Purpose
To evaluate transient, large visual acuity (VA) decreases, termed sporadic vision loss, during anti–vascular endothelial growth factor treatment for neovascular age-related macular degeneration (AMD).
Design
Cohort within a randomized clinical trial.
Methods
setting : Comparison of Age-Related Macular Degeneration Treatments Trials (CATT). study population : Total of 1185 CATT patients. main outcome measures : Incidence of sporadic vision loss and odds ratio (OR) for association with patient and ocular factors. Sporadic vision loss was a decline of ≥15 letters from the previous visit, followed by a return at the next visit to no more than 5 letters worse than the visit before the VA loss.
Results
There were 143 sporadic vision loss events in 122 of 1185 patients (10.3%). Mean VA at 2 years for those with and without sporadic vision loss was 58.5 (∼20/63) and 68.4 (∼20/40) letters, respectively ( P < .001). Among patients treated pro re nata, no injection was given for 27.6% (27/98) of sporadic vision loss events. Multivariate analysis demonstrated that baseline predictors for sporadic vision loss included worse baseline VA (OR 2.92, 95% confidence interval [CI]:1.65–5.17 for ≤20/200 compared with ≥20/40), scar (OR 2.21, 95% CI:1.22–4.01), intraretinal foveal fluid on optical coherence tomography (OR 1.80, 95% CI:1.11–2.91), and medical history of anxiety (OR 1.90, 95% CI:1.12–3.24) and syncope (OR 2.75, 95% CI:1.45–5.22). Refraction decreased the likelihood of sporadic vision loss (OR 0.62, 95%CI: 0.42–0.91).
Conclusions
Approximately 10% of CATT patients had sporadic vision loss. Baseline predictors included AMD-related factors and factors independent of AMD. These data are relevant for clinicians in practice and those involved in clinical trials.
Visual acuity (VA) has been the primary outcome measure for every major clinical trial for neovascular age-related macular degeneration (AMD). Previous studies have established that VA measurement administered under a standard protocol that includes refraction provides a reliable outcome measure. Still, VA scores can be affected by multiple factors, some of which have little to do with the condition of the eye. Health issues that are not primarily ocular, such as depression and neurologic disease, can impact VA measurement or visual function. In addition, clinicians occasionally see patients in follow-up who have a worse VA measurement without any change on clinical examination.
As part of their analysis of vision loss during the Minimally Classic/Occult Trial of the Anti-VEGF Antibody Ranibizumab in the Treatment of Neovascular AMD (MARINA) and Anti-VEGF Antibody for the Treatment of Predominantly Classic Choroidal Neovascularization in AMD (ANCHOR) trials, Wolf and associates identified patients that had acute loss of ≥15 letters within any 1-month period. A total of 106 of 758 ranibizumab-treated patients (13.9%) experienced an acute loss of vision during the first year, and several had more than 1 episode of acute vision loss. Although they concluded that continued treatment was beneficial, there was no clear relationship between patient characteristics and acute vision loss, including an analysis of study eye adverse events (AEs) or serious adverse events (SAEs). It is possible that other factors in addition to progressive AMD disease were involved in some of these acute vision loss events.
Given that significant resources are devoted to studying a treatment’s effects on VA in AMD patients, we have sought further understanding of factors that influence this outcome measurement. The Comparison of Age-Related Macular Degeneration Treatments Trials (CATT) was a 2-year study that evaluated the efficacy of ranibizumab compared with bevacizumab, as well as monthly compared with as-needed treatments. The CATT database provides an unprecedented opportunity to investigate AMD patients as it expands on MARINA and ANCHOR data, providing treatment regimen, drug, and optical coherence tomography (OCT) correlations. We previously reported the frequency of sustained VA loss and its associated factors within CATT. Here, we report similarly for sporadic VA loss within CATT. Rather than studying patients with only an acute loss of ≥15 letters, we were interested in patients who had a decline of ≥15 letters from the previous visit, followed by a return of vision at the next visit. Although changes of 5 and occasionally 10 letters are within test-retest variability, little is known about the causes of transient VA losses of ≥15 letters for AMD patients.
Methods
This study was a secondary analysis of a cohort within a randomized clinical trial (CATT). Previous CATT reports provide a detailed summary of the CATT study design. CATT is registered with http://www.clinicaltrials.gov ( NCT00593450 ). Design features relevant to this report are described here.
Study Patients
Study patients provided written informed consent to participate in CATT. The Institutional Review Board of each study site prospectively approved the CATT study protocol, and the study is in accordance with the Health Insurance Portability and Accountability Act regulations. The inclusion criteria were age ≥50 years, untreated choroidal neovascularization (CNV) from AMD in the study eye, VA of 20/25–20/320, and neovascularization or its sequelae at the foveal center. Baseline medical history was obtained from all patients.
Patients were randomized at study entry to 1 of 4 treatment arms: ranibizumab monthly, bevacizumab monthly, ranibizumab pro re nata (PRN), and bevacizumab PRN. At 1 year, study patients in the monthly groups were randomized again 1:1 to continued monthly treatment or PRN treatment. PRN treatment was given when there were signs of active neovascularization, defined as fluid on OCT, hemorrhage, decreased VA compared with the prior visit, or leakage or increased lesion size on fluorescein angiography.
All patients had monthly VA measurements using an electronic VA testing system by certified VA examiners who were masked to the patients’ treatment assignment. Protocol refraction before measurement of VA was required at baseline and at weeks 4, 12, 24, 36, 52, 64, 76, 88, and 104. For efficiency, refractions were not routinely performed at every visit.
Imaging Procedures
Stereoscopic color fundus photography and fluorescein angiography were performed by certified photographers at baseline, 52 weeks, and 104 weeks. Stratus (version 4.0 or higher) time-domain OCT systems (Carl Zeiss Meditec, Dublin, California, USA) were used for first-year visits and most second-year visits. Spectral-domain OCT images were obtained for 23% of second-year visits. OCT images were obtained monthly in the PRN arms. Certified technicians masked to the patients’ treatment assignment followed standardized procedures and performed OCT imaging with macular thickness maps and fast macular thickness maps. OCT scans were independently analyzed by 2 certified OCT readers at the CATT OCT Reading Center, and photographs were analyzed by 2 certified readers at the CATT Photography Reading Center. Details about image acquisition and analysis by the reading centers are previously described.
Data Analysis
Sporadic vision loss required VA data from 3 consecutive visits (ie, VA1, VA2, and VA3). Sporadic vision loss was defined as a decline of ≥15 letters from the previous visit (ie, VA1 − VA2 ≥ 15 letters), followed by a return at the next visit to no more than 5 letters worse than the visit before the VA loss (ie, VA3 − VA1 ≥ −5 letters). Five letters was chosen for the latter part of this definition since 89% of test-retest electronic VA measurements reportedly are within 5 letters. Sporadic vision loss of 30 letters was defined as a decline of ≥30 letters from the previous visit, followed by a return at the next visit to no more than 5 letters worse than the visit before the VA loss.
The incidence of sporadic vision loss loss was calculated as the proportion of eyes with sporadic vision loss within 2 years among all CATT patients. Mean VA during the study was compared between eyes with sporadic vision loss and all other study eyes. VA, fundus photograph features, and OCT features were compared at 2 years between eyes with and without sporadic vision loss. As noted, the 2-group t test or the paired t test was used for comparison of means. Fisher exact test or McNemar test was used for comparison of proportions.
For the 27 events of sporadic vision loss that did not coincide with an injection, investigators for these events were queried about the possible cause of vision loss, whether new hemorrhage at the macula was present, and why no injection was given.
For the evaluation of baseline medical history associations with sporadic vision loss, we focused on neurologic and psychological histories because of their potential effects on visual function measurements. Additionally, a Functional Comorbidity Index was used to determine if patients with more comorbidities in their baseline history had an increased risk for sporadic vision loss. The Functional Comorbidity Index is an established measure of comorbid disease that correlates with physical function as the outcome of interest. This index contains 18 items such as visual impairment, congestive heart failure, arthritis, asthma, depression, anxiety, and neurologic disease. The Functional Comorbidity Index is scored by summing the number of specific comorbidities in a patient’s medical history. A score of 0 indicates no relevant comorbidities, while a score of 18 indicates the highest number of comorbid illnesses.
The association of sporadic vision loss and nonocular SAEs was investigated using nonocular SAEs reported within 30 days (before or after) of the time of sporadic vision loss events. These time frames were chosen as we were interested in knowing if sporadic vision loss has an association with a patient that is still recovering from a recent systemic SAE or that is becoming systemically ill and about to have an SAE. To investigate these potential associations, we matched sporadic vision loss patients (cases) with patients without sporadic vision loss (controls). The matching criteria were: drug, regimen, age (±3 years), Functional Comorbidity Index score (±2 points), and the number of visits with measured VA. To maximize the use of the controls, we allowed 1 case to have more than 1 control if available (ie, 1:n matching).
The evaluation of factors associated with sporadic vision loss was first performed by univariate analysis using repeated measures logistic regression models to accommodate patients with more than 1 event of sporadic vision loss. Multivariate analyses started with the factors with a P < .20 in univariate analysis, and the final multivariate analysis model was developed using a backward selection procedure by keeping only predictors with P < .05, with the exception of the drug and regimen groups. Adjusted odds ratios (OR) of sporadic vision loss and the 95% confidence intervals (95% CI) were calculated from the final multivariate logistic regression model for repeated measures. All data analyses were performed using SAS v9.2 (SAS Inc, Cary, North Carolina, USA). Two-sided P < .05 was considered statistically significant.
Results
Incidence and Visual Acuity
Over 2 years, 122 of the 1185 patients (10.3%) had at least 1 event of sporadic vision loss. There were 143 sporadic vision loss events. One hundred and two of 122 patients (83.6%) had only 1 sporadic vision loss event; 19 (15.6%) had 2 events; and 1 patient (0.82%) had 4 events. There were 10 patients (0.8%) of the 1185 patients who developed sporadic vision loss of 30 letters, including 1 patient who had 2 events of this. The time to first sporadic vision loss event was evenly distributed across the entire duration of the study. For 59 of 143 sporadic vision loss events (41.3%), the patient had a VA of 20/40 or better at the study visit preceding the sporadic vision loss. At all time points throughout the study, the patients with sporadic vision loss had a worse mean VA than patients without sporadic vision loss ( Figure ).
Optical Coherence Tomography Features and Injections Around the Time of Sporadic Vision Loss Among Eyes Treated Pro Re Nata
Sporadic vision loss events occurred 98 times in 83 eyes treated according to the PRN dosing regimen. OCT analysis of the 98 events showed that the mean retinal thickness was 169 μm at the visit before the sporadic vision loss, 183 μm at the time of sporadic vision loss, and 151 μm at the visit afterwards ( Table 1 ). Among all CATT patients, a change in OCT retinal thickness had a weak correlation with a change in VA (data not shown), and only 13 of these 98 sporadic vision loss events (13.3%) among eyes treated PRN coincided with an increase of retinal thickness of 50 μm or more. Foveal fluid was seen in 25 of the 98 events (25.5%) before the sporadic vision loss, in 37 (37.8%) at the time of sporadic vision loss, and in 17 (17.4%) afterwards. Subretinal fluid at the fovea was seen in 12 events (12.2%) before the sporadic vision loss, in 14 (14.3%) at the time of sporadic vision loss, and in 5 (5.1%) afterwards.
| 4 Weeks Before Sporadic Vision Loss | At Sporadic Vision Loss | 4 Weeks After Sporadic Vision Loss | P Value b (At vs Before Sporadic Vision Loss) | P Value b (At vs After Sporadic Vision Loss) | P Value b (Before vs After Sporadic Vision Loss) | |
|---|---|---|---|---|---|---|
| Events with injections in pro re nata groups, n (%) | 43 (43.9%) | 71 (72.4%) | 38 (38.8%) | <.001 | <.001 | .45 |
| Retinal thickness at foveal center (μm) | ||||||
| <120 | 24 (24.5%) | 21 (21.4%) | 28 (28.6%) | .28 | .006 | .43 |
| 120–212 | 55 (56.1%) | 50 (51.0%) | 58 (59.2%) | |||
| >212 | 17 (17.4%) | 25 (25.5%) | 12 (12.2%) | |||
| Mean (SE) | 169 (8) | 183 (10) | 151 (6) | .15 | <.001 | .007 |
| Retinal fluid at foveal center | ||||||
| No | 69 (70.4%) | 59 (60.2%) | 79 (80.6%) | .08 | <.001 | .07 |
| Yes | 25 (25.5%) | 37 (37.8%) | 17 (17.4%) | |||
| Subretinal fluid at foveal center | ||||||
| No | 82 (83.7%) | 80 (81.6%) | 90 (91.8%) | .78 | .007 | .01 |
| Yes | 12 (12.2%) | 14 (14.3%) | 5 (5.1%) | |||
a The totals may not add to 98 because of missing values in less than 5%.
b McNemar test for comparing proportions, paired t test for comparing means.
Of the 98 events among eyes treated PRN, 43 (43.9%) had a study injection at the prior visit and 71 (72.4%) had an injection at the visit when sporadic vision loss was noted. Among the 27 patients that were not treated at the time of sporadic vision loss, 6 (22.2%) had intraretinal or subretinal fluid at the fovea. Investigators were queried about these 27 events, and responses for 21 of these events were received. No identifiable cause for vision loss was found for 11 of these 21 events. For the remaining events, the cause of sporadic vision loss was thought to be related to a change in systemic health (3/21), progression of non-neovascular AMD (3/21), dry eyes (2/21), cataract (1/21), and increased subretinal fluid from neovascular AMD (1/21). The 1 patient that that had increased subretinal fluid refused treatment on that day, and the other patients were not treated because the investigator did not think there were signs of neovascular AMD activity. None of the responding investigators indicated that there was new hemorrhage at the macula.
Two-Year Visual Acuity and Morphologic Features Associated With Sporadic Vision Loss
A total of 113 patients that had sporadic vision loss were available for data analysis of 2-year VA and morphology. At 2 years, the mean VA of sporadic vision loss patients was 58.5 letters (∼20/63), as compared with 68.4 letters (∼20/40) for those patients without sporadic vision loss ( P < .001) ( Table 2 ). The mean VA change from baseline was 3.1 letters for patients with sporadic vision loss, compared with 6.7 letters for patients without sporadic vision loss ( P = .03). Forty-four of 113 patients (38.9%) with sporadic vision loss were 20/40 or better, as compared with 610 of 921 patients (66.2%) without sporadic vision loss ( P < .001). Fifty-six of 113 sporadic vision loss patients (49.6%) had a scar, as compared with 371 of 921 patients (40.3%) without sporadic vision loss ( P = .04). Sixteen of 113 sporadic vision loss patients (14.2%) had no pathology at the foveal center, compared with 188 of 921 patients (20.4%) without sporadic vision loss ( P = .02). Also, patients with sporadic vision loss had a larger total area of CNV lesion (9.97 mm 2 vs 8.04 mm 2 , P = .02). The presence of geographic atrophy was not significantly associated with sporadic vision loss ( P = .27). OCT analysis showed that the percent with fluid and the mean retinal thickness were not associated with sporadic vision loss ( P > .05).
| Visual Acuity and Morphology Features at Year 2 | With Sporadic Vision Loss (N = 113) | Without Sporadic Vision Loss (N = 921) | P Value a |
|---|---|---|---|
| Visual acuity at year 2, n (%) | |||
| 20/40 or better | 44 (38.9%) | 610 (66.2%) | <.001 |
| Worse than 20/40 | 69 (61.1%) | 311 (33.8%) | |
| Mean (SE) | 58.5 (1.8) | 68.4 (0.6) | <.001 |
| Mean (SE) change from baseline | 3.05 (1.88) | 6.74 (0.53) | .03 |
| Features of fundus photographs/fluorescein angiogram, n (%) | |||
| Scar anywhere | 56 (49.6%) | 371 (40.3%) | .04 |
| Geographic atrophy anywhere | 28 (24.8%) | 188 (20.4%) | .27 |
| Pathology in foveal center, n (%) | |||
| No pathology | 16 (14.2%) | 188 (20.4%) | .02 |
| Fluid | 3 (2.6%) | 30 (3.3%) | |
| CNV/SPED | 15 (13.3%) | 166 (18.0%) | |
| Scar | 38 (33.6%) | 191 (20.7%) | |
| Geographic atrophy | 11 (9.7%) | 52 (5.7%) | |
| RPE tear | 1 (0.9%) | 8 (0.9%) | |
| Other | 29 (25.7%) | 286 (31.1%) | |
| Total area of CNV lesion (mm 2 ) | |||
| Mean (SE) | 9.97 (0.85) | 8.04 (0.27) | .02 |
| Mean (SE) change from baseline | 2.46 (0.84) | 1.86 (0.22) | .39 |
| OCT features | |||
| Intraretinal fluid: Yes (%) | 66 (60.6%) | 460 (51.8%) | .10 |
| Subretinal fluid: Yes (%) | 29 (27.9%) | 325 (36.9%) | .08 |
| Sub-RPE fluid: Yes (%) | 32 (32.3%) | 332 (38.2%) | .27 |
| Retinal thickness at foveal center (μm) | <.001 | ||
| <120 | 43 (38.7%) | 203 (22.4%) | |
| 120–212 | 50 (45.1%) | 593 (65.5%) | |
| >212 | 18 (16.2%) | 110 (12.1%) | |
| Mean (SE) | 147 (8) | 162 (3) | .06 |
| Mean (SE) change from baseline | −92 (13) | −53 (4) | .004 |
| Subretinal tissue complex thickness at foveal center (μm): | |||
| Mean (SE) | 124 (9) | 128 (4) | .77 |
| Mean (SE) change from baseline | −100 (15) | −80 (5) | .21 |
a Fisher exact test for comparing proportions; 2-groups t test for comparing means.
Association of Serious Adverse Events With Sporadic Vision Loss
There were 11 events (10 patients) of sporadic vision loss of 30 letters, which met criteria for an ocular SAE. The causes reported by the investigator were related to AMD (5/11), related to central retinal vein occlusion (1/11), and possibly related to systemic health condition (3/11). There was no clear cause stated for the vision loss in 2 of these 11 events. Furthermore, an evaluation of ocular and systemic AEs did not show any significant associations (data not shown).
Using a matched case-control approach, we also evaluated whether a nonocular SAE within 30 days (before or after) was associated with sporadic vision loss. Among 94 matched case-control pairs that met criteria for analysis, 6 of 94 patients (6.4%) with sporadic vision loss had a nonocular SAE within 30 days compared with 9 of 199 matched controls (4.5%) without sporadic vision loss ( P = .48). Similarly, 47 of 122 patients (38.5%) with sporadic vision loss had a nonocular SAE during the 2 years of the trial, compared with 377 of 1063 patients (35.5%) without sporadic vision loss ( P = .55).
Baseline Medical History and Ocular Predictors of Sporadic Vision Loss
The univariate analysis ( Supplemental Table 1 , available at AJO.com ) showed that a baseline neurologic history and a baseline psychological history were risk factors for sporadic vision loss. Sixty-five of 546 patients (11.9%) with a neurologic history had sporadic vision loss, compared with 57 of 639 patients (8.9%) without a neurologic history ( P = .04). Thirty-two of 232 patients (13.8%) with a psychological history had sporadic vision loss, compared with 90 of 953 patients (9.4%) without a psychological history ( P = .02). Within the broad category of psychological disorders, subcategory analysis showed an “anxiety” history for 12 of 122 (9.8%) sporadic vision loss patients and only 43 of 1063 patients (4.1%) without sporadic vision loss ( P = .01) ( Supplemental Table 2 , available at AJO.com ). Additionally, the neurologic history subcategory of “syncope” was present for 10 of 122 patients (8.2%) with sporadic vision loss, compared with 28 of 1063 patients (2.6%) without sporadic vision loss ( P = .004). Of note, the 1 patient that had 2 events of sporadic vision loss of 30 letters had a baseline history including early Alzheimer disease and anxiety with hallucinations; for both of these events, the investigator did not find an ocular cause and thought that the medical history played a role. To further analyze whether patients with more comorbidities in their medical history had an increased risk for sporadic vision loss events, we applied a Functional Comorbidity Index to the data. However, there was no significant association between the Functional Comorbidity Index values and sporadic vision loss.
Univariate analysis of baseline ocular and OCT features are provided in the online supplement ( Supplemental Tables 3 and 4 , available at AJO.com ).
In multivariate analysis, history of a psychological disorder (OR 1.52, 95% CI: 1.03–2.25) was an independent predictor ( Table 3 ). Further analysis of psychological subcategories demonstrated that an anxiety history was the driving force for this association (OR 1.90, 95% CI: 1.12–3.24). Although a neurologic history was not a significant independent predictor, further subcategory analysis showed that a syncope history was an independent predictor (OR 2.75, 95% CI: 1.45–5.22). Other independent baseline predictors for sporadic vision loss included worse baseline VA (OR 2.92, 95% CI: 1.65–5.17 for baseline VA of 20/200–20/320 compared with 20/25–20/40), baseline scar (OR 2.21; 95% CI: 1.22–4.01), and OCT presence of foveal intraretinal fluid (OR 1.80; 95% CI: 1.11–2.91) ( Table 3 ). Drug or treatment regimen was not associated with sporadic vision loss ( P > .10).
| Baseline Characteristics | Patients at Baseline, N | Sporadic Vision Loss in 2 Years, n (%) | Odds Ratio (95% CI) | P Value a |
|---|---|---|---|---|
| Baseline visual acuity in study eye | ||||
| 20/25–40 | 410 | 29 (7.1%) | 1.00 | .002 |
| 20/50–80 | 431 | 41 (9.5%) | 1.43 (0.89, 2.27) | |
| 20/100–160 | 233 | 32 (13.7%) | 1.88 (1.15, 3.08) | |
| 20/200–320 | 78 | 18 (23.1%) | 2.92 (1.65, 5.17) | |
| Refraction when visual acuity measured (by visit) | ||||
| No | 17 877 | 107 (0.6%) | 1.00 | .01 |
| Yes | 9153 | 34 (0.4%) | 0.62 (0.42, 0.91) | |
| Psychological disorder | ||||
| No | 922 | 88 (9.5%) | 1.00 | .03 |
| Yes | 230 | 32 (13.9%) | 1.52 (1.03, 2.25) | |
| Baseline fibrotic or atrophic scar | ||||
| No | 1108 | 109 (9.8%) | 1.00 | .009 |
| Yes | 44 | 11 (25.0%) | 2.21 (1.22, 4.01) | |
| Intraretinal fluid | ||||
| No fluid | 275 | 20 (7.3%) | 1.00 | .04 |
| Fluid not in foveal center | 315 | 28 (8.9%) | 1.33 (0.76, 2.34) | |
| Fluid in foveal center | 562 | 72 (12.8%) | 1.80 (1.11, 2.91) | |
| Drug | ||||
| Ranibizumab | 584 | 64 (11.0%) | 1.00 | .41 |
| Bevacizumab | 568 | 56 (9.9%) | 0.86 (0.61, 1.23) | |
| Regimen | ||||
| Monthly | 303 | 32 (10.6%) | 1.00 | .14 |
| Switched | 266 | 22 (8.3%) | – | |
| Pro re nata | 583 | 66 (11.3%) | 1.32 (0.91, 1.92) | |
a From generalized linear model using generalized estimating equation to account for correlation from multiple events of sporadic visual acuity loss in some eyes. Initial model includes baseline visual acuity of study eye, lesion type, fibrotic or atrophic scar, retinal fluid, psychological disorder, neurologic disorder, refraction status, drug, and regimen.
Association of Refraction Status With Sporadic Vision Loss
Refractions were performed approximately every 3 months, and multivariate analysis showed that refraction decreased the likelihood of sporadic vision loss (OR 0.62; 95% CI: 0.42–0.91) ( Table 3 ). As seen in the Figure , refractions generally gave a small but consistent VA boost for all patients. After anti-VEGF therapy stabilized the vision (after 12 weeks), refractions were associated with a mean VA score 1.21 letters (95% CI: 1.00–1.42) better than visits without refraction.
Results
Incidence and Visual Acuity
Over 2 years, 122 of the 1185 patients (10.3%) had at least 1 event of sporadic vision loss. There were 143 sporadic vision loss events. One hundred and two of 122 patients (83.6%) had only 1 sporadic vision loss event; 19 (15.6%) had 2 events; and 1 patient (0.82%) had 4 events. There were 10 patients (0.8%) of the 1185 patients who developed sporadic vision loss of 30 letters, including 1 patient who had 2 events of this. The time to first sporadic vision loss event was evenly distributed across the entire duration of the study. For 59 of 143 sporadic vision loss events (41.3%), the patient had a VA of 20/40 or better at the study visit preceding the sporadic vision loss. At all time points throughout the study, the patients with sporadic vision loss had a worse mean VA than patients without sporadic vision loss ( Figure ).
Optical Coherence Tomography Features and Injections Around the Time of Sporadic Vision Loss Among Eyes Treated Pro Re Nata
Sporadic vision loss events occurred 98 times in 83 eyes treated according to the PRN dosing regimen. OCT analysis of the 98 events showed that the mean retinal thickness was 169 μm at the visit before the sporadic vision loss, 183 μm at the time of sporadic vision loss, and 151 μm at the visit afterwards ( Table 1 ). Among all CATT patients, a change in OCT retinal thickness had a weak correlation with a change in VA (data not shown), and only 13 of these 98 sporadic vision loss events (13.3%) among eyes treated PRN coincided with an increase of retinal thickness of 50 μm or more. Foveal fluid was seen in 25 of the 98 events (25.5%) before the sporadic vision loss, in 37 (37.8%) at the time of sporadic vision loss, and in 17 (17.4%) afterwards. Subretinal fluid at the fovea was seen in 12 events (12.2%) before the sporadic vision loss, in 14 (14.3%) at the time of sporadic vision loss, and in 5 (5.1%) afterwards.
| 4 Weeks Before Sporadic Vision Loss | At Sporadic Vision Loss | 4 Weeks After Sporadic Vision Loss | P Value b (At vs Before Sporadic Vision Loss) | P Value b (At vs After Sporadic Vision Loss) | P Value b (Before vs After Sporadic Vision Loss) | |
|---|---|---|---|---|---|---|
| Events with injections in pro re nata groups, n (%) | 43 (43.9%) | 71 (72.4%) | 38 (38.8%) | <.001 | <.001 | .45 |
| Retinal thickness at foveal center (μm) | ||||||
| <120 | 24 (24.5%) | 21 (21.4%) | 28 (28.6%) | .28 | .006 | .43 |
| 120–212 | 55 (56.1%) | 50 (51.0%) | 58 (59.2%) | |||
| >212 | 17 (17.4%) | 25 (25.5%) | 12 (12.2%) | |||
| Mean (SE) | 169 (8) | 183 (10) | 151 (6) | .15 | <.001 | .007 |
| Retinal fluid at foveal center | ||||||
| No | 69 (70.4%) | 59 (60.2%) | 79 (80.6%) | .08 | <.001 | .07 |
| Yes | 25 (25.5%) | 37 (37.8%) | 17 (17.4%) | |||
| Subretinal fluid at foveal center | ||||||
| No | 82 (83.7%) | 80 (81.6%) | 90 (91.8%) | .78 | .007 | .01 |
| Yes | 12 (12.2%) | 14 (14.3%) | 5 (5.1%) | |||
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