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Original Study

Peripapillary Perfused Capillary Density in Acute Angle-Closure Glaucoma: An Optical Coherence Tomography Angiography Study

Suwan, Yanin MD; Fard, Masoud Aghsaei MD; Petpiroon, Purit MD; Supakontanasan, Wasu MD; Pruksacholavit, Rotjaporn MD; Tantraworasin, Apichat MD, PhD‡,§; Teekhasaenee, Chaiwat MD; Ritch, Robert MD||

Author Information
Asia-Pacific Journal of Ophthalmology: March-April 2021 - Volume 10 - Issue 2 - p 167-172
doi: 10.1097/APO.0000000000000370
  • Open

Abstract

Acute angle-closure (AAC) is characterized by severe symptoms and distinct clinical findings. In AAC, intraocular pressure (IOP) increases dramatically because of the sudden blockage of the drainage angle by the peripheral iris. Prolonged IOP elevation leads to glaucomatous damage to the optic nerve head, loss of optic nerve axons, and subsequent progressive loss of the visual field when left untreated. In a previous study, circumpapillary retinal nerve fiber layer (cpRNFL) thickness was markedly thinner in acute primary angle closure (APAC) eyes than in age-matched normal eyes.1

An acute attack leads to an initial increase followed by an accelerated decrease in cpRNFL and ganglion cell complex (GCC) thickness despite normal IOP, open-angle, and unchanged cup-to-disc ratio.2–8 Prolonged duration from acute attack onset to IOP-lowering treatment is reportedly associated with cpRNFL and GCC loss after APAC.5,9 Although mechanical compression of the optic disc has generally been accepted as the leading mechanism underlying glaucomatous damage to angle closure, particularly APAC,10 vascular dysregulation may play a role in the pathogenesis of angle-closure glaucoma. Retinal ganglion cells and their axons undergo apoptosis after exposure to an extremely high IOP during an acute attack.10

Noninvasive optical coherence tomography angiography (OCTA) allows rapid and accurate quantitative assessments of the optic nerve head and peripapillary microvasculature to the capillary level. Split-spectrum amplitude-decorrelation angiography, an OCTA algorithm, compares the decorrelation signals among serial B-scan OCT images obtained at the same cross-section to construct an image of blood flow.11–13 Reduction in peripapillary vessel density in different types of glaucomas on OCTA has been reported.14–18 Additionally, the diagnostic capabilities of vessel density measurements have been shown to be comparable to those of RNFL measurements in both primary open-angle glaucoma (POAG) and primary angle-closure glaucoma (PACG).17

Recent studies have reported that peripapillary retinal and choroidal perfusion was decreased in acute and chronic PACG eyes compared with that in primary angle-closure suspect or fellow eyes.10,19,20 Wang et al19 have reported lower peripapillary retinal vessel density in APAC eyes than in fellow eyes once IOP was normalized after an acute attack; Zhang et al10 have reported similar findings.

Thus, the aim of the present study was to compare peripapillary perfused capillary density (PCD) on OCTA among resolved AAC, POAG, and control eyes.

MATERIALS AND METHODS

This prospective, cross-sectional, observational study was approved by the institutional review board of Ramathibodi Hospital, Mahidol University. This study was performed in compliance with the Health Insurance Portability and Accountability Act and the tenets of the Declaration of Helsinki. All patients provided written informed consent.

Participants

This study included eyes of patients with resolved AAC or POAG of varying severities as well as healthy controls. All participants were recruited between February 1, 2017 and August 31, 2018. The inclusion criteria for all participants were age of >20 years and the best-corrected visual acuity of ≥20/40.

AAC was defined based on the following criteria: (1) presence of at least 2 of the following symptoms: periocular pain or headache, nausea and/or vomiting, decreased vision, and rainbow-colored halos around lights; (2) documentation of IOP ≥ 21 mm Hg using Goldmann applanation tonometry; (3) presence of at least 4 of the after slit-lamp biomicroscopic findings: ciliary injection, corneal epithelial edema, fixed mid-dilated pupil, glaukomflecken, and shallow peripheral anterior chamber; and (5) presence of invisible posterior trabecular meshwork of >180 degrees on gonioscopy. Patients with >180-degree open angles on gonioscopy before the use of antiglaucoma medication were excluded. IOP in all AAC eyes had been controlled without the use of antiglaucoma medications after laser peripheral iridotomy, laser peripheral iridoplasty, or phacoemulsification with or without goniosynechialysis. At the time of this study, optic disc swelling in the affected eye had subsided.

POAG was defined based on the following criteria: presence of (1) a glaucomatous-appearing optic nerve, (2) an open anterior chamber angle, and (3) cpRNFL thinning on OCT outside the 95% CI of normal distribution. A glaucomatous visual field defect was defined as the presence of at least 3 contiguous points at a 5% level of significance on the pattern deviation plot, with one of the three points at a 1% level of significance, excluding points on the edge of the field, and a glaucoma hemifield test result outside the normal limits in at least 2 consecutive baseline visual field tests (P < 0.5), consistent with a glaucomatous pattern. The cutoffs for low test reliability included 25% false positives, 25% false negatives, and 25% fixation losses. Regarding the categorization of POAG eyes according to severity, mild was defined as a mean deviation (MD) of less than −6 dB, moderate as MD of −6 to −12 dB, and severe as MD of more than −12 dB.

Control eyes were defined as eyes without any evidence of retinal pathology or glaucoma, an IOP of ≤21 mm Hg, an open anterior chamber angle, a healthy optic disc appearance, and no visual field or RNFL defects.

The exclusion criteria common to all participants were the presence of eyes with recurrent/subacute angle closure, an increased cup-to-disc ratio, secondary angle closure, history of ocular surgery other than uncomplicated cataract surgery, high hyperopia or myopia (greater than +6 or −6 D of the spherical equivalent refractive error or more than ±3 D astigmatism), opacities of the ocular media, vitreoretinal diseases or nonglaucomatous optic neuropathy, chronic ocular or systemic corticosteroid use, cardiovascular diseases apart from systemic hypertension, or diabetes mellitus. Both eyes of each participant were imaged and analyzed.

Clinical Examinations

After a complete resolution of an acute attack, all participants underwent a detailed ophthalmic examination including medical history review, systolic and diastolic blood pressure measurements, antiglaucoma medication assessments, best-corrected visual acuity (Snellen) determination, anterior segment slit-lamp biomicroscopy, IOP measurement using Goldmann applanation tonometer, dilated fundus examination using a 78D noncontact slit-lamp lens (Volk Optical, Mentor, OH, USA), and A-scan biometry. Data regarding the attack IOP (IOP before treatment), duration of increased IOP (duration from onset of AAC to normalization of IOP), and the period from acute attack onset to OCTA imaging were also collected. Visual field examinations were performed with the Humphrey Visual Field Analyzer (Humphrey Instrument Model 740; Carl Zeiss Meditec) using the 24-2 Swedish Interactive Thresholding Algorithm Standard program. cpRNFL thickness was analyzed using OCT (OptoVue, Inc., Fremont, CA, USA).

Optical Coherence Tomography Angiography

All OCTA images were obtained using a commercial spectral-domain OCT system (AngioVue Software Version 2017.1.1.151, OptoVue, Inc.). Each patient underwent a single imaging session comprising 2 volumetric raster scans (1 vertical and 1 horizontal) centered at the optic nerve head and covering 4.5 × 4.5 mm2. Each raster scan comprised 400 brightness scans, which were each obtained twice, yielding a total of 400 × 400 brightness scans. Each brightness scan comprised 400 amplitude scans. At an amplitude scan rate of 70,000 A-scans per second, each raster scan was completed in <3 s. The split-spectrum amplitude-decorrelation angiography algorithm was used to produce images of perfused vessels.21,22 The vessels located between the internal limiting membrane and the retinal nerve fiber layer posterior boundary were analyzed to sample the radial peripapillary capillary vasculature. After reviewing the raw images (investigator, YS), images with significant background noise, motion artifacts, signal strength index of <40, and segmentation error within the regions of interest were excluded.13

Optical Coherence Tomography Angiography Image Analysis

OCTA images were analyzed using a custom MATLAB program (The Mathworks, Inc., Natick, MA, USA) to calculate global, annular, and sectoral (superior, inferior, temporal, and nasal) PCDs, as described previously.23

Annular and Sectoral Perfused Capillary Densities

PCD was calculated after major vessel removal using the thresholding technique. After determining the center of each image, 2 concentric circles with diameters of 3.45 and 1.95 mm were drawn, producing an annular area with a width of 0.75 mm. Annular PCD (%) was calculated by dividing the number of pixels associated with perfused capillaries by the number of pixels in the entire ring. Each 90-degree sectoral PCD in the ring was also assessed.23

Global Perfused Capillary Density

Global PCD (%) was calculated by dividing the number of pixels associated with perfused capillaries by the number of pixels in the entire image after the removal of the major vessels.

Statistical Analysis

The Shapiro–Wilk test was used to assess the distribution of numerical data. Descriptive statistics were mean and standard deviation (SD) for Gaussian distribution variables and median (interquartile range) for non-Gaussian distribution variables. Categorical variables were compared using the Fisher exact test, whereas continuous variables were compared using analysis of variance or Kruskal-Wallis H test to assess differences among the 3 study groups depend on data distribution. Multiple comparisons between the groups within each analysis were performed using the Bonferroni correction test. A marginal model of generalized estimating equations adjusted for age, sex, and interocular correlation was used to identify the effects of experimental groups on PCD. Further subgroup analysis in AAC, we used a marginal model of generalized estimating equations with adjustment for age and sex. All statistical analyses were performed using Stata, version 14 (StataCorp, College Station, TX, USA). P < 0.05 was considered significant.

RESULTS

Study Population

Initially, 164 eyes of 128 patients met the inclusion criteria of this study. Among the 164 eyes, 1 AAC eye and 1 POAG eye were excluded because of unacceptable OCTA image quality and/or eye movement. Thus, 44 eyes of 40 patients with resolved AAC [mean (SD) age, 62.0 (7.2) years; 32 (78%) women], 69 eyes of 40 patients with POAG [58.9 (11.8) years; 22 (55%) women], and 49 eyes of 48 healthy controls [63.0 (11.3) years; 28 (57%) women] were included in this study. Among the 4 patients who had bilateral AAC, 1 patient simultaneously developed AAC in both eyes. There were no significant differences in axial length, systolic blood pressure, diastolic blood pressure, and mean arterial pressure among the 3 study groups. Among patients with AAC, all eyes (100%) had undergone cataract surgery with or without goniosynechialysis. Patient demographics are summarized in Table 1. There were significant differences in global and sectoral cpRNFL thicknesses among the 3 study groups (all P < 0.001). Pairwise comparisons revealed significant differences in global cpRFNL thickness between the experimental and control groups (all P < 0.001); however, there was no difference between the AAC and POAG groups (P = 0.091; Table 2).

TABLE 1 - Clinical and Demographic Characteristics of Subgroups
Characteristics AAC Group(n = 44) POAG Group(n = 69) Control Group(n = 49) P Value
Age, y, mean (SD) 62.4 (7.1) 58.(11.8) 63.1 (11.3) 0.085
Female, n (%) 32 (78.0) 22 (55.0) 28 (57.1) 0.016
Axial length, mm, mean (SD) 22.7 (1.1) 23.9 (1.0) 22.4 (0.5) 0.973
Systolic blood pressure, mm Hg, mean (SD) 130.2 (27.5) 129.5 (19.3) NA 0.672
Diastolic blood pressure, mm Hg, mean (SD) 77.1 (8.4) 75.9 (7.9) NA 0.815
Mean arterial pressure, mm Hg, mean (SD) 94.8 (13.2) 93.7 (10.6) NA 0.691
RFNL thickness, microns, mean (SD)
 Global 90.2 (20.8) 83.7 (13.6) 102.0 (6.4) <0.001
 Superior 106.7 (26.6) 106.3 (19.1) 122.0 (8.1) <0.001
 Inferior 110.0 (30.1) 91.9 (23.8) 126.2 (10.0) <0.001
 Nasal 72.5 (17.7) 68.9 (13.8) 82.7 (8.5) <0.001
 Temporal 73.1 (18.7) 66.7 (13.6) 76.6 (8.4) <0.001
Glaucoma severity, mild: moderate: severe 20:4:8 44:15:10 NA 0.372
Visual field MD, dB −4.7 (−13.4, −3.6) −5.0 (−8.9, −3.0) NA 0.619
Visual field PSD, dB 3.9 (2.0–7.5) 6.8 (3.4–11.9) NA 0.005
Attack IOP, mm Hg, mean (SD) 52.7 (12.3) NA NA
Duration of increased IOP, days, median (IQR) 3 (1–11.5) NA NA
Duration from attack onset to imaging, days, median (IQR) 385 (168–1851) NA NA
Number of antiglaucoma medications, median (IQR) 0 (0–0) 1 (1–2) NA
PCD, mean (SD)
 Global 20.3 (8.5) 20.5 (8.5) 27.9 (7.5) <0.001
 Annular 22.4 (9.3) 25.0 (10.3) 30.7 (8.0) <0.001
AAC indicates acute angle closure; IOP, intraocular pressure; NA, not applicable; PCD, peripapillary perfused capillary density; POAG, primary open-angle glaucoma; RNFL, retinal nerve fiber layer; SD, standard deviation.
Visual field data are available in 32 eyes.

TABLE 2 - Post Hoc Comparisons of PCD and Global cpRNFL Thickness among the AAC, POAG, and Control Groups
PCD
Global AAC POAG Control
 AAC 1 1.000 <0.001
 POAG 1 <0.001
 Control 1
Annular AAC POAG Control
 AAC 1 0.507 <0.001
 POAG 1 0.005
 Control 1
cpRNFL thickness
AAC POAG Control
 AAC 1 0.091 <0.001
 POAG 1 <0.001
 Control 1
AAC indicates acute angle closure; cpRNFL, circumpapillary retinal nerve fiber layer; PCD, peripapillary perfused capillary density; POAG, primary open-angle glaucoma.Analyzed by Bonferroni correction.
Significant mean difference at the 0.05 level.

Perfused Capillary Density

There were significant differences in global, annular, and all 4 sectoral PCDs among the 3 study groups (all P < 0.001). OCTA images in grayscale from each group are shown in Figure 1. Pairwise comparisons revealed significant differences in both annular and global PCDs across all groups (all P < 0.001), except between the AAC and POAG groups (P = 1.000 and P = 0.507 for global and annular PCDs, respectively; Table 2).

FIGURE 1
FIGURE 1:
Optical coherence tomography angiography (OCTA) images of the 3 groups. (Left column) OCTA images in grayscale. (Right column) OCTA images with 2 concentric circles with diameters of 3.45 and 1.95 mm. Major vessels (in cyan) were removed using customized software.

When POAG was further classified according to glaucoma severity, there were significant differences in global, annular, and sectoral PCDs among the AAC, mild-to-severe POAG, and control groups (all P = 0.030; Table 3). Pairwise comparisons revealed significant differences in global PCD between each of the POAG stage and control groups and between the AAC and control groups (P < 0.018); however, there were no differences between each of the POAG stage and AAC groups (P > 0.985; Table 4).

TABLE 3 - Comparisons of Global, Annular, and Sectoral PCDs among the AAC, Mild-to-Severe POAG, and Control Groups
PCD, %, Mean (SD) AAC(n = 44) POAG-Mild(n = 44) POAG-Moderate(n = 15) POAG-Severe(n = 10) Control(n = 49) P Value
Global 20.3 (8.5) 21.6 (8.6) 20.1 (9.2) 15.1 (5.6) 27.9 (7.5) <0.001
Annular 22.4 (9.3) 26.3 (10.2) 24.3 (11.5) 19.1 (7.8) 30.7 (8.0) <0.001
Superior 18.4 (10.0) 23.0 (10.2) 20.0 (9.4) 17.1 (8.9) 29.3 (7.5) <0.001
Nasal 21.6 (9.5) 28.4 (14.6) 26.6 (14.6) 22.9 (9.6) 27.6 (8.4) 0.030
Inferior 20.8 (9.9) 22.7 (9.9) 19.9 (13.5) 11.9 (6.8) 29.8 (8.6) <0.001
Temporal 27.7 (11.7) 29.6 (12.7) 29.4 (13.5) 21.8 (8.7) 35.1 (10.7) 0.006
AAC indicates acute angle closure; PCD, peripapillary perfused capillary density; POAG, primary open-angle glaucoma; SD, standard deviation.
P value among 4 groups (1-way ANOVA).

TABLE 4 - Post Hoc Comparisons of Global and Annular PCDs Among the AAC, Mild-to-Severe POAG, and Control Groups
PCD AAC(n = 44) POAG-Mild(n = 44) POAG-Moderate(n = 15) POAG-Severe(n = 10) Control(n = 49)
Global
AAC 1 1.000 1.000 0.985 0.000
POAG-mild 1 1.000 0.413 0.003
POAG-moderate 1 1.000 0.018
POAG-severe 1 0.001
Control 1
Annular
AAC 1 0.572 1.000 1.000 0.000
POAG-mild 1 1.000 0.481 0.268
POAG-moderate 1 1.000 0.263
POAG-severe 1 0.014
Control 1
AAC indicates acute angle closure; PCD, peripapillary perfused capillary density; POAG, primary open-angle glaucoma.Analyzed by Bonferroni correction.
Significant mean difference at the 0.05 level.

After adjusting for age and sex, the mean difference in global PCD between each of the glaucoma groups and the control group was the highest in the severe POAG group (−14.2; 95% CI, −19.9 to −8.5; P < 0.001), followed by the AAC (−8.5; 95% CI, −11.7 to −5.3; P < 0.001), moderate POAG (−8.2; 95% CI, −12.3 to −4.0; P < 0.001), and mild POAG (–6.9, 95% CI, −10.2 to −3.5; P < 0.001) groups (Table 5). In subgroup analysis of AAC group, after adjusting for age and sex, the attack IOP significantly affected global PCD [mean difference (95% CI) = 0.2 (0.1, –0.4), P = 0.040], but not in annular PCD [mean difference (95% CI) = 0.2 (–0.1, +0.5), P = 0.055]. In contrast, the duration of increased IOP did not affect PCD [mean difference (95% CI) = –0.1 (–0.4, +0.1), P = 0.258 for global and –0.2 (–0.4, +0.1), P = 0.168 for annular PCDs]. In addition, the period from acute attack onset to OCTA imaging did not affect PCD [mean difference (95% CI) = 0.1(–0.1, +0.1), P = 0.722 for global and –0.1(–0.1, +0.1), P = 0.863 for annular PCDs].

TABLE 5 - Mean Difference in Global and Annular PCD Among the 5 Groups Compared with the Control Group
Global PCD Mean Difference 95% Confidence Interval P Value
Control Reference
AAC −8.512 ± 1.626 −11.697, −5.325 <0.001
POAG-mild −6.855 ± 1.713 −10.213, −3.497 <0.001
POAG-moderate −8.173 ± 2.123 −12.335, −4.012 <0.001
POAG-severe −14.200 ± 2.909 −19.902, −8.498 <0.001
AAC Reference
POAG-mild 0.680 ± 2.009 −3.258, 4.619 0.735
POAG-moderate 0.202 ± 2.761 −5.210, 5.613 0.942
POAG-severe −3.433 ± 3.545 −11.381, 2.515 0.211
Annular PCD
Control Reference
AAC −9.320 ± 1.853 −12.952, −5.687 <0.001
POAG-mild −4.653 ± 1.953 −8.481, −0.826 0.017
POAG-moderate −6.672 ± 2.431 −11.438, −1.908 0.006
POAG-severe −12.785 ± 3.332 −19.316, −6.255 <0.001
AAC Reference
POAG-mild 3.327 ± 2.266 −1.114, 7.767 0.142
POAG-moderate 2.904 ± 3.113 −3.198, 9.006 0.351
POAG-severe −2.169 ± 3.910 −9.832, 5.494 0.579
AAC indicates acute angle closure; PCD, peripapillary perfused capillary density; POAG, primary open-angle glaucoma.Analyzed by the marginal model of generalized estimating equation.

DISCUSSION

OCTA is a novel noninvasive and quantitative imaging modality for the retinal microvasculature. Using OCTA and a customized analysis algorithm, we found a significant reduction in PCD in eyes with a single episode of AAC compared with that in control eyes. An increase in IOP between 40 and 50 mm Hg can severely affect retinal perfusion.24 In this study, all eyes showed normal IOP when they underwent OCTA, as confirmed by the long duration from acute attack onset to imaging. Mechanical compression of the optic disc because of high IOP is the primary mechanism underlying damage to angle closure. Therefore, reduced retinal vessel density may be a consequence of ischemia caused by extremely high IOP occurring during an acute attack. Decreased vascular density may elicit a synergistic effect with mechanical compression induced by IOP, leading to cpRNFL loss after an acute attack.25

Recent studies have reported reduced retinal vessel density in the peripapillary area on OCTA in AAC eyes compared with that in primary angle-closure suspect eyes.19,10 In the present study, cpRNFL thickness was significantly different between the affected and control eyes, which is consistent with the results reported by Zhang et al.10 In contrast, Wang et al19 have reported a similar cpRNFL thickness between AAC and fellow eyes. These conflicting results can be explained by different degrees of residual damage due to acute attacks among the enrolled AAC eyes. Meanwhile, our findings corroborate those reported by Moghimi et al25 regarding the progressive loss of peripapillary vessel density and thinning of cpRNFL at 6 weeks after an AAC episode.

We enrolled healthy eyes to eliminate the possibility of unnoted subacute angle closure attacks in the fellow eyes (natural internal controls) of AAC eyes, which may lead to errors in the measurement of accurate vessel density. Moreover, we used a generalized estimating equation model to eliminate potential interocular correlations in the same participant. Although previous studies have reported a potential effect of axial length on retinal vessel density,26,27 axial length showed a multicollinearity effect in the experimental groups (r = 0.503, P < 0.001); thus, we omitted axial length as an adjusted factor.

Recently, choroidal microvascular dropout has been shown to be significantly lower in PACG eyes than in POAG eyes.20 However, to better understand the association between peripapillary retinal and choroidal microvascular disturbances, further research is warranted.

Regarding subgroup analyses of POAG stages, both global and annular PCDs were significantly different among the 5 groups. However, there were no differences between each of the POAG stage and AAC groups. Multivariate analysis revealed that the degree of decrease in PCD in eyes with a single episode of AAC was similar to that in eyes with mild-to-severe POAG. These findings suggest that even a single acute attack can lead to significant damage to the neurons and peripapillary microvasculature.

The present study has several limitations. First, we attempted to enroll eyes with a single episode of AAC. However, we may not have been able to exclude eyes with asymptomatic sub-AAC glaucoma. An ideal study should include imaging participants before the episode of an acute attack; however, because this was not possible, we implemented the next best approach. As such, we excluded eyes with a history of subacute or recurrent angle-closure glaucoma and/or an increased cup-to-disc ratio.

In conclusion, this study provides a detailed comparison of peripapillary microvascular alterations among AAC, POAG, and control eyes. Overall, we found a greater loss of PCD in eyes with a single episode of AAC than in control eyes. Additionally, we found that the degree of microvascular attenuation in AAC eyes was not different from that in POAG eyes. Considering the cross-sectional design, the causality between decreased PCD and IOP-induced glaucomatous damage in AAC remains to be determined. Moreover, alterations in peripapillary vasculature with the rapid normalization of IOP on prompt treatment after an episode of AAC are yet to be established. From the current evidence, we suggest not to continue using antiglaucoma medication after the normalization of IOP. Further research is imperative to explain the association between PCD alterations and IOP-induced glaucomatous damage as well as the synergistic effects of microvascular attenuation on glaucomatous damage.

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Keywords:

angle closure; glaucoma; imaging; OCTA; primary open-angle glaucoma

Copyright © 2021 Asia-Pacific Academy of Ophthalmology. Published by Wolters Kluwer Health, Inc. on behalf of the Asia-Pacific Academy of Ophthalmology.