Swept-Source Optical Coherence Tomography Angiography in Vitreomacular Traction Syndrome

Zofia Anna Nawrocka; Zofia Nawrocka; Jerzy Nawrocki

doi:10.1177/24741264211045867

. 2021 Nov 8;6(1):31–39. doi: 10.1177/24741264211045867

Swept-Source Optical Coherence Tomography Angiography in Vitreomacular Traction Syndrome

Zofia Anna Nawrocka ^1,^✉, Zofia Nawrocka ¹, Jerzy Nawrocki ¹

PMCID: PMC9976224 PMID: 37007724

Abstract

Purpose:

A swept-source optical coherence tomography angiography (SS-OCTA) analysis of vasculature in vitreomacular traction (VMT) before and after surgery as well as 15 months’ “watchful waiting” follow-up data.

Methods:

A retrospective analysis of 38 eyes. Patients were divided into group 1: untreated (20 eyes); group 2: untreated, spontaneous release of traction (4 eyes); and group 3: vitrectomy (14 eyes).

Results:

In all cases, SS-OCTA of the choriocapillaris revealed a hyporeflective area, which disappeared after traction release. In group 1, none of the analyzed factors significantly changed. In group 2, visual acuity (VA) improved from 0.3 logMAR to 0.1 logMAR. None of the following parameters significantly changed: central choroidal thickness, superficial fovea avascular zone (sFAZ), deep fovea avascular zone (dFAZ), and vessel densities. In 1 eye a lamellar macular hole formed. Factors increasing the chances of spontaneous release of traction were width of traction and central retinal thickness (P < .05). In group 3, VA improved from 0.27 Snellen (0.6 logMAR) to 0.44 Snellen (0.4 logMAR) (P < .05). Postoperative OCTA revealed significant decreases in central retinal thickness (P < .001), the parameters sFAZ, and dFAZ (P < .05).

Conclusions:

sFAZ and dFAZ decreased after vitrectomy but not after spontaneous release of traction. VA was better in eyes with spontaneous release of traction. The degree of improvement in VA was greater in the vitrectomy group. In all cases a hyporeflective area is visible in the choriocapillaris layer in SS-OCTA. It disappears when traction is released. Early treatment, at least in patients with lower VA, might be beneficial.

Keywords: OCT-A, swept-source OCT angiography, vitrectomy, vitreomacular adhesion, vitreomacular traction, VMTS

Introduction

Vitreomacular traction (VMT) is defined as perifoveal vitreous cortex detachment. It coexists with macular cortex attachment and is associated with retinal anatomic changes such as macular pseudocysts, macular schisis, cystoid macular edema, and subretinal fluid.¹

Because the disease is reported to be symptomatic in only about 1.5% of cases, there is a paucity of data on its natural history in the peer-reviewed literature.^2
-4 Despite the lack of natural course data and the lack of clear indications for treatment, multiple treatment options are available, such as “watchful waiting,” ocriplasmin, gas injection, or vitrectomy. Observation has shown that the traction may spontaneously release, although this event is unpredictable.⁵ Detailed analysis of the anatomy and function in either spontaneous resolution or after treatment of VMT is required to allow the physician and patient to make decisions regarding specific cases. Rapid developments in swept-source optical coherence tomography (SS-OCT) and swept-source optical coherence tomography angiography (SS-OCTA) imaging methods have provided greater insight into understanding changes in the retina and their influence on functional results in patients with VMT syndrome (VMTS).

The aim of this study is the analysis of retinal and choroidal vasculature in SS-OCTA in patients with a natural course of VMT as well as in patients scheduled for surgery. To the authors’ knowledge, this is the first SS-OCTA–documented follow-up study of patients with VMT.

Methods

A retrospective database review of patients with the diagnosis “idiopathic symptomatic vitreomacular traction” was performed at the “Jasne Blonia” Ophthalmic Clinic (Lodz, Poland). Of these, 38 eyes of 38 patients met the additional inclusion criteria of having had at least 2 OCTA examinations. This cohort was composed of nontreated patients with a natural course of the disease and patients treated by vitrectomy. Exclusion criteria were severe glaucoma, previous treatment with antivascular endothelial growth factor injections, previous vitreoretinal surgery, uveitis, high myopia, and previous ocriplasmin or intravitreal gas injection. Moreover, patients with the following diagnoses were not included in the present study: diabetic retinopathy, retinal vascular occlusion, optic neuropathy, age-related macular degeneration, or polypoidal choroidal neovascularization.

In all eyes, a complete ophthalmic examination was performed and SS-OCT as well as SS-OCTA (Triton, Topcon) images were captured at the initial visit and during follow-up. SS-OCTA examinations were performed at the same time of day in each case to avoid potential diurnal variations. The following data were collected during each follow-up control: best-corrected visual acuity (VA), age, phakic status, and OCT and OCTA features. The status of posterior vitreous detachment was analyzed, and any intraretinal changes were recorded. Central retinal thickness (CRT), central choroidal thickness (CCT), and maximal horizontal surface adhesion were all measured, as were the area of the vessel layers and the vessel density at the level of superficial and deep choroidal vessels and at the level of choriocapillaris. All diameters were measured manually by 2 experienced examiners (Z.A.N., J.N.). In addition, the number of months of follow-up was noted.

After acquisition, OCTA images were automatically segmented in all B scans according to the manufacturer’s default setting to produce en face images of the superficial capillary plexus, deep capillary plexus, avascular zone, and choriocapillaris. Images were reviewed to ensure correct segmentation. The fovea avascular zone (FAZ) area (in squared millimeters) was manually measured, at both the level of superficial capillary plexus and deep capillary plexus. Each en face image was exported into Adobe Photoshop and converted to black and white. Automatic threshold selections were obtained from the gray-level histograms to determine the percentage of white and black pixels. Images were transformed in the stamp mode in Adobe Photoshop. The balance (white/dark) was set to 25/17. Retinal perfusion was calculated by scoring the percentage of white pixels in relation to the number of total pixels, according to published protocols.^6
-8

The indication for surgery was decreased VA and/or metamorphopsia not spontaneously resolving for at least 3 months. After core vitrectomy, the posterior vitreous was stained with MembraneBlue (DORC). After posterior vitreous detachment, another staining was performed to visualize the internal limiting membrane (ILM), which was then removed.

Statistical analysis was performed with IBM SPSS Statistics. Best-corrected VA measurements in decimal Snellen were converted to logMAR. Wilcoxon signed rank test was performed for paired groups and chi-square test was used to compare categorical variables. The influence of particular factors on VA was analyzed with Spearman correlation analysis and multivariable analysis.

Šidák correction was used if the simple effect proved statistically significant. A P value of less than .05 was considered statistically significant but a result greater than .05 and less than .1 was considered a significant statistical tendency.

Results

The 38 study eyes with VMT were divided into 3 groups: untreated patients whose VMT resolved naturally (group 1; n = 20 eyes); untreated patients whose VMT spontaneously released (group 2; n = 4 eyes); and patients who underwent surgery for VMT (group 3; n = 14 eyes). None of the eyes in the study presented with epiretinal membrane (ERM) formation at any time. All groups’ VA was similar at baseline in (F _2,32 = 2.17; P = .130; η² = 0.12), and no significant differences in initial CRT between groups were presented: (F _2,32 = 2.21; P = .126; η² = 0.12) (Table 1).

Table 1.

Baseline Data of Groups 1, 2, and 3 and Simple Effects of Bifactorial Analysis of Variance.^a

Parameter	Group 1		Group 2		Group 3		F	P	η²
Parameter	M	SD	M	SD	M	SD	F	P	η²
VA, Snellen (logMAR)	0.42 (0.4)	0.28 (0.5)	0.52 (0.3)	0.19 (0.7)	0.27 (0.6)	0.15 (0.8)	2.17	.130	0.12
CRT, μm	341.05	128.15	296.50	60.47	415	114.80	2.21	.126	0.12
CCT, μm	241.25	69.61	221.75	35.51	278.23	196.63	0.45	.640	0.03
Maximal horizontal surface adhesion, μm	962.53	1592.04	330	76.88	1241	1977	0.61	.444	0.03
sFAZ, μm	348.25	153.19	275.69	83.76	246.08	198.61	1.46	.247	0.08
dFAZ, μm	421.79	219.12	425.13	224.34	334.14	268.54	0.34	.713	0.03
sVD, %	43.43	6.68	44.69	8.15	42.38	7.96	0.15	.858	0.01
dVD, %	46.13	6.44	41.15	2.94	42.68	6.43	1.61	.217	0.10
Choriocapillaris, %	79.75	7.00	78.10	6.47	80.78	2.07	0.34	.718	0.02

Open in a new tab

Abbreviations: CCT, central choroidal thickness; CRT, central retinal thickness; dFAZ, deep fovea avascular zone; dVD, deep vessel density; M, mean; sFAZ, superficial fovea avascular zone; sVD, superficial vessel density; VA, visual acuity—Snellen (logMAR).

^aGroup 1, untreated (n = 20 eyes). Group 2, untreated, spontaneous release of traction (n = 4 eyes). Group 3, vitrectomy (n = 14 eyes).

Group 1

During the 15-month observation period of 20 eyes, no significant changes were found in any of the following parameters: VA (F _1,32 = 0.07; P = .797; η² = 0); CRT (F _1,34 = 2.68; P = .111; η² = 0.07); and CCT (237 µm) (F _1,34 = 0.95; P = .337; η² = 0.03).

Although in individual cases superficial fovea avascular zone (sFAZ) and deep fovea avascular zone (dFAZ) measurements either increased, decreased, or remained stable, none of those changes had statistical significance (F _1,32 = 0.48; P = .495; η² = 0.02). Mean sFAZ was 494 μm², and mean dFAZ was 697 µm²).

No changes in vessel density over time were noted in the superficial and deep retinal vessels layers nor in the choriocapillaris.

Group 2

Traction spontaneously released in 4 of 24 untreated eyes (16.7%) (Figure 1). VA improved from 0.52 Snellen (0.3 logMAR) to 0.70 Snellen (0.1 logMAR), which was statistically significant (F _1,32 = 4.48; P = .042; η² = 0.12). CRT significantly decreased (F _1,34 = 5.36; P = .027; η² = 0.14), whereas CCT remained stable (F _1,34 = 0.05; P = .817; η² = 0).

sFAZ did not change after spontaneous release of traction (F _1,32 = 0.15; P = .700; η² = 0.01). There were no discernable changes in dFAZ, and no changes in vessel density over time were noted in the superficial and deep retinal vessels layers nor in the choriocapillaris.

In 1 eye, a lamellar macular hole formed after spontaneous release of traction (Figure 2), and this was still present at the end of the 15-month follow-up period.

Group 3

In 14 patients, vitrectomy with ILM peeling was performed. After surgery, a significant decrease was found in CRT (F _1,34 = 17.37; P < .001; η² = 0.34). This was greater than the CRT decrease noted in the untreated, spontaneous release group (group 2). CCT showed no statistically significant change after surgery (F _1,34 = 0.77; P = .385; η² = 0.02). We noted no change or increase in traction in eyes in which OCT scans from different time points were available before surgery. A comparison of the 3 presented groups is summarized in Table 2.

Table 2.

Final Results in Groups 1, 2, and 3 and Simple Effects of Bifactorial Analysis of Variance.^a

Parameter	Group 1		Group 2		Group 3		F	P	η²
Parameter	M	SD	M	SD	M	SD	F	P	η²
VA, Snellen (logMAR)	0.41 (0.4)	0.26 (0.6)	0.70 (0.1)	0.38 (0.4)	0.44 (0.4)	0.23 (0.6)	2.01	.150	0.11
CRT, μm	388.25^b	127.05	147.25^c	35.34	266^b	153.78	7.16	.003	0.30
CCT, μm	254.60	94.48	207	49.34	247.31	79.18	0.76	.474	0.04
Maximal horizontal surface adhesion, μm	633.79	560.64	0	0	0	0	4.93	.038	0.18
sFAZ, μm	331.15^c	153.76	297.20^b,c	56.91	161.26^b	132.42	5.23	.011	0.25
dFAZ, μm	537.26^c	336.02	414.34^b,c	125.53	192.19^b	174.06	4.50	.021	0.25
sVD, %	44.60	7.43	38.47	2.89	42.20	8.63	1.17	.325	0.08
dVD, %	45.36	6.05	53.23	13.91	42.80	6.90	2.75	.081	0.16
Choriocapillaris, %	78.19	7.19	77.23	5.52	80.78	2.77	0.85	.436	0.06
Observation time	15	3	15	4	12	2

Open in a new tab

^a Post hoc Šidák test was used. P < .05 was considered statistically significant. Group 1, untreated (n = 20 eyes). Group 2, untreated, spontaneous release of traction (n = 4 eyes). Group 3, vitrectomy (n = 14 eyes).

^b,c Statistically significant difference. Groups with the same letter do not differ statistically significantly from one another; groups with different letters are statistically significantly different.

SS-OCTA data from 6 months after surgery were included in the final analysis. Areas of sFAZ (F _1,32 = 6.46; P = .016; η² = 0.17) and dFAZ (F _2,26 = 4.50; P = .021; η² = 0.26) decreased after surgery (Figure 3). No changes in vessel density over time were noted in the superficial and deep retinal vessels layers nor in the choriocapillaris.

Figure 3. — A 74-year-old woman with vitreomacular traction before and after surgery. Visual acuity improved from 0.4 Snellen (0.4 logMAR) to 0.6 Snellen (0.2 logMAR). (A) Swept-source optical coherence tomography (SS-OCT) shows vitreomacular traction. (B) Automatic segmentation of SS-OCT angiography (SS-OCTA) before surgery. (C) SS-OCTA of the superficial retinal vessel layer. (D) SS-OCTA of the deep retinal vessel layer, where a slight deformation of the fovea avascular zone is visible. (E) In an SS-OCTA image of the choriocapillaris, central hyperreflectivity is visible. (F) SS-OCT after surgery. (G) Automatic segmentation of SS-OCTA after surgery. (H) SS-OCTA of the superficial retinal vessel layer and (I) deep retinal vessel layer, in the latter of which slight deformation of the fovea avascular zone remains visible. (J) SS-OCTA of the choriocapillaris level after surgery. No abnormalities in reflectivity are visible.

One year after surgery, VA improved from 0.27 Snellen (0.6 logMAR) to 0.44 Snellen (0.4 logMAR), which was statistically significant: F _1,32 = 10.03; P = .003; η² = 0.61. Even though final VAs were lower than in the untreated, spontaneous release of traction group (group 2), the degree of improvement in VA was greater in the vitrectomy group (group 3), as indicated by the greater F value: 10.03 in group 3 vs 4.48 in group 2.

Multiple regression analysis revealed that initial VA depended on initial CRT (P < .05) and initial central choroidal thickness (P < .05). Final VA did not statistically significantly depend on any of the analyzed factors.

Comparison of Groups

If the simple effect proved statistically significant in final analysis, analyses with the Šidák correction followed.

Final CRT results were lower in group 2 (P = .041) and group 3 (P = .006), after spontaneous or surgical release of traction when compared with group 1.

We noted a statistically significant reduction of sFAZ and dFAZ in eyes after surgery. Even though initial sFAZ was similar between groups (F _2,32 = 1.46; P = .247; η² = 0.08), the final sFAZ was lower in group 3 than in the other groups (P = .009). dFAZ was also similar between groups at the initial visit and was lower in postsurgical group 3 when compared with groups 1 and 2 (combined) at the final visit (P = .018).

Stepwise regression analysis revealed that in groups 1 and 2 the final width of traction was determined in 66.1% of cases by the initial width of traction and CRT (F _2,16 = 18.52; P < .001). This implied that patients with wider traction and increased CRT were less likely to develop spontaneous resolution of traction. The fact that these 2 factors explain only 66.1% of these cases might mean there is a high possibility of random events in VMTS, as no other anatomic factor analyzed with OCT and OCTA helped to explain these findings. The mean width of traction in eyes with complete spontaneous release was 396.8 µm (group 2) and was 962 µm in eyes in which the traction remained visible (group 1).

Choriocapillaris

In all cases of VMTS, a hyporeflective area could be seen in the choriocapillaris layer in SS-OCTA (Figures 1E and 3E). This may be a shadowing artifact caused by either dense vitreous or intraretinal fluid. It was not visible in eyes with vitreomacular adhesion (VMA) only (Figure 2C), and it disappeared when traction was released, either spontaneously or after vitrectomy.

Conclusions

The sFAZ and dFAZ decreased after vitrectomy with ILM peeling but not in eyes after spontaneous release of traction. Hyporeflective areas visible at the level of the choriocapillaris disappeared in all eyes after release of traction. Initial VA negatively correlated with CRT and CCT. Initial and final VAs were better in eyes with spontaneous release of traction, but improvement in VA was higher in the vitrectomy group.

One of the largest OCT-based studies of tractional eye diseases to date was composed of 556 eyes of 400 patients with the diagnosis of VMT, VMA, or macular hole.⁵ Stalmans⁵ reported spontaneous resolution of traction in 22.7% (46/203) of eyes with VMT. Improved VA was noted in 34% of those eyes for which data were available (14/41), and the remaining eyes mostly showed no change. In a multicenter, noncomparative case series of 230 eyes by Tzu et al,⁹ spontaneous release of VMT was reported in 32% of cases. In our present study, we recorded spontaneous release of traction in 4 of 38 eyes (10.5%), which, given our relatively small number of cases, seems comparable to other studies.^4,10

It has been previously reported that eyes with higher VA more often experience spontaneous resolution of VMT when compared with eyes with worse vision.⁴ We noted better initial and final VA in patients with spontaneous resolution when compared with vitrectomized eyes or eyes with no spontaneous release of traction. However, the degree of VA improvement was greater in our patients after surgery than after spontaneous release. One potential explanation for this finding is the “ceiling effect.” Baseline VA was at a relatively high level, thus only limited visual improvement was possible, whereas the eyes in group 3 that had worse baseline VA could achieve a greater range of recovery after surgery. We must also take into consideration that, owing to the small number of patients with spontaneous release of traction, our statistical analyses must be interpreted with caution.

To our knowledge there are no earlier papers reporting on SS-OCTA findings in VMT. However, some comparisons can be made with the SS-OCTA findings from other vitreomacular interface disease studies while allowing for their potentially different pathologies.

In our VMT study we found no change in sFAZ after spontaneous release of traction, but a decrease in sFAZ and dFAZ was noted after vitrectomy with ILM peeling, as has been reported in full-thickness macular hole (FTMH) cases.¹¹ It might be explained by the fact that in spontaneous release only the vitreous is detached and during vitrectomy usually ILM is also removed. ILM removal might induce some repairing processes, which in turn might be responsible for changes in the FAZ area. An increase in dFAZ areas was observed after diabetic retinopathy¹² and after vitrectomy for ERM in patients with diabetes.¹³ The clinical relevance of the decrease in FAZ area in the present study is not completely understood, but in most cases increased FAZ areas are associated with some extent of ischemia. Because we observed higher VA gains and a reduction in FAZ areas in patients who underwent surgery, early treatment, at least in patients with lower VAs, might be beneficial.

We found no relationship between dFAZ and CRT in our VMT study, whereas in both ERM and FTMH, dFAZ negatively corresponded to final CRT.^14,15 We found that in VMT, CRT decreased after spontaneous release and even more so after vitrectomy with ILM peeling. In our study CCT remained stable after spontaneous release and after vitrectomy with ILM peeling, whereas CCT decreased after surgery for idiopathic ERM.¹⁶

Higher vessel density has been reported in eyes with idiopathic ERM when compared with healthy eyes, and vessel density in the superficial retinal vessel plexus decreases after ILM peeling for ERM and for FTMH.^17
-19 We found no changes in vessel densities after spontaneous release nor after vitrectomy with ILM peeling in VMT. A weakness of our study may be the small number of cases, which could have influenced this and other findings. A potential weakness of many of the aforementioned studies exists in comparing FAZ between eyes with either ERM or FTMH with their fellow eyes. Knowing that macular disease is more common in fellow eyes than in the general population, fellow eyes might not necessarily be good models.

Incomplete normalization of the FAZ areas, or an abnormal size of FAZ, might be associated with incomplete visual recovery in patients with vitreomacular interface diseases. We found that VA significantly improved after spontaneous release of traction and an even greater improvement was seen after vitrectomy with ILM peeling; postoperative visual gain was not associated with FAZ changes nor with any of the other analyzed OCT and OCTA parameters.

Initial VA in all the VMT cases we studied, however, did depend on initial CCT and CRT. We suggest 2 explanations: First, prolonged traction may be responsible for the increase in CRT, which in turn leads to some defects at the cellular level and an increase in oxygen requirements, which can cause a secondary increase in CCT thickness. If we assume that the choroid has a role in vitreomacular interface diseases, the primary increase in CCT might cause secondary changes in the retina, which would, for example, make photoreceptors more susceptible to defects caused by traction.

In all cases of VMTS, a hyporeflective area with central hyperreflectivity encircled with hyporeflectivity was visible in the choriocapillaris layer in SS-OCTA (see Figure 1E and 3E). It was not visible in eyes with VMA only (see Figure 2C) and was no longer visible after traction was released either spontaneously or after vitrectomy; therefore, it was probably a shadowing artifact. We suspect it might have been caused either by dense vitreous or intraretinal fluid visible in some cases of VMT. However, some form of hyporeflectivity remained visible in some cases at the level of choriocapillaris. In fellow eyes of FTMH, in which vitreomacular diseases are observed more often than in the general population, a central change of reflectivity is often observed at the level of the choriocapillaris.²⁰ Even eyes with no OCT-visible abnormality develop a central hyporeflective area.¹⁵ Blood flow in the choroid was lower in eyes with idiopathic ERM than in controls.²¹ Thus, it would require further studies to estimate whether those hyporeflective areas are in reality caused only by a shadowing artifact or are owing to some circulation deficit caused by either traction or some idiopathic changes.

A bias of the present study is its retrospective nature and small sample size. However, it is still the biggest study analyzing SS-OCTA in VMT. Another bias is the fact that the decision to perform surgery was highly subjective. It is not to be excluded that VA improvement after surgery was associated with the surgeons’ experience in qualifying appropriate patients for surgery. Moreover, measurements of FAZ areas in distorted fovea might be inaccurate, despite manual correction of segmentation.

Using SS-OCTA in VMT, we found the sFAZ and dFAZ decreased after vitrectomy with ILM peeling but not in eyes after spontaneous release of traction.

For 15 months’ follow-up, we found no changes in vessel densities after spontaneous release nor after vitrectomy with ILM peeling.

Initial and final VA was better in eyes with spontaneous release of traction than in the other groups. However, the degree of improvement in VA was greater in the vitrectomy group. CCT and CRT negatively correlated with initial, but not with final, VA. None of the SS-OCTA parameters examined in this study significantly correlated with final VA. Hyporeflective areas visible at the level of the choriocapillaris disappeared in all eyes after release of traction, and sFAZ and dFAZ decreased after vitrectomy with ILM peeling but not in eyes after spontaneous release of traction. Higher VA gains and a reduction in FAZ areas were observed in patients who underwent surgery. Early treatment, at least in patients with lower VAs, might be beneficial.

Footnotes

Authors’ Note: This manuscript was presented online at the Deutsche Ophthalmologische Gesellschaft Congress on October 7, 2020.

Ethical Approval: This retrospective study was approved by the ethics committee of the “Jasne Blonia” Ophthalmic Clinic. All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards.

Statement of Informed Consent: This type of study (retrospective study) does not require formal consent.

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iD: Zofia Anna Nawrocka, MD, PhD Inline graphic https://orcid.org/0000-0001-8376-9218

References

1. Duker JS, Kaiser PK, Binder S, et al. The International Vitreomacular Traction Study Group classification of vitreomacular adhesion, traction, and macular hole. Ophthalmology. 2013;120(12):2611–2619. doi:10.1016/j.ophtha.2013.07.042 [DOI] [PubMed] [Google Scholar]
2. Shao L, Wei W. Vitreomacular traction syndrome. Chin Med J (Engl). 2014;127(8):1566–1571. doi:10.3760/cma.j.issn.0366-6999.20140211 [PubMed] [Google Scholar]
3. Odrobina D, Michalewska Z, Michalewski J, Dzięgielewski K, Nawrocki J. Long-term evaluation of vitreomacular traction disorder in spectral domain optical coherence tomography. Retina. 2011;31(2):324–331. doi:10.1097/iae.0b013e3181eef08c [DOI] [PubMed] [Google Scholar]
4. Errera MH, Liyanage SE, Petrou P, et al. A study of the natural history of vitreomacular traction syndrome by OCT. Ophthalmology. 2018;125(5):701–707. doi:10.1016/j.ophtha.2017.10.035 [DOI] [PubMed] [Google Scholar]
5. Stalmans P. A retrospective cohort study in patients with tractional diseases of the vitreomacular interface (ReCoVit). Graefes Arch Clin Exp Ophthalmol. 2016;254(4):617–628. doi:10.1007/s00417-016-3294-1 [DOI] [PMC free article] [PubMed] [Google Scholar]
6. Siegfried F, Rommel F, Rothe M, Grisanti S, Mahdy Ranjbar M. Evaluating diurnal changes in choroidal sublayer perfusion using optical coherence tomography angiography. Acta Ophthalmol. 2019;97(8):e1062–e1068. doi:10.1111/aos.14140 [DOI] [PubMed] [Google Scholar]
7. Rommel F, Siegfried F, Sochurek JAM, et al. Mapping diurnal variations in choroidal sublayer perfusion in patients with idiopathic epiretinal membrane: an optical coherence tomography angiography study. Int J Retina Vitreous. 2019;5:12. doi:10.1186/s40942-019-0162-2 [DOI] [PMC free article] [PubMed] [Google Scholar]
8. Nicolò M, Rosa R, Musetti D, Musolino M, Saccheggiani M, Traverso CE. Choroidal vascular flow area in central serous chorioretinopathy using swept-source optical coherence tomography angiography. Invest Ophthalmol Vis Sci. 2017;58(4):2002–2010. doi:10.1167/iovs.17-21417 [DOI] [PubMed] [Google Scholar]
9. Tzu JH, John VJ, Flynn HW, Jr, et al. Clinical course of vitreomacular traction managed initially by observation. Ophthalmic Surg Lasers Imaging Retina. 2015;46(5):571–576. doi:10.3928/23258160-20150521-09 [DOI] [PubMed] [Google Scholar]
10. Hikichi T, Yoshida A, Trempe CL. Course of vitreomacular traction syndrome. Am J Ophthalmol. 1955;119(1):55–61. doi:10.1016/s0002-9394(14)73813-9 [DOI] [PubMed] [Google Scholar]
11. Kim YJ, Jo J, Lee JY, Yoon YH, Kim JG. Macular capillary plexuses after macular hole surgery: an optical coherence tomography angiography study. Br J Ophthalmol. 2018;102(7):966–970. doi:10.1136/bjophthalmol-2017-311132 [DOI] [PubMed] [Google Scholar]
12. Freiberg FJ, Pfau M, Wons J, Wirth MA, Becker MD, Michels S. Optical coherence tomography angiography of the foveal avascular zone in diabetic retinopathy. Graefes Arch Clin Exp Ophthalmol. 2016;254(6):1051–1058. doi:10.1007/s00417-015-3148-2 [DOI] [PMC free article] [PubMed] [Google Scholar]
13. Romano MR, Cennamo G, Schiemer S, Rossi C, Sparnelli F, Cennamo G. Deep and superficial OCT angiography changes after macular peeling: idiopathic vs diabetic epiretinal membranes. Graefes Arch Clin Exp Ophthalmol. 2017;255(4):681–689. doi:10.1007/s00417-016-3534-4 [DOI] [PubMed] [Google Scholar]
14. Michalewska Z, Nawrocki J. Swept-source OCT angiography of full-thickness macular holes: appearance and artifacts. Ophthalmic Surg Lasers Imaging Retina. 2018;49(2):111–121. doi:10.3928/23258160-20180129-05 [DOI] [PubMed] [Google Scholar]
15. Yoon YS, Woo JM, Woo JE, Min JK. Superficial foveal avascular zone area changes before and after idiopathic epiretinal membrane surgery. Int J Opthalmol. 2018;11(10):1711–1715. doi:10.18240/ijo.2018.10.21 [DOI] [PMC free article] [PubMed] [Google Scholar]
16. Michalewska Z, Michalewski J, Adelman RA, Zawiślak E, Nawrocki J. Choroidal thickness measured with swept source OCT before and after vitrectomy with ILM peeling for idiopathic epiretinal membranes. Retina. 2015;35(3):487–491. doi:10.1097/IAE.0000000000000350 [DOI] [PubMed] [Google Scholar]
17. Michalewska Z, Nawrocki J. Swept-source optical coherence tomography angiography reveals internal limiting membrane peeling alters deep retinal vasculature. Retina. 2018;38(suppl 1):S154–S160. doi:10.1097/IAE.0000000000002199 [DOI] [PubMed] [Google Scholar]
18. Nelis P, Alten F, Clemens CR, Heiduschka P, Eter N. Quantification of changes in foveal capillary architecture caused by idiopathic epiretinal membranes using OCT angiography. Graefes Arch Clin Exp Ophthalmol. 2018;255(7):1319–1324. doi:10.1007/s00417-017-3640-y [DOI] [PubMed] [Google Scholar]
19. Mastropasqua L, Borrelli E, Carpineto P, et al. Microvascular changes after vitrectomy with internal limiting membrane peeling: an optical coherence tomography angiography study. Int Ophthalmol. 2018;38(4):1465–1472. doi:10.1007/s10792-017-0608-1 [DOI] [PubMed] [Google Scholar]
20. Michalewska Z, Michalewski J, Sikorski BL, et al. A study of macular hole formation by serial spectral optical coherence tomography. Clin Exp Ophthalmol. 2009;37(4):373–383. doi:10.1111/j.1442-9071.2009.02041.x [DOI] [PubMed] [Google Scholar]
21. Chen H, Chi W, Cai X, et al. Macular microvasculature features before and after vitrectomy in idiopathic macular epiretinal membrane: an OCT angiography analysis. Eye (Lond). 2018;33(4):619–628. doi:10.1038/s41433-018-0272-3 [DOI] [PMC free article] [PubMed] [Google Scholar]

[bibr1-24741264211045867] 1. Duker JS, Kaiser PK, Binder S, et al. The International Vitreomacular Traction Study Group classification of vitreomacular adhesion, traction, and macular hole. Ophthalmology. 2013;120(12):2611–2619. doi:10.1016/j.ophtha.2013.07.042 [DOI] [PubMed] [Google Scholar]

[bibr2-24741264211045867] 2. Shao L, Wei W. Vitreomacular traction syndrome. Chin Med J (Engl). 2014;127(8):1566–1571. doi:10.3760/cma.j.issn.0366-6999.20140211 [PubMed] [Google Scholar]

[bibr3-24741264211045867] 3. Odrobina D, Michalewska Z, Michalewski J, Dzięgielewski K, Nawrocki J. Long-term evaluation of vitreomacular traction disorder in spectral domain optical coherence tomography. Retina. 2011;31(2):324–331. doi:10.1097/iae.0b013e3181eef08c [DOI] [PubMed] [Google Scholar]

[bibr4-24741264211045867] 4. Errera MH, Liyanage SE, Petrou P, et al. A study of the natural history of vitreomacular traction syndrome by OCT. Ophthalmology. 2018;125(5):701–707. doi:10.1016/j.ophtha.2017.10.035 [DOI] [PubMed] [Google Scholar]

[bibr5-24741264211045867] 5. Stalmans P. A retrospective cohort study in patients with tractional diseases of the vitreomacular interface (ReCoVit). Graefes Arch Clin Exp Ophthalmol. 2016;254(4):617–628. doi:10.1007/s00417-016-3294-1 [DOI] [PMC free article] [PubMed] [Google Scholar]

[bibr6-24741264211045867] 6. Siegfried F, Rommel F, Rothe M, Grisanti S, Mahdy Ranjbar M. Evaluating diurnal changes in choroidal sublayer perfusion using optical coherence tomography angiography. Acta Ophthalmol. 2019;97(8):e1062–e1068. doi:10.1111/aos.14140 [DOI] [PubMed] [Google Scholar]

[bibr7-24741264211045867] 7. Rommel F, Siegfried F, Sochurek JAM, et al. Mapping diurnal variations in choroidal sublayer perfusion in patients with idiopathic epiretinal membrane: an optical coherence tomography angiography study. Int J Retina Vitreous. 2019;5:12. doi:10.1186/s40942-019-0162-2 [DOI] [PMC free article] [PubMed] [Google Scholar]

[bibr8-24741264211045867] 8. Nicolò M, Rosa R, Musetti D, Musolino M, Saccheggiani M, Traverso CE. Choroidal vascular flow area in central serous chorioretinopathy using swept-source optical coherence tomography angiography. Invest Ophthalmol Vis Sci. 2017;58(4):2002–2010. doi:10.1167/iovs.17-21417 [DOI] [PubMed] [Google Scholar]

[bibr9-24741264211045867] 9. Tzu JH, John VJ, Flynn HW, Jr, et al. Clinical course of vitreomacular traction managed initially by observation. Ophthalmic Surg Lasers Imaging Retina. 2015;46(5):571–576. doi:10.3928/23258160-20150521-09 [DOI] [PubMed] [Google Scholar]

[bibr10-24741264211045867] 10. Hikichi T, Yoshida A, Trempe CL. Course of vitreomacular traction syndrome. Am J Ophthalmol. 1955;119(1):55–61. doi:10.1016/s0002-9394(14)73813-9 [DOI] [PubMed] [Google Scholar]

[bibr11-24741264211045867] 11. Kim YJ, Jo J, Lee JY, Yoon YH, Kim JG. Macular capillary plexuses after macular hole surgery: an optical coherence tomography angiography study. Br J Ophthalmol. 2018;102(7):966–970. doi:10.1136/bjophthalmol-2017-311132 [DOI] [PubMed] [Google Scholar]

[bibr12-24741264211045867] 12. Freiberg FJ, Pfau M, Wons J, Wirth MA, Becker MD, Michels S. Optical coherence tomography angiography of the foveal avascular zone in diabetic retinopathy. Graefes Arch Clin Exp Ophthalmol. 2016;254(6):1051–1058. doi:10.1007/s00417-015-3148-2 [DOI] [PMC free article] [PubMed] [Google Scholar]

[bibr13-24741264211045867] 13. Romano MR, Cennamo G, Schiemer S, Rossi C, Sparnelli F, Cennamo G. Deep and superficial OCT angiography changes after macular peeling: idiopathic vs diabetic epiretinal membranes. Graefes Arch Clin Exp Ophthalmol. 2017;255(4):681–689. doi:10.1007/s00417-016-3534-4 [DOI] [PubMed] [Google Scholar]

[bibr14-24741264211045867] 14. Michalewska Z, Nawrocki J. Swept-source OCT angiography of full-thickness macular holes: appearance and artifacts. Ophthalmic Surg Lasers Imaging Retina. 2018;49(2):111–121. doi:10.3928/23258160-20180129-05 [DOI] [PubMed] [Google Scholar]

[bibr15-24741264211045867] 15. Yoon YS, Woo JM, Woo JE, Min JK. Superficial foveal avascular zone area changes before and after idiopathic epiretinal membrane surgery. Int J Opthalmol. 2018;11(10):1711–1715. doi:10.18240/ijo.2018.10.21 [DOI] [PMC free article] [PubMed] [Google Scholar]

[bibr16-24741264211045867] 16. Michalewska Z, Michalewski J, Adelman RA, Zawiślak E, Nawrocki J. Choroidal thickness measured with swept source OCT before and after vitrectomy with ILM peeling for idiopathic epiretinal membranes. Retina. 2015;35(3):487–491. doi:10.1097/IAE.0000000000000350 [DOI] [PubMed] [Google Scholar]

[bibr17-24741264211045867] 17. Michalewska Z, Nawrocki J. Swept-source optical coherence tomography angiography reveals internal limiting membrane peeling alters deep retinal vasculature. Retina. 2018;38(suppl 1):S154–S160. doi:10.1097/IAE.0000000000002199 [DOI] [PubMed] [Google Scholar]

[bibr18-24741264211045867] 18. Nelis P, Alten F, Clemens CR, Heiduschka P, Eter N. Quantification of changes in foveal capillary architecture caused by idiopathic epiretinal membranes using OCT angiography. Graefes Arch Clin Exp Ophthalmol. 2018;255(7):1319–1324. doi:10.1007/s00417-017-3640-y [DOI] [PubMed] [Google Scholar]

[bibr19-24741264211045867] 19. Mastropasqua L, Borrelli E, Carpineto P, et al. Microvascular changes after vitrectomy with internal limiting membrane peeling: an optical coherence tomography angiography study. Int Ophthalmol. 2018;38(4):1465–1472. doi:10.1007/s10792-017-0608-1 [DOI] [PubMed] [Google Scholar]

[bibr20-24741264211045867] 20. Michalewska Z, Michalewski J, Sikorski BL, et al. A study of macular hole formation by serial spectral optical coherence tomography. Clin Exp Ophthalmol. 2009;37(4):373–383. doi:10.1111/j.1442-9071.2009.02041.x [DOI] [PubMed] [Google Scholar]

[bibr21-24741264211045867] 21. Chen H, Chi W, Cai X, et al. Macular microvasculature features before and after vitrectomy in idiopathic macular epiretinal membrane: an OCT angiography analysis. Eye (Lond). 2018;33(4):619–628. doi:10.1038/s41433-018-0272-3 [DOI] [PMC free article] [PubMed] [Google Scholar]

PERMALINK

Swept-Source Optical Coherence Tomography Angiography in Vitreomacular Traction Syndrome

Zofia Anna Nawrocka, MD, PhD

Zofia Nawrocka, MD, PhD

Jerzy Nawrocki, MD, PhD