Abstract
In recent years, optical coherence tomography (OCT) biomarkers for specific retinal diseases have been found to be associated with treatment outcome and disease recurrence. The main purposes of this study were to identify OCT biomarkers for myopic choroidal neovascularization (mCNV) treated with intravitreal injection of anti‐vascular endothelial growth factor (anti‐VEGF). OCT features in 43 eyes of 39 patients with mCNV treated with anti‐VEGF with at least 1 year of follow‐up were retrospectively analyzed. Eyes with subretinal hyperreflective material (SHM) in baseline spectral‐domain OCT (SD‐OCT) had significantly more visual improvement than eyes without SHM at month 6 (p = 0.007) and had a trend of more visual improvement than eyes without SHM (p = 0.058) at month 12. Eyes with subretinal fluid (SRF) at baseline had significantly more central retinal thickness (CRT) decrease than patients without SRF at month 6 and 12 (p = 0.012 and 0.006 respectively). In univariate regression analysis, dome‐shaped macula (DSM), SRF in baseline OCT image and fuzzy border of mCNV when entering pro re nata (PRN) injection protocol tended to have higher risk of disease recurrence in 1 year (odds ratio: 14.86 (p = 0.003), 3.75 (p = 0.049) and 22.92 (p < 0.001) respectively). However, they were not significant in multivariate regression analysis. OCT biomarkers at baseline could provide prognostic information for mCNV management.
Keywords: choroidal neovascularization, myopia, optical coherence tomography biomarker, vascular endothelial growth factor
1. INTRODUCTION
Pathologic myopia (PM) is one of the leading causes of low vision or blindness and is reported as varying from 5.8% to 31.3% in several studies globally. 1 Myopic choroidal neovascularization (mCNV) is one of the major vision‐threatening complications of pathologic myopia. Intravitreal injection of vascular endothelial growth factor inhibitors (anti‐VEGF) is currently the first‐line medical treatment for mCNV, while optical coherence tomography (OCT) can be extremely useful for physicians in evaluating treatment response concerning follow‐up of patients with CNV. Several baseline OCT biomarkers, such as CNV size and location, outer retina integrity, and subfoveal choroidal thickness have been reported to be associated with visual prognosis; 2 , 3 , 4 , 5 however, inconsistent consensus remains in the prediction of visual outcome while literature analyzing biomarkers for disease recurrence is lacking, so new imaging biomarkers in mCNV require further research.
In this study, we investigated baseline OCT biomarkers for not only visual gain but disease recurrence in mCNV as well after treatment with intravitreal injection of anti‐VEGF within 12 months.
2. METHODS
A retrospective review of medical records of patients who received intravitreal anti‐VEGF injections for treatment‐naive eyes mCNV from January 2018 to November 2021 was conducted, with the study being approved by the Institutional Review Board and Ethics Committee of the hospital and adhering to the tenets of the Declaration of Helsinki. Due to the retrospective nature of this research that utilized pre‐existing information of the patient group, informed consent was waived. All cases were assigned a number code and no personally identifiable information was revealed.
The inclusion criteria included treatment‐naïve patients who were under follow‐up for a minimum of 12 months; the presence of myopia with a spherical equivalent (S.E.) refractive error ≤ −6 D or axial length ≥ 26.5 mm; active CNV secondary to pathologic myopia defined as presence of leakage from CNV seen by fluorescein angiography and presence of intraretinal cyst (IRC) or subretinal fluid (SRF) or increase of central retinal thickness (CRT) seen by spectral‐domain optical coherence tomography (SD‐OCT); and a best corrected visual acuity (BCVA) of 3/60–6/12, which conforms to the range of reimbursement from the Taiwan National Health Insurance Scheme.
The exclusion criteria were prior treatments for CNV including photodynamic therapy (PDT) and thermal laser photocoagulation and intravitreal injection of anti‐VEGF; history of intraocular surgery, except cataract surgery; any intraocular surgery during the follow‐up period; subfoveal and juxtafoveal myopic traction maculopathy; and CNV secondary to ocular pathology other than pathologic myopia such as age‐related macular degeneration, choroiditis, angioid streaks or trauma.
Data variables collected included age, sex, BCVA (converted to the logarithm of the minimum angle of resolution: logMAR), intraocular pressure (IOP) and fundus photography, fundus fluorescein angiography, CRT and optical characteristics according to OCT (Spectralis HRA + OCT imaging; Heidelberg Engineering, Heidelberg, Germany) and treatment. Myopic maculopathy was graded into five categories according to the International Photographic Classification and Grading System using color fundus photographs: category 0, no myopic retinal lesions, category 1, tessellated fundus only; category 2, diffuse chorioretinal atrophy; category 3, patchy chorioretinal atrophy; category 4, macular atrophy. 6
On the baseline SD‐OCT image, CRT was calculated by built‐in software. Subfoveal choroidal thickness (SFCT) was measured as the distance from the outer border of the RPE at the point of the thinnest inner retinal layers on as a foveal point to the inner surface of the sclera using a manual caliper function of the built‐in software. Baseline CNV location was classified into three groups: subfoveal, juxtafoveal and extrafoveal, with subfoveal CNV defined as the location of CNV under the geometric center of the foveal avascular zone (FAZ); juxtafoveal CNV defined as the location of CNV at 1–199 μm from the geometric center of the foveal avascular zone (FAZ); while extrafoveal CNV was defined as the location of CNV at ≥200 μm from the geometric center of the foveal avascular zone (FAZ). We further measured the highest CNV height and widest CNV width with a manual caliper function of the built‐in software in OCT as well as the CNV size on fluorescein angiography by the built‐in software.
Baseline OCT biomarkers including pigment epithelial detachment (PED), SRF, IRC, subretinal hyperreflective material (SHM), ellipsoid zone (EZ) disruption and external limiting membrane (ELM) disruption were also recorded. Dome‐shaped macula (DSM) was defined according to the literature with a bulge of retinal pigment epithelium (RPE), choroid and sclera of more than 50 μm in height above a line connecting the RPE on both sides outside of the DSM. 4
The treatment protocol and follow‐up period received for patients in this study were in accordance with the PRN regimen in a previous report. 7 The anti‐VEGF agents used in this study included bevacizumab, ranibizumab and aflibercept. If the signs of active disease (e.g., intraretinal or subretinal fluid) occurred on OCT or mCNV leakage noted in the fluorescein angiography (FA), then the patient would receive additional injection. Typically, after intravitreal injection of anti‐VEGF, SHM regresses gradually along with slight thickening of RPE. We further reviewed the SD‐OCT image when entering PRN injection protocol. If there was few remaining SHM and blurry margin of RPE layer, we recorded it as fuzzy border of the CNV.
The primary endpoint of the current study was to determine the predictive factors of visual and anatomical outcome and recurrence of disease activity, with secondary endpoints focused on evaluating the mean change of BCVA and CRT.
Data were presented as the mean and standard deviation for continuous variables, and as for categorical variables, presented as numbers with percentages in parentheses. Data with skewed distribution would be expressed as medians (IQR) instead. The Student t test was used to compare logMAR and OCT characteristic changes from baseline at months 6 and 12 while the generalized estimating equations (GEE) model was used to estimate the changes of visual acuity and CRT varying with time. The association between the variable of interest and within‐1‐year retreatment was identified by univariate and multivariate logistic regression. The level of significance was set at p < 0.05, and all statistical tests were performed using IBM SPSS 26 (IBM Corp. Released 2019. Armonk, NY: IBM Corp).
3. RESULTS
Forty‐three eyes of 39 patients were enrolled in the study. The baseline clinical characteristics are shown in Table 1. The mean age was 49.4 ± 12.6 years and females were predominant in our study. The mean axial length was 29.1 ± 1.3 mm. Dome‐shaped macula was noted in 10 (23.3%) patients. Location of mCNV was subfoveal in 33 (76.7%) eyes. Median subfoveal choroidal thickness was 60 μm (1st quartile: 36 μm, 3rd quartile: 83 μm). Mean CNV height was 170.8 ± 94.2 μm at baseline and mean CNV width was 1043.3 ± 685.8 μm at baseline. For baseline OCT biomarker, 42 (97.7%) eyes showed EZ disruption; 42 (97.7%) eyes showed ELM disruption; 38 (88.4%) eyes showed SHM; 2 (4.65%) eyes showed PED; while 17 (39.5%) patients had SRF and six (14.0%) patients had IRC. Baseline logMAR BCVA was 0.52 ± 0.38 and baseline CRT was 330.5 ± 69.1 μm.
TABLE 1.
Baseline clinical characteristics of study subjects
| Characteristics | Statistics (n = 43) |
|---|---|
| Age | 49.4 ± 12.6 (range: 23–79) |
| Female sex | 40 (93.02%) |
| Laterality | |
| Left | 16 (37.21%) |
| Right | 27 (62.79%) |
| Lens status | |
| Phakic | 29 (67.44%) |
| Pseudophakic | 14 (32.56%) |
| Axial length, mm | 29.1 ± 1.3 (range: 25.1–31.7) |
| MM category | |
| Normal (C0) | 2 (5.00%) |
| Tessellated (c1) | 2 (5.00%) |
| Peripapillary diffuse CR atrophy (C2) | 28 (70.00%) |
| Patchy atrophy (C3) | 5 (12.50%) |
| Macular atrophy (C4) | 3 (7.50%) |
| Spherical equivalent, diopter | −9.6 ± 5.8 |
| DSM | |
| N | 33 (76.74%) |
| Y | 10 (23.26%) |
| CNV location | |
| Subfovea | 33 (76.74%) |
| Juxtafovea | 7 (16.28%) |
| Extrafovea | 3 (6.98%) |
| CNV, μm or mm2 | |
| Height, μm | 170.8 ± 94.2 |
| Width, μm | 1043.3 ± 685.8 |
| Size, mm2 | 0.40 ± 0.42 |
| Baseline SFCT, μm | 60 (36–83) |
| Baseline OCT biomarker | |
| EZ disruption | 42 (97.67%) |
| ELM disruption | 42 (97.67%) |
| SHM | 38 (88.37%) |
| PED | 2 (4.65%) |
| SRF | 17 (39.53%) |
| IRC | 6 (13.95%) |
Abbreviations: CNV, choroidal neovascularization; DSM, dome‐shaped macula; ELM, external limiting membrane; EZ, ellipsoid zone; IRC, intraretinal cyst; OCT, optical coherence tomography; PED, pigment epithelioid detachment; SFCT, subfoveal choroidal neovascularization; SHM, subretinal hyperreflective material; SRF, subretinal fluid.
Mean BCVA and CRT at baseline and months 1, 3, 6 and 12 are shown in Table 2. Visual improvement was most achieved at months 3 and 6 with a gain of 0.18 and 0.17 respectively, estimated by GEE model. CRT decreased at month 1 and was maintained over all 12 months.
TABLE 2.
Best corrected visual acuity and central retinal thickness changes during 12 months
| logMAR BCVA | CRT | |||
|---|---|---|---|---|
| Mean ± SD | GEE estimates | Mean ± SD | GEE estimates | |
| Baseline | 0.52 ± 0.38 | ref. group | 330.49 ± 69.19 | ref. group |
| 1 month | 0.42 ± 0.35 | −0.10 (−0.19 ~ −0.01) | 292.37 ± 55.07 | −38.12 (−53.35 ~ −22.88) |
| 3 month | 0.35 ± 0.38 | −0.18 (−0.28 ~ −0.07) | 291.49 ± 53.39 | −39.00 (−54.50 ~ −23.50) |
| 6 month | 0.35 ± 0.39 | −0.17 (−0.28 ~ −0.07) | 295.35 ± 55.78 | −35.14 (−51.29 ~ −18.99) |
| 12 month | 0.39 ± 0.45 | −0.13 (−0.26 ~ 0.00) | 286.09 ± 56.63 | −44.40 (−61.36 ~ −27.43) |
Abbreviations: BCVA, best corrected visual acuity; CRT, central retinal thickness; GEE, generalized estimating equations; ref., reference.
The average number of injections was 3.8 ± 2.4. Twenty‐nine (67.4%) eyes entered PRN injection protocol without fuzzy border of CNV, and 4 eyes (13.8%) had disease recurrence during the 1‐year follow‐up. The other 14 (32.6%) eyes entered PRN protocol with fuzzy border of CNV (Figure 1), and 11 eyes (78.6%) had disease recurrence in 1 year. Eyes entering PRN protocol with fuzzy border of CNV had significantly higher risk of recurrence than those without (p < 0.001); however, there was no significant difference on visual and CRT change at 1 year between the group with or without fuzzy border when entering PRN protocol (p = 0.185 and 0.707 respectively).
FIGURE 1.
A 53‐year‐old female patient with mCNV. (A) Initial OCT image showed juxtafoveal CNV with SHM (arrow) and few SRF. (B) After 1 injection of aflibercept, the OCT image showed no SRF and obvious decrease of CRT. However, there was still fuzzy border (arrow) of CNV (C) 4 months later, and patient suffered from the recurrence of CNV (arrow) with increased CRT.
The predictive factors for visual improvement and thickness changes are shown in Table 3. Eyes with SHM at baseline had significantly more visual improvement than eyes without SHM at month 6 (p = 0.007), and a trend of more visual improvement than eyes without SHM at month 12 (p = 0.058). Eyes with SRF in the baseline SD‐OCT image had significantly more CRT decrease than patients without SRF at months 6 and 12 (p = 0.012 and 0.006 respectively). Baseline CNV height was negatively correlated with the CRT changes at months 6 and 12. (p = 0.017 and 0.008 respectively) There was no significant association between visual gain and CRT changes with CNV width and size.
TABLE 3.
Best corrected visual acuity and central retinal thickness changes from baseline at 6 months and 12 months compared between baseline OCT characteristics.
| logMAR BCVA | CRT | |||||
|---|---|---|---|---|---|---|
| Baseline OCT | Baseline | Diff6M | Diff12M | Baseline | Diff6M | Diff12M |
| DSM | ||||||
| N (33) | 0.5 ± 0.40 | −0.2 ± 0.35 | −0.2 ± 0.42 | 325.1 ± 56.78 | −32.7 ± 58.37 | −42.6 ± 60.16 |
| Y (10) | 0.5 ± 0.35 | −0.01 ± 0.37 | 0.03 ± 0.48 | 348.4 ± 102.03 | −43.1 ± 41.84 | −50.3 ± 49.79 |
| p‐value | 0.484 | 0.103 | 0.172 | 0.356 | 0.605 | 0.715 |
| SHRM | ||||||
| N (5) | 0.5 ± 0.38 | 0.2 ± 0.28 | 0.2 ± 0.27 | 306.2 ± 27.96 | −26.6 ± 21.24 | −39.4 ± 35.54 |
| Y (38) | 0.5 ± 0.39 | −0.2 ± 0.35 | −0.2 ± 0.44 | 333.7 ± 72.52 | −36.3 ± 57.75 | −45.1 ± 60.05 |
| p‐value | 0.693 | 0.007 | 0.058 | 0.41 | 0.715 | 0.839 |
| SRF | ||||||
| N (26) | 0.5 ± 0.39 | −0.2 ± 0.31 | −0.1 ± 0.42 | 315.9 ± 56.42 | −18.5 ± 40.67 | −25.4 ± 48.96 |
| Y (17) | 0.5 ± 0.37 | −0.2 ± 0.45 | −0.2 ± 0.48 | 352.8 ± 81.97 | −60.6 ± 64.25 | −73.4 ± 58.63 |
| p‐value | 0.946 | 0.773 | 0.732 | 0.088 | 0.012 | 0.006 |
| IRC | ||||||
| N (37) | 0.5 ± 0.38 | −0.2 ± 0.37 | −0.1 ± 0.44 | 324.8 ± 57.72 | −33.0 ± 56.23 | −40.9 ± 58.41 |
| Y (6) | 0.6 ± 0.40 | −0.3 ± 0.36 | −0.5 ± 0.28 | 365.3 ± 120.52 | −48.3 ± 45.99 | −66.2 ± 49.91 |
| p‐value | 0.689 | 0.400 | 0.068 | 0.187 | 0.531 | 0.323 |
| CNV width | ||||||
| Pearson's r | 0.15 | 0.111 | 0.023 | 0.26 | −0.138 | −0.18 |
| p‐value | 0.334 | 0.478 | 0.887 | 0.096 | 0.377 | 0.247 |
| CNV height | ||||||
| Pearson's r | 0.26 | −0.241 | −0.27 | 0.52 | −0.364 | −0.4 |
| p‐value | 0.10 | 0.12 | 0.084 | <0.001 | 0.017 | 0.008 |
| CNV size | ||||||
| Pearson's r | 0.05 | −0.067 | 0.043 | 0.15 | −0.096 | −0.09 |
| p‐value | 0.759 | 0.668 | 0.788 | 0.324 | 0.542 | 0.566 |
| SFCT | ||||||
| Pearson's r | −0.18 | 0.273 | 0.282 | −0.14 | 0.093 | 0.042 |
| p‐value | 0.255 | 0.076 | 0.070 | 0.376 | 0.554 | 0.789 |
Abbreviations: BCVA, best corrected visual acuity; CRT, central retinal thickness; DSM, dome‐shaped macula; ELM, external limiting membrane; EZ, ellipsoid zone; IRC, intraretinal cyst; OCT, optical coherence tomography; PED, pigment epithelioid detachment; SHM, subretinal hyperreflective material; SRF, subretinal fluid.
The predictive factors for disease recurrence in 1 year are shown in Table 4. Patients with DSM, with SRF at baseline and with fuzzy border of CNV when entering PRN injection protocol tended to have higher risk of disease recurrence (odds ratio: 14.86 (p = 0.003), 3.75 (p = 0.049) and 22.92 (p < 0.001) respectively).
TABLE 4.
Associations between the factors and recurrence in 1 year, univariate analysis by logistic regression
| Variable | Odds ratio (95% CI) | p‐value |
|---|---|---|
| Age | 1.02 (0.97–1.08) | 0.407 |
| Axial length | 1.12 (0.67–1.86) | 0.663 |
| MM category | ||
| Normal (C0) | 1 (reference) | |
| Tessellated (C1) | 1.00 (0.03– +Inf) | >0.999 |
| Peripapillary diffuse CR atrophy (C2) | 1.06 (0.08– +Inf) | 0.9655 |
| Patchy atrophy (C3) | 2.22 (0.14– +Inf) | 0.5714 |
| Macular atrophy (C4) | 1.00 (0.00– +Inf) | |
| Dome‐shaped macula | 14.86 (2.56–86.35) | 0.003 |
| Baseline CNV width | 1.00 (1.00–1.00) | 0.327 |
| Baseline CNV height | 1.00 (0.99–1.00) | 0.458 |
| Baseline CNV size | 2.04 (0.44–9.37) | 0.359 |
| Baseline SFCT | 1.00 (0.99–1.01) | 0.925 |
| Baseline OCT biomarker | ||
| EZ disruption (Y vs. N) | Estimate diverges | 0.999 |
| ELM disruption (Y vs. N) | Estimate diverges | 0.999 |
| SHM (Y vs. N) | 0.31 (0.05–2.09) | 0.228 |
| PED (Y vs. N) | Estimate diverges | 0.999 |
| SRF (Y vs. N) | 3.75 (1.00–14.02) | 0.049 |
| IRC (Y vs. N) | 0.92 (0.15–5.74) | 0.932 |
| CNV with or without fuzzy border when entering PRN injection protocol: With vs. Without | 22.92 (4.37–120.10) | <0.001 |
Abbreviations: CNV, choroidal neovascularization; DSM, dome‐shaped macula; ELM, external limiting membrane; EZ, ellipsoid zone; IRC, intraretinal cyst; OCT, optical coherence tomography; PED, pigment epithelioid detachment; PRN, pro‐re nata; SFCT, subfoveal choroidal neovascularization; SHM, subretinal hyperreflective material; SRF, subretinal fluid.
4. DISCUSSION
In our study, eyes with naive mCNV receiving intravitreal injection of anti‐VEGF achieved significant improvement of visual and anatomical parameters during 1‐year follow‐up. The mean number of injections was 3.8 ± 2.4. The results were compatible with the literature. RADIANCE and MYRROR studies both showed significant visual and anatomical improvement over a period of 48 weeks 8 , 9 ; similarly, data from real world studies also showed visual and anatomical improvement after treatment. 10 , 11 , 12
Our study showed that eyes with SHM at baseline had significantly more visual improvement at 6 months and a tendency of more visual improvement at 12 months compared with eyes without SHM at baseline. SHM is a tomographic feature seen on OCT as a hyperreflective material located between the neurosensory retina and RPE layer, and could be made up of fluid, fibrin, blood, scar, and macular neovascular membranes. 12 Battaglia Parodi et al. also reported patients presenting with hyperreflective exudation who displayed greater final BCVA improvement. 13 An earlier retrospective study by Bruyere et al showed that subretinal hyperreflective exudation was an SD‐OCT finding that correlated with signs of active mCNV but did not correlate with significant visual improvement at 6 months. 14 Due to limitations of the small case number and different inclusion criteria in different series, the exact role of SHM in the prognosis of myopia CNV remains unclear, so further investigation is warranted.
Other factors, including better baseline VA, lower S.E., EZ and ELM integrity, nonsubfoveal CNV location and smaller CNV area were reported to be associated with better VA at 12 months or revealed more visual improvement in previous studies. 2 , 3 , 4 , 5 In our study, we did not analyze S.E. due to some of our study subjects having had refractive surgery before; additionally, CNV area was not a predicting factor of visual improvement. Multiple factors might affect visual acuity in mCNV patients including CNV location, expansion of chorioretinal atrophy or cataract progression. We intend to further explore these factors in future studies.
In our study, SRF and greater CNV height in baseline OCT image were associated with more decrease of CRT at 6 and 12 months. It is easy to understand that eyes with SRF and greater CNV height usually have higher CRT at baseline and will gain more CRT decrease when CNV activity decrease.
Previous studies have shown possible risk factors related to mCNV recurrence including new onset and progressive lacquer crack, age, gender, duration of myopic CNV, baseline SFCT as well as CNV size; however, the conclusion is still controversial. Our study showed SRF in baseline OCT image, DSM and presence of fuzzy border of CNV when entering PRN injection protocol were associated with higher risk of disease recurrence in univariate analysis. The multivariate analysis did not show significant result. Differing from exudative AMD, mCNV usually has lower disease activity with minimal SRF in OCT image, 7 although the presence of SRF has been reported as a sign of CNV activity in exudative AMD patients. 15 SRF was detected at baseline in 17 eyes (39.5%) in our study. It is speculated that high disease activity at baseline might lead to more recurrence during follow‐up. Wang et al. reported that the risk of recurrence was much higher in patients with a thicker macula than in those with a thinner macula. 3
Dome‐shaped macula (DSM) was first described by Gaucher and coworkers in 2008 who observed a dome‐shaped elevation on OCT within the region of a posterior staphyloma (PS) seen exclusively in highly myopic eyes. 16 It was initially thought to be an inward bulging of the sclera, but was later proven to be caused by a localized thickening of sclera by Imamura et al. 17 The focal area of increased scleral thickness has been thought to mechanically increase choroidal fluid outflow resistance with increased hydrostatic pressure within the choroid, leading to large, hyperpermeable choroidal patchy vessels. These patchy vessels may further cause focal RPE dysfunction, leading to formation of PED, serous retinal detachment and even choroidal neovascularization. Cai et al. reported that there were no differences in visual and CRT improvement for mCNV with and without a DSM after anti‐VEGF treatment for 1 year 18 ; however, in their study, patients without DSM showed greater reduction of CRT in the first month, which might imply that patients without a DSM might be more sensitive to the anti‐VEGF treatment at the early stage. Wang et al. reported that eyes with CNV in the DSM group had a larger CNV area than those in the non‐DSM group, 19 so the VEGF level might be higher in DSM eyes with CNV, which might lead to more risk of recurrence.
In SD‐OCT, most active myopic CNV appears as a dome‐shaped hyperreflective elevation above the retinal pigment epithelium. Due to its low activity, myopic CNV is usually not accompanied by apparent subretinal fluid in many cases. Accordingly, unlike exudative AMD, it is hard to monitor disease activity in the early recurrence. In the study by Intronini et al., hyper‐reflective lesion with fuzzy borders appeared more meaningful than CRT in the evaluation of myopic CNV activity. 20 Our study found that eyes entering the PRN protocol with fuzzy border had significantly higher risk of disease recurrence within 1 year. This sign could be a potential marker to plan treatment interventions.
Ng et al. conducted a retrospective cohort study investigating factors associated with need for retreatment for mCNV during a mean follow‐up period of 25.1 months. 21 They found that larger baseline CNV size could possess higher risk for retreatment. Apposite their study, ours had relatively small sample size and we only followed up for 1 year.
There are some limitations in the current study. Firstly, this is a retrospective study with a small sample size with short‐time follow‐up. Secondly, different anti‐VEGF agents were used in some patients. Although there was a lack of a prospective randomized controlled head‐to‐head trial of different anti‐VEGF agents for mCNV treatment, several retrospective studies have shown similar efficacy of these agents. 22 , 23
In conclusion, our study showed baseline OCT biomarkers could provide prognostic information in the treatment of mCNV. SHM might indicate better visual outcome at 1 year. Myopic CNV in eyes with DSM, SRF at baseline and fuzzy CNV border when entering PRN protocol were risk factors for disease recurrence in 1 year; accordingly, close follow‐up for these patients was required. Further studies with larger sample sizes and more precise study design are needed to assess the value of these image biomarkers.
CONFLICT OF INTEREST STATEMENT
The authors declare no competing interests.
ACKNOWLEDGMENT
The authors would like to thank Y.C. Chang, P.K. Liu, K.C. Cheng, H.J. Wu, H.J. Lai and X.Z. Lin for providing materials and helpful advisement.
Lee DY, Wu P‐Y, Sheu S‐J. Optical coherence tomography biomarkers for myopic choroidal neovascularization treated with anti‐vascular endothelial growth factor. Kaohsiung J Med Sci. 2023;39(6):637–643. 10.1002/kjm2.12669
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