## 4 Discussion
also did not find any differences [31]. These results align with our study where we did not find any difference in the CVI in the total analyzed sample. However, in our study, patients who were dexamethasone responders, with a reduction in CMT, had a significantly lower CVI following treatment as compared to baseline. [PERSON] et al. showed a significant reduction in CVI and LA in the third month post-dexamethasone injection in patients with DME resistant to anti-VEGF therapy. The authors attributed these results to a reduction in vasodilation induced by the local effects of the corticosteroid [32]. In our study, although not statistically significant, we also observed a progressive reduction in LA during the follow-up, confirming the local effects of the corticosteroid, albeit limited. Therefore, we agree with these authors that the reduction in LA in our study could potentially be attributed to the effects of corticosteroids on choroidal vasculature. Similar results emerged from the recent study by [PERSON] et al., who reported a reduction in LA, TA, and CVI in the third month post-intravitreal dexamethasone injection in patients with DME refractory to anti-VEGF. These authors observed a progressive decrease in LA, TA, and CVI values during follow-up and hypothesized that this trend could be explained by the pharmacokinetics of intravitreal dexamethasone [33]. Animal model studies showed that dexamethasone reaches peak concentration in the second month after intravitreal injection and becomes undetectable after the 180 th day [33; 34]. Even in our study, CVI decreased significantly in the fourth month after intravitreal injection, suggesting a prolonged action of dexamethasone on the choroid even after the second month. In our study, we also found a positive correlation between the CVI and CMT in the second month, suggesting that higher CMT values are associated with higher CVI values. It is reasonable to hypothesize that this behavior is related to the response to intravitreal dexamethasone; in responder patients, there is a greater reduction in CVI and vice versa. Interestingly, a correlation emerged between baseline CVI and CMT in the second month. We could speculate that higher baseline CVI may suggest a greater acute inflammatory response at the choroidal level, which is reasonably associated with greater difficulty for dexamethasone to induce complete fluid reabsorption. Our results contrast with those of [PERSON] et al., who reported a greater reduction in CMT in patients with high baseline CVI, with a moderately significant relationship [32]. However, we are only the second group to study this relationship, and our analyzed population sample differs from that of [PERSON] et al., who included patients with DME refractory to anti-VEGF, whereas the majority of patients in our sample were treatment-naive patients. The effect of intravitreal injections on the CVI has been explored to a limited extent, even in the context of anti-VEGF therapy. [PERSON] et al. reported a reduction in CVI at three and six months following the intravitreal injection of anti-VEGF [35]. [PERSON] et al. conducted a study investigating both the effect of anti-VEGF on CVI and the prognostic value of baseline CVI in predicting a functional response to intravitreal injection. Their findings demonstrated that patients with a higher baseline CVI tended to achieve greater visual acuity gains regarding letter scores compared to those with a lower baseline CVI. The authors also included in their analysis the influence of retinal morphological parameters related to inflammation, such as the presence of subretinal fluid (SRF), the number of hyperreflective foci (HRF), the extent of disruption of the inner limiting membrane and ellipsoid zone (EZ), and the presence of disorganization of the retinal inner layers (DRIL), on visual recovery post-intravitreal anti-VEGF injection in relation to the CVI.