Macular hole closure following anti-vascular endothelial growth factor injection in an eye with myopic choroidal neovascularization

Dear Editor, I am Cheolmin Yun, from the Department of Ophthalmology, Korea University College of Medicine. I write to present a case report of a female patient with a myopic patient suffering from atrophic choroidal neovascularization (CNV) and a full thickness macular hole (FTMH), who was treated with an intravitreal anti-vascular endothelial growth factor (VEGF) injection without vitrectomy. A FTMH in an eye with high myopia has been suggested to have a poorer anatomical and visual prognosis than in an eye without high myopia [1]. FTMHs were reported in 6.26% of highly myopic eyes, but cases with a CNV and a FTMH in the same eye were not common[2]. Shimada [3] presented cases with a FTMH associated with chorioretinal atrophy adjacent to myopic CNV. They suggested that eyes at the atrophic stage of myopic CNV have a higher risk of developing a FTMH, and recommended periodic optical coherence tomography (OCT) examinations for a FTMH. However, the best therapy for these patients has not been determined. A 68-year-old female presented with a ten-day history of decreased visual acuity OD. Her vision was 1.52 logMAR OD. The anterior segment was normal. The axial length of right eye was 28.71 mm. Fundoscopic examination of the right eye showed a subretinal hemorrhage. Fluorescein angiography (FA) indicated a type 2 CNV located close to the fovea with leakage (Figure 1). The patient underwent spectral-domain optical coherence tomography (SD-OCT, 3D OCT-1000 Mark II, Topcon Corp., Tokyo, Japan) examination using three-dimensional scanning protocols with 128 B-scans (512 A-scans per B-scan with a length of 6 mm). The SD-OCT revealed vitreomacular adhesion (Figure 2), and the patient was diagnosed with myopic CNV. Photodynamic therapy (PDT) was performed with verteporfin (Visudyne; Novartis AG, B俟lach, Switzerland). On the SD-OCT scan obtained ten months after the treatment for CNV, retinoschisis and macular detachment were noted adjacent to the previous CNV lesion. She had no visual symptoms and her vision was 1.52 logMAR. Seventeen months after PDT, the patient presented with visual dimness. Her vision was decreased to 2.00 logMAR. SD-OCT demonstrated a FTMH at the location of the previous macular detachment. However, FA did not show apparent leakage from the CNV. Pars plana vitrectomy was recommended. However, the patient refused the surgery. Three weeks after initial diagnosis of the FTMH, a SD-OCT scan revealed that the FTMH had not resolved. After obtaining informed consent, she underwent intravitreal injection of bevacizumab (Avastin; Genentech, South San Francisco, CA, USA). Five days after the intravitreal injection of bevacizumab, closing of the FTMH was observed on SD-OCT examination. SD-OCT images obtained six weeks after the intravitreal injection showed that the macular edema and subretinal fluid were further decreased. Vitreomacular adhesion, which had been observed on SD-OCT before the anti-VEGF injection, was unchanged after closure of the FTMH. FA did not show any change in the CNV. SD-OCT images obtained three months after the intravitreal injection showed that the macular edema and subretinal fluid were further decreased. The patient's vision recovered to 1.70 logMAR. The macular hole remained closed until twenty months after the intravitreal injection. In our case, the FTMH eventually developed adjacent to the atrophic CNV that had been treated with PDT. Shrinkage and regression of CNV at the atrophic stage were suggested to induce a FTMH by centrifugal and tangential stretching of the extremely thin atrophic retina at the edge of the CNV [3]. The traction force must be one of the reasons for the Macular hole closure following anti-VEGF injection