	45.87 ± 3.02	0.859	0.982	0.841
Central	46.43 ± 2.17	44.79 ± 2.68	46.72 ± 2.12	0.002	0.560	< 0.001
Nasal	44.57 ± 4.54	43.74 ± 5.4	46.89 ± 4.51	0.435	0.023	0.003
Inferotemporal	46.91 ± 5.09	47.11 ± 5.51	45.96 ± 4.9	0.864	0.382	0.311
Lower	49.2 ± 2.19	49.26 ± 1.75	48.78 ± 2.48	0.904	0.362	0.318
Inferonasal	48.55 ± 3.14	47.37 ± 3.32	48.43 ± 5.35	0.199	0.899	0.240
Average	47.20 ± 1.50	47.00 ± 1.41	47.41 ± 1.54	0.537	0.509	0.209
CVI, %, mean ± SD
Superotemporal	36.43 ± 4.32	35.76 ± 4.36	34.52 ± 3.51	0.458	0.027	0.165
Upper	37.68 ± 3.61	36.89 ± 3.45	35.04 ± 3.51	0.316	< 0.001	0.018
Superonasal	37.48 ± 3.95	35.79 ± 3.35	34.2 ± 5.01	0.073	< 0.001	0.087
Temporal	33.73 ± 3.85	32.32 ± 2.77	31.41 ± 2.92	0.051	< 0.001	0.205
Central	35.66 ± 4.63	36.32 ± 2.53	36.15 ± 2.79	0.395	0.502	0.830
Nasal	34.41 ± 4.11	32.05 ± 5.26	32.85 ± 3.8	0.016	0.093	0.409
Inferotemporal	33.89 ± 5.2	31.16 ± 4.73	32.26 ± 4.09	0.010	0.102	0.285
Lower	35.93 ± 3.75	33.63 ± 5.33	33.83 ± 3.82	0.017	0.022	0.837
Inferonasal	30.07 ± 5.39	26.97 ± 6.28	27.76 ± 4.73	0.012	0.047	0.511
Average	35.02 ± 3.2	33.37 ± 2.86	33.09 ± 2.94	0.014	0.003	0.671
Choroidal thickness, µm, mean ± SD
Superotemporal	314.55 ± 78.84	264.53 ± 63.11	244.76 ± 38.88	0.006	< 0.001	0.265
Upper	324.09 ± 85.16	270.63 ± 62.91	263.67 ± 43.17	0.005	< 0.001	0.918
Superonasal	278.07 ± 83.77	239.37 ± 63.88	243.83 ± 43.16	0.060	0.054	0.977
Temporal	278.8 ± 76.86	235.26 ± 53.48	227.26 ± 45.54	0.011	< 0.001	0.849
Central	369.82 ± 83.11	301.79 ± 62.13	316.83 ± 36.33	< 0.001	< 0.001	0.474
Nasal	262.23 ± 79	224.08 ± 67.35	234.96 ± 46.21	0.061	0.145	0.786
Inferotemporal	261.55 ± 95.4	204.08 ± 54.87	219.33 ± 59.28	0.030	0.043	0.535
Lower	249.98 ± 73.92	206.05 ± 57.66	218.22 ± 47.7	0.010	0.054	0.660
Inferonasal	174.59 ± 48.54	150.58 ± 38.29	159.52 ± 45.56	0.017	0.112	0.362

Ethical approval.

All procedures performed in studies involving human participants were in accordance with the ethical standards of the Institutional Review Board of General Hospital of Central Theater Commandand with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

Informed consent.

Informed consent was obtained from all individual participants included in the study.

Data availability

Data are available upon reasonable request. Deidentified participant data that underline the results reported in this article (text, tables and figures) could be shared upon reasonable request sent to the corresponding author.

Author contributions

Conception and design of the research :Bei Xiao; Acquisition of data: Ya Ye, Zhen Huang; Analysis and interpretation of the data : YaYe, Zhen Huang; Statistical analysis: Bei Xiao,Ming Yan; Obtaining financing: Yan-Ping Song; Writing of the manuscript: Bei Xiao; Critical revision of the manuscript for intellectual content :Yan-Ping Song，Bei Xiao

Funding.

The key project of the National Key R&D Program "Research on the Prevention and Treatment of Common Frequent Diseases" (2022YFC2502800).

Competing interests

The authors declare no competing interests.

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No competing interests reported.

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Quantitative Analysis of Choroidal Vascular Structures and Anatomical Changes in Pachychoroid Spectrum Diseases Using ultra-widefield SS-OCTA

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Ultra-widefield SS-OCT analysis

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