Genetic influence on visual outcomes of polypoidal choroidal vasculopathy.

Abstract

Dear Editor, We read with interest the article by Hata et al. [1], which reported that polypoidal choroidal vasculopathy (PCV) patients with the T risk allele of A69S had a higher rate of recurrence and were more likely to experience reduction of visual acuity (VA) during the second year, compared to patients without this allele. These findings may help determine the frequency of follow-up or the optimal treatment regimen for individual patients. In addition to genetic variations, we are curious whether the authors noted any phenotypic differences between the two groups of patients. Differences that are detectable clinically or on imaging modalities such as indocyanine green angiography (ICGA) or fluorescein angiography (FA) may be an important first step in sub-typing PCV patients [2–5]. The combination of clinical, imaging, and genetic features may allow stratification of PCV patients in order to ensure optimal management. Several authors have described different methods of classifying or sub-typing PCV, although most did not correlate this with VA outcomes. In a recent paper [6], a classification system for PCV was described, based on the type of branching vascular network (BVN) seen on ICGA and the presence of leakage seen on FA. Patients with Type A PCV (only interconnecting channels on ICGA) had the best outcomes over 5 years, with intermediate VA outcomes among Type B (BVN present, but no significant leak on FA), and the worst outcomes among Type C (BVN with significant leak on FA) (VA ≥20/40 at 5 years: 80 % vs. 66.7 % vs. 7.7 %, p<0.001). We agree with the authors that BVNmay persist after treatment, and new polyps may develop from either the same region of the BVN, or an entirely new part of it. In Fig. 3 of their article [1], a persistent BVN is observed on ICGA at 1 year, and the recurrent polyps develop at the periphery of the BVN at 2 years. In this paper, the authors mentioned that all eyes in the study, Bhad a polypoidal lesion, a branching vascular network, or type 2 choroidal neovascularization (CNV) beneath the foveal center^ [1]. We would like to confirm whether Btype 2 CNV^ refers to the OCT / anatomic classification of CNV [7]. PCV lesions tend to manifest with the appearance of occult CNV on FA, which usually corresponds to type 1 CNV (located beneath the retinal pigment epithelium). In contrast, type 2 CNV on OCT typically corresponds to classic CNV, which is uncommon in PCV. The authors discussed the potential complications of photodynamic therapy (PDT), including subretinal and breakthrough vitreous hemorrhage. However, even untreated polyps may develop spontaneous hemorrhage, which, in some cases, may be extensive, and sometimes lead to vitreous or suprachoroidal hemorrhage [8]. In addition, complications such as choroidal ischemia and atrophy may result from repeated treatment with full-fluence PDT. This should be avoided in patients with good VA and relatively mild subretinal fluid. In conclusion, we congratulate the authors on their results, which provide additional insights on the role of genetic variations on the outcomes of PCV. * Colin S. Tan Colintan_eye@yahoo.com.sg