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 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 28  |  Issue : 2  |  Page : 116-119

Myopic choroidal neovascular membrane: A retrospective study


Department of Vitreoretinal Services, Giridhar Eye Institute, Kochi, Kerala, India

Date of Web Publication20-Mar-2017

Correspondence Address:
S Sindhu
Fellow National Board (Vitreoretinal Surgery), Giridhar Eye Institute, Kadavathara, Kochi, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/kjo.kjo_25_16

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  Abstract 


Purpose: The purpose of the study was to analyse the fundus fluorescein angiographic (FFA) and Spectral domain Optical coherence tomographic (SD- OCT) patterns of myopic CNVM and to evaluate their response to anti-VEGF.
Materials and Methods: This is a retrospective analysis of 24 treatment naïve eyes diagnosed with myopic CNVM. Eyes with age related macular degeneration, coexisting diabetes mellitus, inflammatory CNVM, idiopathic CNVM and Pseudophakia were excluded.Analysis of degree of myopia, the best corrected visual acuity (BCVA) at presentation and one year after treatment, FFA features, SD-OCT images and the response to intravitreal anti VEGF injections were carried out.
Results: 24 eyes of 21patients ( 6 males, 15 females) were included in the study Mean age of the patients was 44.78 ± 17.40 years.Degree of myopia ranged from -2.5D to -22 D. Fundus fluorescein angiography showed classic CNVM in all eyes with subfoveal location in 19 eyes and juxtafoveal in 5 eyes. SD-OCT imaging showed subretinal hyperreflective material with intraretinal oedema in all eyes. Intravitreal bevacizumab (1.25mg in 0.5ml) was given in 18 eyes and ranibizumab (0.5 mg in 0.5ml) in 6 eyes. Mean number of injections taken was 1.83 (range 1 to 5). At 1 year follow up,13 eyes showed improvement in BCVA (54.16%), 6 worsened (25%), 5 remained stable (20.83%).
Conclusion: Myopic CNVM responds to finite number of anti-VEGF injections anatomically and visually with no associated complications. The worsening is due to degenerative changes rather than recurrence of CNVM.

Keywords: Myopic choroidal neovascular membrane and anti-VEGF


How to cite this article:
Sindhu S, Mahesh G, Rajesh B, Giridhar A. Myopic choroidal neovascular membrane: A retrospective study. Kerala J Ophthalmol 2016;28:116-9

How to cite this URL:
Sindhu S, Mahesh G, Rajesh B, Giridhar A. Myopic choroidal neovascular membrane: A retrospective study. Kerala J Ophthalmol [serial online] 2016 [cited 2019 Nov 12];28:116-9. Available from: http://www.kjophthal.com/text.asp?2016/28/2/116/202470




  Introduction Top


Choroidal neovascular membrane (CNVM) occurs in approximately 5–10% patients of pathological myopia.[1] Myopic CNVM is a vision threatening complication of myopia, and historically it was thought to occur only in pathological myopia; however, now it is recognized that it can occur in any degree of myopia as well as in myopia without any degenerative changes in the fundus.[2] CNVM can be attributed to myopia by refractive status of the eye and by excluding other disorders associated with CNVM.[2]

Aim

The aim of this study was to analyze the fundus fluorescein angiographic (FFA) and spectral domain optical coherence tomographic (SD-OCT) patterns of myopic CNVM and to evaluate their response to anti vascular Endothelial Growth Factor (VEGF).


  Materials and Methods Top


This is a retrospective analysis of 24 treatment naïve eyes diagnosed with myopic CNVM with 1-year follow-up during the period of February 2012 to February 2014.

Exclusion criteria

Eyes with age-related macular degeneration, coexisting diabetes mellitus, inflammatory CNVM, idiopathic CNVM, and pseudophakia were excluded.

Analysis of degree of myopia, best corrected visual acuity (BCVA) at initial presentation and at the end of 1 year, Fundus Fluorescein Angiograhy (FFA) patterns, SD-OCT images, mean number of anti-VEGF injections needed for scarring were carried out. Monthly follow-up was performed for the first 3 months after intravitreal injections, at 6 months, at 1 year, and when the patient was symptomatic. Change in BCVA by more than or less than 2 lines on Snellen chart was considered as improvement or worsening, respectively. Patients with change in visual acuity of less than 2 Snellen lines were considered to be stable.


  Results Top


Twenty-four eyes of 21 patients (6 males and 15 females) were included in the study. Mean age of the patients was 44.78 ± 17.40 years. Lowest age included was 16 years, and 73 was the highest age. Degree of myopia ranged from − 2.5 D to − 22 D. Four patients showed presence of macular scar in other eye with history of previous treatment of CNVM. Three patients developed CNVM in the fellow eye during treatment period. FFA showed classic CNVM in all eyes, with subfoveal location in 19 eyes and juxtafoveal in 5 eyes [Figure 1].
Figure 1: Showing FFA finding of subfoveal classic CNVM in an eye with myopic CNVM

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SD-OCT imaging [Figure 2] showed subretinal hyperreflective material with intraretinal edema in all eyes. None of the eyes showed subretinal fluid.
Figure 2: Showing SD OCT finding of subretinal hyperreflective material in eye with myopic CNVM

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Intravitreal anti-VEGF injections were given at initial presentation and on pro re nata basis. Intravitreal bevacizumab (1.25 mg in 0.5 ml) was given in 18 eyes and ranibizumab (0.5 mg in 0.5 ml) in 6 eyes. Mean number of injections taken was 1.83 (range, 1–5). At 1-year follow up, 13 eyes showed improvement in BCVA (54.16%), 6 worsened (25%), and 5 remained stable (20.83%) [Chart 1]. Chorioretinal atrophy that developed around the regressed CNVM was the cause of worsening in 4 eyes and scar at fovea in 2 eyes.



[Figure 3] shows color fundus and SD OCT images of myopic CNVM eye before and after treatment with anti-VEGF. Twelve eyes showed regression with single injection of anti-VEGF, 8 eyes with 2 injections, and 1 eye with 3 injections. Three eyes showed recurrences, of which 2 eyes regressed with 4 injections and 1 eye with 5 injections [Chart 2].
Figure 3: Showing colour fundus and SD OCT images of eye with myopic CNVM before and after treatment with anti-VEGF

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Overall mean BCVA at baseline was 0.64 log MAR at initial presentation and 0.48 log MAR at 1 year follow up. This difference was found to be statistically significant (P = 0.04) [Table 1].
Table 1: Showing BCVA at baseline and 1 year after treatment

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With respect to visual outcome, there was no statistically significant difference noted with degree of myopia (P = 0.70) and age of the patient (P = 0.59). Analysis of mean number of injections and final BCVA outcome in patients less than 50 years (n = 13), and in patients more than 50 years (n = 11) did not reveal any statistically significant difference with respect to final visual outcome [Table 2].
Table 2: Showing mean number of anti-VEGF injections <than 50 years and >50 years

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  Discussion Top


The most common location of myopic CNVM is subfoveal, followed by juxtafoveal and rarely extrafoveal. In a prospective study by Yodoi et al.[3] in 22 eyes; 12 eyes showed juxtafoveal (54.5%) location of CNVM. Our study showed subfoveal location of CNVM in 19 eyes (79.17%) and juxtafoveal in 5 eyes (20.83%). None of our eyes had CNVM at extrafoveal location.

A study by Yoshida et al. showed that after initial presentation of myopic CNVM, CNVM develops in fellow eye in 35% of the patients within 8 years.[7] In a retrospective study of 73 patients with myopic CNVM, 17 patients (23.29%) presented with bilateral CNVM within 3 years.[8] Our study showed involvement of fellow eye in 3 patients during the treatment period. Probably less number in our study could be attributed to short duration of follow-up.

Myopic CNVM in SD-OCT shows subretinal hyperreflective material between neurosensory retina and retinal pigment epithelium with less subretinal and intraretinal fluid accumulation and absence of pigment epithelial detachment.[4] In our study, all eyes showed subretinal hyperreflective material with intraretinal edema and absence of subretinal fluid.

Several studies have reported an improvement in BCVA of 0.485 to 0.284 log MAR with an mean of 2.45 anti-VEGF injections.[9],[10],[11] Our study showed improvement of BCVA from 0.64 to 0.48 log MAR with mean number of 1.89 anti-VEGF injections.

A study by Gabrriya et al.[12] showed significantly better BCVA outcome as well as significantly less number of mean injections in patients less than 50 years versus above 50 years. Kuo et al.[5] found that difference in visual acuity gain between age groups above and below 50 years was not statistically significant similar to our study.

Our study had 24 eyes,13 eyes below 50 years and 11 eyes above 50 years, the lowest age being 16 and highest 73 years. In a retrospective study done by Kuo et al,[5] 36eyes were included with 25 eyes below 50 years and 31 eyes above 50 years. In a prospective study done by Arias et al[6] in 17 eyes,6 eyes were below 50 years and 11 above 50 years

Kuo et al.[5] also found that spherical equivalent was the predictive factor for final visual acuity in younger patients. In contrast, our study showed no statistically significant difference in final BCVA outcome with respect to degree of myopia. Myopic CNVM can occur at any degree of myopia and not only in eyes with pathological myopia, as postulated by Leveziel et al. and Reynolds et al.[13]

The vision loss in myopic CNVM is attributed to direct damage to photoreceptors, formation of fibrous pigmented scar, and atrophy around the regressed CNVM.[14],[15] Our study showed scar at fovea in 2 eyes and chorioretinal atrophy around regressed CNVM in 4 eyes as the cause of worsening.


  Conclusion Top


Myopic CNVM can occur at any degree of myopia and responds to finite number of anti-VEGF injections anatomically and visually with no associated complications. Age and degree of myopia had no correlation with development of CNVM and final BCVA. The worsening is because of degenerative changes rather than recurrence of CNVM. However, there is need for long-term follow-up as recurrence is commonly seen after first year in eyes with myopic CNVM.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Avila MP, Weiter RJJ, Jalkh AE, Trempe CL, Pruett RC, Schepens CL. Natural history of choroidal neovascularization in degenerative myopia. Ophthalmology 1984;91:1573-81.  Back to cited text no. 1
    
2.
Leveziel N, Yu Y, Reynolds R, Tai A, Meng W, Caillaux V, et al. Genetic factors for choroidal neovascularization associated with high myopia. Invest Ophthalmol Vis Sci 2012;53:5004-9.  Back to cited text no. 2
    
3.
Yodoi Y, Tsujikawa A, Nakanishi H, Otani A, Tamura H, Ojima Y, et al. Central retinal sensitivity after intravitreal injection of bevacizumab for myopic choroidal neovascularization. Am J Ophthalmol 2009;147:816-24.  Back to cited text no. 3
    
4.
Baba T, Ohno-Matsui K, Yoshida T, Yasuzumi K, Futagami S, Tokoro T, et al. OCT of CNV in high myopia, Acta Ophthalmol Scand 2002;80:82-7.  Back to cited text no. 4
    
5.
Kuo JZ, Ong FS, Yeung L, Wu WC, Chen YP, Wang NK, et al. Predictive factors for visual outcome to intravitreal bevacizumab in Chinese patients with myopic choroidal neovascularisation. Retina 2011;31:1835-40.  Back to cited text no. 5
    
6.
Arias MP, Planas N, Prades S. Intravitreal Bevacizumab for choroidal neovascularisation secondary to pathological myopia: 6 month result. Br J Opthalmol 2008;92:1035-9.  Back to cited text no. 6
    
7.
Ohno-Matsui K, Yoshida T, Futagami S, Yasuzumi K, Shimada N, Kojima A, et al. Patchy atrophy and lacquer cracks predispose to the development of choroidal neovascularisation in pathological myopia. Br J Ophthalmol 2003;87:570-3.  Back to cited text no. 7
    
8.
Leveziel N, Caillaux V, Bastuji-Garin S, Zmuda M, Souied EH. Angiographic and optical coherence tomography characteristics of recent myopic choroidal neovascularization. Am J Ophthalmol 2013;155:913-9.  Back to cited text no. 8
    
9.
Chang LK, Spaide RF, Brue C, Freund KB, Klancnik JM Jr, Slakter JS. Bevacizumab treatment for subfoveal choroidal neovascularisation from causes other than age related macular degeneration. Arch Ophthalmol 2008;126:951-4.  Back to cited text no. 9
    
10.
Rheaume MA, Sebag M. Intravitreal bevacizumab for the treatment of choroidal neovasularisation associated with pathological myopia. Can J Ophthalmol 2008;43:565-80.  Back to cited text no. 10
    
11.
Wakabayashi T, Ikuno Y, Gomi F. Different dosing of intravitreal bevacizumab for choroidal neovascularisation because of pathological myopia. Retina 2011;31:880-6.  Back to cited text no. 11
    
12.
Gharbiya M, Allievi F, Mazzeo L, Gabrieli CB. Intravitreal bevacizumab treatment for choroidal neovascularisation in pathological myopia: 12 month results. Am J Ophthalmol 2009;147:84-93.  Back to cited text no. 12
    
13.
Leveziel N, Yu Y, Reynolds R, Tai A, Meng W, Caillaux V, et al. Genetic factors for choroidal neovascularization associated with high myopia. Invest Ophthalmol Vis Sci 2012;53:5004-9.  Back to cited text no. 13
    
14.
Jonas JB, Jonas SB, Jonas RA, Holbach L, Dai Y, Sun X, et al. Parapapillary atrophy: Histological gamma zone and delta zone. PLoS One 2012;7:e47237.  Back to cited text no. 14
    
15.
Yoshida T, Ohno-Matsui K, Yasuzumi K, Kojima A, Shimada N, Futagami S, et al. Myopic choroidal neovascularisation a 10 year follow up. Ophthalmolgy 2003;110:1297-305.  Back to cited text no. 15
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2]



 

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