Ophthalmic Surgery, Lasers and Imaging Retina

Practical Retina 

New Paradigms in Polypoidal Choroidal Vasculopathy Management: The Impact of Recent Multicenter, Randomized Clinical Trials

Colin S. Tan, MBBS, MMed (Ophth), FRCSEd (Ophth); Seenu M. Hariprasad, MD; Louis W. Lim, MBBS

Abstract

Seenu M. Hariprasad
Practical Retina Co-Editor

Just as recently as 2 years ago, in this column, we asked Colin S. Tan, MBBS, MMed (Ophth), FRCSEd (Ophth), and Louis W. Lim, MBBS, to summarize the optimal management of polypoidal choroidal vasculopathy (PCV). Since that time, there have been several randomized clinical trials that have given us further insight on the management of this interesting condition. PCV was once considered to be a variant of wet age-related macular degeneration (AMD). However, it is clear that the unique clinical features and high prevalence in pigmented individuals warrants a distinct approach to this disease that may or may not be different than for wet AMD. Fortunately, given recent Level 1 evidence, the community is beginning to reach consensus regarding a systematic approach to treating this condition.

In this column, Drs. Tan and Lim will provide an up-to-date summary of treatment options for PCV. They will be reviewing numerous clinical trials, including EVEREST, EVEREST II, FUJISAN, PLANET, APOLLO, VAULT, and DRAGON. I am certain their insights and review of current treatment approaches will be educational for the retina community.

Colin S. Tan

Louis W. Lim

Polypoidal choroidal vasculopathy (PCV) is a variant of age-related macular degeneration (AMD) and commonly manifests with Type 1 choroidal neovascularization (CNV).1 PCV is characterized by the presence of abnormal vascular channels that are located in the subretinal pigment epithelial (RPE) space, commonly known as a branching vascular network, and the presence of aneurysmal dilatations (the polyps or polypoidal lesions) (Figure 1). Although PCV occurs more frequently in some populations, especially Asians,2,3 it is a global disease and an important differential to consider in any patient presenting with features of neovascular AMD.4

Figure 1.

Polypoidal choroidal vasculopathy. Color fundus photograph illustrating the orange-red subretinal nodules characteristic of this condition. There is subretinal hemorrhage surrounding the nodule temporal to the optic disc.

Although the treatment outcomes of PCV have been explored in various publications,5–7 it is only in recent years that we have the results of randomized, controlled clinical trials to facilitate evidence-based management of this important disease. The past year has been particularly exciting, with the results of 1-year data from two large multicenter, randomized controlled trials on PCV being reported. In this paper, we will explore the results of some of the multicenter, randomized, controlled clinical trials on PCV and discuss how these influence the management paradigms of PCV. It is important, however, to remember that the results of different clinical trials cannot be compared directly, as the baseline characteristics of the study populations may be different. Important considerations include differences in baseline best-corrected visual acuity (BCVA), central subfield thickness, and CNV type diagnosed using fluorescein angiography.

An important consideration in the management of any clinical condition is to first confirm that the diagnosis is made accurately. Currently, the gold standard for diagnosis of PCV is indocyanine green angiography (ICGA).8–10 However, a hyperfluorescent lesion seen on ICGA may not necessarily be a polyp. Common misdiagnoses include typical neovascular AMD, retinal angiomatous proliferations, retinal microaneurysms, and artifacts arising from prominent choroidal vessels beneath a region of RPE atrophy.4 Therefore, it is imperative to use established diagnostic criteria in evaluating whether a lesion is indeed PCV, such as the diagnostic criteria used and validated in the EVEREST and EVEREST II studies.9,11,12

In most clinical trials of retinal diseases, important outcome measures include changes in BCVA and retinal thickness measured using optical coherence tomography (OCT). For PCV studies, however, another important consideration is the rate of polyp closure or regression. Polyps that remain patent may bleed or leak, which results in worsening of…

Seenu M. Hariprasad Practical Retina Co-Editor

Seenu M. Hariprasad
Practical Retina Co-Editor

Just as recently as 2 years ago, in this column, we asked Colin S. Tan, MBBS, MMed (Ophth), FRCSEd (Ophth), and Louis W. Lim, MBBS, to summarize the optimal management of polypoidal choroidal vasculopathy (PCV). Since that time, there have been several randomized clinical trials that have given us further insight on the management of this interesting condition. PCV was once considered to be a variant of wet age-related macular degeneration (AMD). However, it is clear that the unique clinical features and high prevalence in pigmented individuals warrants a distinct approach to this disease that may or may not be different than for wet AMD. Fortunately, given recent Level 1 evidence, the community is beginning to reach consensus regarding a systematic approach to treating this condition.

In this column, Drs. Tan and Lim will provide an up-to-date summary of treatment options for PCV. They will be reviewing numerous clinical trials, including EVEREST, EVEREST II, FUJISAN, PLANET, APOLLO, VAULT, and DRAGON. I am certain their insights and review of current treatment approaches will be educational for the retina community.

Colin S. Tan

Colin S. Tan

Louis W. Lim

Louis W. Lim

Polypoidal choroidal vasculopathy (PCV) is a variant of age-related macular degeneration (AMD) and commonly manifests with Type 1 choroidal neovascularization (CNV).1 PCV is characterized by the presence of abnormal vascular channels that are located in the subretinal pigment epithelial (RPE) space, commonly known as a branching vascular network, and the presence of aneurysmal dilatations (the polyps or polypoidal lesions) (Figure 1). Although PCV occurs more frequently in some populations, especially Asians,2,3 it is a global disease and an important differential to consider in any patient presenting with features of neovascular AMD.4

Polypoidal choroidal vasculopathy. Color fundus photograph illustrating the orange-red subretinal nodules characteristic of this condition. There is subretinal hemorrhage surrounding the nodule temporal to the optic disc.

Figure 1.

Polypoidal choroidal vasculopathy. Color fundus photograph illustrating the orange-red subretinal nodules characteristic of this condition. There is subretinal hemorrhage surrounding the nodule temporal to the optic disc.

Although the treatment outcomes of PCV have been explored in various publications,5–7 it is only in recent years that we have the results of randomized, controlled clinical trials to facilitate evidence-based management of this important disease. The past year has been particularly exciting, with the results of 1-year data from two large multicenter, randomized controlled trials on PCV being reported. In this paper, we will explore the results of some of the multicenter, randomized, controlled clinical trials on PCV and discuss how these influence the management paradigms of PCV. It is important, however, to remember that the results of different clinical trials cannot be compared directly, as the baseline characteristics of the study populations may be different. Important considerations include differences in baseline best-corrected visual acuity (BCVA), central subfield thickness, and CNV type diagnosed using fluorescein angiography.

Diagnosis of PCV

An important consideration in the management of any clinical condition is to first confirm that the diagnosis is made accurately. Currently, the gold standard for diagnosis of PCV is indocyanine green angiography (ICGA).8–10 However, a hyperfluorescent lesion seen on ICGA may not necessarily be a polyp. Common misdiagnoses include typical neovascular AMD, retinal angiomatous proliferations, retinal microaneurysms, and artifacts arising from prominent choroidal vessels beneath a region of RPE atrophy.4 Therefore, it is imperative to use established diagnostic criteria in evaluating whether a lesion is indeed PCV, such as the diagnostic criteria used and validated in the EVEREST and EVEREST II studies.9,11,12

Clinical Outcome Measures in PCV Studies

In most clinical trials of retinal diseases, important outcome measures include changes in BCVA and retinal thickness measured using optical coherence tomography (OCT). For PCV studies, however, another important consideration is the rate of polyp closure or regression. Polyps that remain patent may bleed or leak, which results in worsening of VA.13 In addition, some cases may develop large subretinal hemorrhages (Figure 2), often termed as “massive submacular hemorrhage,” which may be associated with a poor prognosis and result in significant visual loss.13–15

Massive submacular hemorrhage. The submacular hemorrhage involves a large region of the macula. Centrally, there are orange-red subretinal nodules characteristic of polypoidal choroidal vasculopathy, with a large pigment epithelial detachment superiorly.

Figure 2.

Massive submacular hemorrhage. The submacular hemorrhage involves a large region of the macula. Centrally, there are orange-red subretinal nodules characteristic of polypoidal choroidal vasculopathy, with a large pigment epithelial detachment superiorly.

The Role of Photodynamic Therapy in PCV Management

In earlier studies on PCV, it was reported that although treatment with anti-vascular endothelial growth factor (VEGF) agents resulted in improvements in VA and reduction in retinal thickness on OCT, the polyps often remained patent.16,17 As previously discussed, this may pose a risk of continued or recurrent hemorrhage and exudation. When photodynamic therapy (PDT) with verteporfin (Visudyne; Novartis International AG, Basel, Switzerland) is used, either alone or together with anti-VEGF agents, the rate of polyp regression is much higher (Figure 3).

Treatment of polypoidal choroidal vasculopathy (PCV). (A) Indocyanine green angiography (ICGA) on presentation, illustrating characteristic polypoidal lesions and a branching vascular network (BVN). (B) Optical coherence tomography (OCT) on presentation, showing subretinal fluid, intraretinal cysts, and elevation of the retinal pigment epithelium (RPE) caused by the PCV lesion. The sharp elevation of RPE near the fovea corresponds to a polypoidal lesion. (C) ICGA following treatment with photodynamic therapy and a course of anti-vascular endothelial growth factor agents. The polypoidal lesions have resolved, although the BVN is still present. (D) OCT scan taken after treatment, showing resolution of the subretinal and intraretinal fluid. The RPE elevation has also reduced in height.

Figure 3.

Treatment of polypoidal choroidal vasculopathy (PCV). (A) Indocyanine green angiography (ICGA) on presentation, illustrating characteristic polypoidal lesions and a branching vascular network (BVN). (B) Optical coherence tomography (OCT) on presentation, showing subretinal fluid, intraretinal cysts, and elevation of the retinal pigment epithelium (RPE) caused by the PCV lesion. The sharp elevation of RPE near the fovea corresponds to a polypoidal lesion. (C) ICGA following treatment with photodynamic therapy and a course of anti-vascular endothelial growth factor agents. The polypoidal lesions have resolved, although the BVN is still present. (D) OCT scan taken after treatment, showing resolution of the subretinal and intraretinal fluid. The RPE elevation has also reduced in height.

Multicenter Clinical Trials on Treatment of PCV with PDT

The results of several multicenter clinical trials of the treatment of PCV with PDT can be seen in Table 1.

Outcomes of Clinical Trials on PCV

Table 1:

Outcomes of Clinical Trials on PCV

The first multicenter, randomized, controlled trial to address the efficacy of PDT was the EVEREST study,11 in which 61 patients with PCV were randomized into one of three treatment arms: verteporfin PDT combined with intravitreal ranibizumab (Lucentis; Genetech, South San Francisco, CA), PDT with sham injection, or intravitreal ranibizumab with sham PDT. At the primary endpoint of the study (6 months), complete polyp regression was observed in 77.8% of patients in the group receiving PDT and ranibizumab and 71.4% of the group receiving PDT monotherapy, compared to only 28.6% in the ranibizumab monotherapy group. The group receiving combination therapy experienced a larger gain in VA and greater reduction in retinal thickness compared to the ranibizumab monotherapy group, although the differences were not statistically significant.

Due to the relatively small sample size, the EVEREST study was not powered to detect a difference in VA or retinal thickness among the treatment arms. This, together with the short study duration (6 months), were limitations of this study and formed the impetus for a larger subsequent study.

The EVEREST II study12 was a 24-month, multicenter, randomized, double-masked study that compared the efficacy of PDT combined with ranibizumab against ranibizumab and sham PDT among patients with symptomatic macular PCV. From 42 sites in Asia, 322 patients with PCV were randomized equally into each of the two study arms. In both EVEREST and EVEREST II, the diagnosis of PCV was confirmed by a Central Reading Center (Fundus Image Reading Center, National Healthcare Group Eye Institute, Singapore) using standardized diagnostic criteria.9

Patients were treated with three loading doses of ranibizumab monthly, followed by additional ranibizumab injections pro re nata (PRN) based on prespecified retreatment criteria. Patients in the combination arm received verteporfin PDT at the start and PRN at three monthly intervals if polyps were detected on ICGA, whereas those in the monotherapy group received sham PDT.

At month 12, patients in the combination arm gained 8.3 letters, compared to 5.1 for the monotherapy arm (P = .01), and 24.5% gained 15 letters or more compared to 14.0% in the monotherapy arm (P = .03). Complete polyp regression was significantly higher in the combination arm, and almost double that of the monotherapy arm (69.3% vs. 34.7%; P < .001). The mean reduction in central subfield retinal thickness was greater in the combination arm (least squares mean, −164.9 μm vs. −113.4 μm; P < .001). Correspondingly, the percentage of patients with disease activity at month 11 was 20.5% in the combination arm compared to 50.0% in the monotherapy arm.

In addition to better treatment efficacy, patients treated with combination PDT and ranibizumab also required fewer injections. The median number of ranibizumab injections was four compared to seven for the monotherapy arm. Overall, 61.0% of patients in the combination arm only required one PDT treatment (at baseline) during the 12-month period.

Despite the proven efficacy of PDT combined with anti-VEGF agents, some clinicians have debated whether all patients with PCV require PDT. To attempt to address this, randomized clinical trials have been conducted on deferred PDT, or rescue PDT.

The FUJISAN study18 was a prospective, randomized clinical trial where patients received ranibizumab with either PDT at baseline or deferred PDT (at 3 months). Both groups experienced similar gains in VA (8.1 letters vs. 8.8, respectively), whereas the reduction in retinal thickness was greater among the group receiving initial PDT (−184.5 μm vs. −145.6 μm). In this study, the mean number of ranibizumab injections during the 12-month period was 4.5 and 6.8, respectively.

The PLANET study19 was a randomized, double-blind study where 310 patients diagnosed with PCV received three initial monthly doses of aflibercept (Eylea; Regeneron, Tarrytown, NY). At week 12, all patients were randomized into two arms: the first received aflibercept every 4 weeks with active PDT only if specific treatment criteria were met (termed “rescue PDT”), whereas the other group received aflibercept every 4 weeks and sham rescue PDT.

At month 12, VA gains were similar in both groups (10.8 vs. 10.7 letters), as were the reduction in CSFT (−143.5 μm vs. −137.7 μm). The percentage of patients with complete polyp regression at week 52 was 44.8% for the active rescue PDT group and 38.9% for the sham rescue PDT group. Of note, fewer than 15% of patients in either group required rescue PDT treatment, based on the study treatment protocol.

Prospective, Multicenter Clinical Trials on PCV Treated with Anti-VEGF Monotherapy (Table 2)

Outcomes of Clinical Trials on PCV

Table 2:

Outcomes of Clinical Trials on PCV Treated With Anti-VEGF Monotherapy

Although PDT has been shown to be effective in treating PCV, some ophthalmologists believe that PCV can be effectively treated using anti-VEGF monotherapy. In addition to outcomes of the anti-VEGF monotherapy arms of the randomized controlled trials discussed above, evidence for the efficacy of anti-VEGF monotherapy can be obtained from several prospective, multicenter, noncomparative, single-arm studies where PCV patients were treated using anti-VEGF agents alone.

The APOLLO study6 was an open-label, prospective, multicenter, single-arm clinical trial of 50 patients with PCV treated with intravitreal aflibercept monthly for 3 months, then every 2 months (at months 4, 6, 8, 10, and 12). After 12 months, mean gain in VA was 10.5 letters, with 72.5% of patients reported to have complete polyp regression. The mean central subfield thickness decreased from 355.7 μm at baseline to 238.5 μm at 12 months (P < .0001).

Similarly, the VAULT study20 treated 40 patients with PCV with intravitreal aflibercept monthly for 3 months, then every 2 months thereafter. At month 12, the mean gain in VA was 9.0 letters, and 66.7% of patients were reported to have complete polyp regression. Mean subfield macular thickness decreased from 365.2 μm to 253.6 μm (P < .001), and a dry macula was reported in 60.0% of eyes at month 12.

The DRAGON study21 was a 24-month, phase 4, randomized, double-masked, controlled, multicenter study that examined the treatment outcomes of ranibizumab monthly for the first 12 months compared to ranibizumab PRN. After month 12, patients in both treatment arms were treated with ranibizumab PRN. Among the cohort of 333 patients, 139 (41.7%) were diagnosed by the reading center to have PCV. Of these, the mean gain in VA at month 24 was 12.3 letters for the group treated initially with monthly therapy and 9.7 for the group treated with PRN.

Conclusion

The 1-year results from two large, prospective, multicenter clinical trials, EVEREST II and PLANET, provide important information that influences the paradigm of PCV management. It has been shown that combining PDT with an anti-VEGF agent increases the rate of complete polyp regression and reduces the treatment burden. The optimal time to perform PDT (whether at the initial treatment or in a deferred or rescue mode) remains the subject of discussion. Additional considerations for future studies will include identifying which patients will benefit from early PDT and those in which PDT may safely be deferred. On the other hand, treatment with anti-VEGF monotherapy has been shown to result in improvements in VA and reduction in central macular thickness, although its efficacy in terms of complete polyp closure is variable.

References

  1. Khan S, Engelbert M, Imamura Y, Freund KB. Polypoidal choroidal vasculopathy: Simultaneous indocyanine green angiography and eye-tracked spectral domain optical coherence tomography findings. Retina. 2012;32(6):1057–1068. doi:10.1097/IAE.0b013e31823beb14 [CrossRef]
  2. Maruko I, Iida T, Saito M, Nagayama D, Saito K. Clinical characteristics of exudative age-related macular degeneration in Japanese patients. Am J Ophthalmol. 2007;144(1):15–22. doi:10.1016/j.ajo.2007.03.047 [CrossRef]
  3. Lim TH, Laude A, Tan CS. Polypoidal choroidal vasculopathy: An angiographic discussion. Eye (Lond). 2010;24(3):483–490. doi:10.1038/eye.2009.323 [CrossRef]
  4. Tan CS, Ngo WK, Lim LW, Tan NW, Lim THEVEREST Study Group. EVEREST study report 3: Diagnostic challenges of polypoidal choroidal vasculopathy. Lessons learnt from screening failures in the EVEREST study. Graefes Arch Clin Exp Ophthalmol. 2016;254(10):1923–1930. doi:10.1007/s00417-016-3333-y [CrossRef]
  5. Cho HJ, Kim KM, Kim HS, et al. Intravitreal aflibercept and ranibizumab injections for polypoidal choroidal vasculopathy. Am J Ophthalmol. 2016;165:1–6. doi:10.1016/j.ajo.2016.02.019 [CrossRef]
  6. Oshima Y, Kimoto K, Yoshida N, et al. One-year outcomes following intravitreal aflibercept for polypoidal choroidal vasculopathy in Japanese patients: The APOLLO Study. Ophthalmologica. 2017;238(3):163–171. doi:10.1159/000477448 [CrossRef]
  7. Gomi F, Ohji M, Sayanagi K, et al. One-year outcomes of photodynamic therapy in age-related macular degeneration and polypoidal choroidal vasculopathy in Japanese patients. Ophthalmology. 2008;115(1):141–146. doi:10.1016/j.ophtha.2007.02.031 [CrossRef]
  8. Tan CS, Ngo WK, Lim LW, Lim TH. A novel classification of the vascular patterns of polypoidal choroidal vasculopathy and its relation to clinical outcomes. Br J Ophthalmol. 2014;98(11):1528–1533. doi:10.1136/bjophthalmol-2014-305059 [CrossRef]
  9. Tan CS, Ngo WK, Chen JP, Tan NW, Lim THEVEREST Study Group. EVEREST study report 2: Imaging and grading protocol, and baseline characteristics of a randomised controlled trial of polypoidal choroidal vasculopathy. Br J Ophthalmol. 2015;99(5):624–648. doi:10.1136/bjophthalmol-2014-305674 [CrossRef]
  10. Tan CS, Lim TH, Hariprasad SM. Current management of polypoidal choroidal vasculopathy. Ophthalmic Surg Lasers Imaging Retina. 2015;46(8):786–791. doi:10.3928/23258160-20150909-02 [CrossRef]
  11. Koh A, Lee WK, Chen LJ, et al. EVEREST study: Efficacy and safety of verteporfin photodynamic therapy in combination with ranibizumab or alone versus ranibizumab monotherapy in patients with symptomatic macular polypoidal choroidal vasculopathy. Retina. 2012;32(8):1453–1464. doi:10.1097/IAE.0b013e31824f91e8 [CrossRef]
  12. Koh A, Lai TYY, Takahashi K, et al. Efficacy and safety of ranibizumab with or without verteporfin photodynamic therapy for polypoidal choroidal vasculopathy: A randomized clinical trial. JAMA Ophthalmol. 2017;135(11):1206–1213. doi:10.1001/jamaophthalmol.2017.4030 [CrossRef]
  13. Tan CS, Wong HT, Lim BA, Hee OK, Lim TH. Polypoidal choroidal vasculopathy causing massive suprachoroidal haemorrhage. Eye (Lond). 2007;21(1):132–133. doi:10.1038/sj.eye.6702455 [CrossRef]
  14. Cho JH, Ryoo NK, Cho KH, Park SJ, Park KH, Woo SJ. Incidence rate of massive submacular hemorrhage and its risk factors in polypoidal choroidal vasculopathy. Am J Ophthalmol. 2016;169:79–88. doi:10.1016/j.ajo.2016.06.014 [CrossRef]
  15. Lin TC, Hwang DK, Lee FL, Chen SJ. Visual prognosis of massive submacular hemorrhage in polypoidal choroidal vasculopathy with or without combination treatment. J Chin Med Assoc. 2016;79(3):159–165. doi:10.1016/j.jcma.2015.11.004 [CrossRef]
  16. Cho HJ, Baek JS, Lee DW, Kim CG, Kim JW. Short-term effectiveness of intravitreal bevacizumab vs. ranibizumab injections for patients with polypoidal choroidal vasculopathy. Korean J Ophthalmol. 2012;26(3):157–162. doi:10.3341/kjo.2012.26.3.157 [CrossRef]
  17. Kokame GT, Yeung L, Teramoto K, Lai JC, Wee R. Polypoidal choroidal vasculopathy exudation and haemorrhage: Results of monthly ranibizumab therapy at one year. Ophthalmologica. 2014;231(2):94–102. doi:10.1159/000354072 [CrossRef]
  18. Gomi F, Oshima Y, Mori R, et al. Initial versus delayed photodynamic therapy in combination with ranibizumab for treatment of polypoidal choroidal vasculopathy: The Fujisan Study. Retina. 2015;35(8):1569–1576. doi:10.1097/IAE.0000000000000526 [CrossRef]
  19. Iida T. Results of the planet study. Paper presented at: Asia-Pacific Vitreo-retina Society Annual Meeting. ; December 9, 2016. ; Bangkok, Thailand. .
  20. Lee JE, Shin JP, Kim HW, et al. Efficacy of fixed-dosing aflibercept for treating polypoidal choroidal vasculopathy: 1-year results of the VAULT study. Graefes Arch Clin Exp Ophthalmol. 2017;255(3):493–502. doi:10.1007/s00417-016-3489-5 [CrossRef]
  21. Li X, Zhu A, Egger A, et al. Ranibizumab 0.5 mg in patients with polypoidal choroidal vasculopathy: Results from the DRAGON study. Paper presented at: American Academy of Ophthalmology. ; October 15–18, 2016. ; Chicago, IL. .

Outcomes of Clinical Trials on PCV

EVEREST11 EVEREST II12* FUJISAN18 PLANET19#
Type of Study Prospective, multicenter, randomized, controlled clinical trial Prospective, multicenter, randomized, controlled clinical trial Prospective, multicenter, randomized clinical trial Prospective, multicenter, randomized, controlled clinical trial
Number of Patients 59 322 72 310
Duration of Study (Months) 6 24 12 24
Treatment PDT + ranibizumab PDT + sham injection Ranibizumab + sham PDT PDT + ranibizumab Ranibizumab + sham PDT PDT + ranibizumab (initial) PDT + ranibizumab (delayed) Aflibercept + rescue PDT Aflibercept + sham rescue PDT
Baseline VA (Letters) 56.6 ± 20.9 57.2 ± 12.8 49.0 ± 18.1 61.1 ± 12.6 61.2 ± 13.9 54.3 ± 17.9 54.9 ± 13.1 59.0 (11.5) 57.7 (11.3)
Gain in VA (Letters) 10.9 ± 10.9 7.5 ± 10.7 9.2 ± 12.4 8.3 ± 1.0 5.1 ± 1.1 8.1 ± 1.8 8.8 ± 1.8 10.8 10.7
Reduction in CRT (µm) 145.6 ± 119.0 98.1 ± 104.3 65.7 ± 114.3 164.9 113.4 184.5 ± 31.1 145.6 ± 20.6 143.5 137.7
Complete Polyp Regression (%) 77.8 71.4 28.6 69.3 34.7 62.1 54.8 44.8 38.9

Outcomes of Clinical Trials on PCV Treated With Anti-VEGF Monotherapy

APOLLO6 VAULT20 DRAGON21
Type of Study Open-label, prospective, multicenter, single-arm, single-dose clinical trial Prospective, multicenter, interventional, single-arm, single-dose clinical trial Phase 4, randomized, double-masked, controlled, multicenter study
Number of Patients With PCV 50 40 139
Duration of Study (Months) 12 12 24
Treatment Aflibercept Aflibercept Ranibizumab
Baseline VA (Letters) 0.33 ± 0.34 (83.5 ± 83) 55.1 ± 18.2 54.1 ± 12.3 (monthly); 54.6 ± 11.9 (PRN)
Gain in VA (Letters) 0.21 (10.5) 9.0 ± 18.1 12.3 (monthly); 9.7 (PRN)
Reduction in CRT (μm) 117 111.6 176.1 (monthly); 157.5 (PRN)
Complete Polyp Regression (%) 72.5 66.7
Authors

Colin S. Tan, MBBS, MMed (Ophth), FRCSEd (Ophth), can be reached at National Healthcare Group Eye Institute, Tan Tock Seng Hospital, 11 Jalan Tan Tock Seng, Singapore; email: Colintan_eye@yahoo.com.sg.

Seenu M. Hariprasad, MD, can be reached at the Department of Ophthalmology and Visual Science, University of Chicago, 5841 S. Maryland Avenue, MC2114, Chicago, IL 60637; email: retina@uchicago.edu.

Louis W. Lim, MBBS, can be reached at National Healthcare Group Eye Institute, Tan Tock Seng Hospital, 11 Jalan Tan Tock Seng, Singapore; email: limwy1987@gmail.com.

Disclosures: Dr. Tan received a grant from the National Medical Research Council, Singapore, and has received honoraria and conference support from Bayer and Novartis outside the submitted work. Dr. Hariprasad is a consultant or on the speakers bureau for Alcon, Allergan, Bayer, OD-OS, Clearside Biomedical, Ocular Therapeutix, Alimera Sciences, Leica, Spark, and Regeneron. Dr. Lim reports no relevant financial disclosures.

10.3928/23258160-20171215-01

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