The typical choroidal phenotype of the pachychoroidal spectrum disorders includes a diffuse or focal increase in the choroidal thickness . This is typically associated with abnormally dilated Haller layer vessels, the pachyvessels, and an attenuation of the inner choroid or Sattler’s layer and choriocapillaris. The pachyvessels are a well-established choroidal feature in eyes with pachychoroidal spectrum disorders [5,12,13,17–19]. The results of a study of PCV  showed that the distribution of the subfoveal choroidal thickness was bimodal with peaks at 170 and 390 μm. This suggested that PCV may consists of two overlapping phenotypes with one having markedly increased subfoveal choroidal thickness. However, in over 90% of pachyvessel (+) and pachyvessel (-) groups, the pachyvessels were observed below the assumed lesions, and these pachyvessels occupied nearly the full thickness of the choroid. This emphasizes the attenuation of the inner choroidal layers. A recent study  reported that pachyvessels were present in 46% of eyes with typical neovascular AMD, 85% of eyes with a thin choroidal PCV, and 96% of eyes with a thick choroid PCV, and 100% eyes with CSC.
Our results showed that pachyvessels were detected in 55.8% of eyes with PCV which is much lower than that reported . The reason for this difference may be due to differences in the ethnicity and race. Although there are no objective size criteria for pachyvessels, the higher incidence of pachyvessel in PCV supports the role of choroidal vessel dilatations in the pathogenesis of these diseases.
We found that the mean SFCT was significantly thinner in the pachyvessels (+) group than in the pachyvessels (-) group. It has been supposed that this may occur when the luminal volume increases secondary to the outer choroidal vessel dilation is offset by a reduction in tissue volume from a concurrent atrophy of the inner choroidal vasculature [3,17]. Thus, it is possible for an eye to have normal or even subnormal choroidal thickness but still have the pachychoroid disease phenotype .
Pachyvessels and attenuation of inner choroid seem to be key features of the pachychoroidal changes in eyes with PCV. A loss of the choriocapillaris may produce a relatively ischemic environment leading to the overexpression of angiogenic factors. While the exact pathogenic mechanisms for these choroidal changes remain to be validated, some plausible hypotheses including an engorgement of the vortex veins, choroidal vascular hyperpermeability, and choroidal venous hypertension can be considered [7,20,21].
The results of a recent study showed that pachyvessels were associated with choriocapillaris flow impairment by location and size . Whether the occurrence of dilated Haller pachyvessels is a primary event or secondary to the inner choroidal attenuation is still under investigation. It is possible that ischemic, inflammatory, or involutional insults to the inner choroidal circulation can result in a loss of the inner choroid leading to arteriovenous shunting with the resultant venous dilation.
Although the choroidal changes are possibly involved in the pathogenesis of PCV, it remains unclear whether the PCV phenotypes with varying choroidal thickness have similar neovascular processes and clinical characteristics. These dilated large choroidal vessels under the disease foci can be associated with disease development or progression.
We investigated the association between the pachyvessels and the SFCT, and between the pachyvessels and the clinical characteristics of eyes with PCV. There were no significant differences in the incidence of SRF, PED, and hemorrhages between the pachyvessels (+) group and pachyvessels (-) group confirming earlier results . They found that there was not a significant difference in the central retinal thickness and presence of PED and hemorrhages between the thin SFCT group and thick SFCT group.
However, our results showed that the PCV eyes with SRF and hemorrhages in the pachyvessels (+) group had significantly thinner SFCT than that of pachyvessels (-) group especially the eyes with hemorrhages. Although there was not a significant difference in SFCT between eyes with SRF, PED, and hemorrhages, this may have been because of the small number of eyes studied. The PCV eyes in pachyvessels (+) group with hemorrhages had the thinnest choroid. These findings suggest that the choroidal changes are possibly involved in the pathogenesis of PCV and the thin choroid may likely be the cause of the hemorrhages because of the ischemic condition.
It has been reported that an increased SFCT and choroidal vascular hyperpermeability are associated with poor outcomes for anti-VEGF treatment [7,23–25]. Our results suggested that the thin choroid may be a risk of hemorrhages.
An earlier study reported that some of the fellow eyes in patients with PCV had pachyvessels in the absence of neovascular or polypoidal sequelae . This suggested that the pachychoroid features were not a reaction to the neovascularization.
Our findings showed that pachyvessels were detected in 46.3％ of the fellow eyes and most of the fellow eyes (78.3%) in pachyvessels (+) group had pachyvessels. This is consistent with published observations in non-Asian cohorts [12,13]. Our data also suggested that the fellow eyes had a potentially of developing pathogenic changes of the choroid.
This study has several limitations including its retrospective and noncomparative design. There is no consensus for defining the thickness of the subfoveal choroid. In addition, the thickness can be influenced by various factors, such as age, axial length, and refractive error . Furthermore, there are no objective size criteria or definition for pachyvessels. Further investigations may define these vessels in more detail.
In conclusion, pachyvessels were present in 55.8% of eyes with PCV, and these eyes had a significantly thinner SFCT. The presence of pachyvessels and attenuation of the inner choroid seem to be due to the pathological changes in eyes with PCV.