2018 AAO Retina Subday: Simultaneous Inhibition of VEGF and Ang-2 with Genentech's Faricimab in Neovascular AMD: STAIRWAY Phase 2 Results

1Nimesh Patel, MD Vitreoretinal Fellow Bascom Palmer Eye Institute Nicole Topilow, MD Ophthalmology Resident Bascom Palmer Eye Institute The Mandarin Oriental hotel provided a grand setting for the annual meeting. The day began with organizer, Dr. Philip J. Rosenfeld, providing some history of Angiogenesis. He discussed how far the field has come since the first meeting and that we are only in the dawn of ocular pharmacotherapy.
2 Dr. Philip Luthert started the presentations with his interesting theory that the cause for the pattern of parafoveal geographic atrophy in AMD is related to a competition between cones and rods for metabolites. Next, Dr. Jean-Francois Korobelnik discussed new data regarding the prevalence of AMD. It appears that the incidence of late AMD is decreasing. This could be due to improving dietary health and decreasing rates of smoking. His group found that if a patient does not have early AMD at age 73, then they are very unlikely to develop late AMD in their lifetime.
3 After this, Dr. Emily Y. Chew presented preliminary data from the AREDS2 study with a 10-year follow up. Beta-carotene continues to be associated with a two-fold increase risk of lung cancer. The treatment effect of the AREDS2 formula is maintained throughout the duration of the study. The studies involving lampalizumab did not show a benefit in progression but did provide important natural history data. Dr. Nancy M. Holekamp discussed natural history of geographic atrophy (GA) progression from the Proxima A and Proxima B studies. There was GA growth and consistent visual acuity decline. There was a discussion that with these findings, VA could indeed be a reliable endpoint for future GA studies.
4 Genetics in AMD has been an been an emerging area of study. Dr. Johanna M. Seddon presented a polygenic risk model that can predict to a certain degree which patients are more likely to progress from intermediate to late AMD.
5 Dr. Karl G. Csaky showed an evaluation of the association of high-risk SNPs with GA progression in the lampalizumab phase III trial. GA progression was not strongly associated with the SNPs tested. A theory as to why this is in contrary to the prior presentation was that there may exist a difference in the mechanisms behind progression from intermediate to late AMD and progression in GA.
6 Next, Dr. Lawrence A. Yannuzzi showed amazing cases of cuticular drusen and discussed three phenotypes. He noted that it is necessary in mixed cases to use multimodal imaging with autofluorescence. The clinical impact of this classification is that the progression rates were significantly different between the phenotypes.
7 The focus shifted to imaging and one of the pioneers of OCT, Dr. James G. Fujimoto, showed results using ultrahigh speed and ultrahigh resolution OCT for investigating the choriocapillaris. He showed that it is possible to increase the scan rate and improve the assessment of flow and pulsatility in the choriocapillaris in the cardiac cycle. Dr. Ruikang Wang discussed the assessment of the choriocapillaris using OCTA. He showed how retinal projection artifact from drusen and the RPE needs to be removed before choriocapillaris quantification.
8 Continuing on this topic, Dr. Nadia K. Waheed showed that choriocapillaris loss can be seen prior to and may be associated with atrophy progression, although longitudinal studies are needed. Widespread clinical correlation could be limited by segmentation difficulties in segmentation as well as image processing requiring complex analysis and quality control.
9 Dr. Philip J. Rosenfeld closed the first session by presenting on the flow voids in choriocapillaris imaging. There was a continued increase in flow deficits in the central macula as age increases in normal patients. This is important to establish a model of normal controls for future studies.   Interestingly, the area of the choriocapillaris loss that was most associated with atrophy progression was not directly adjacent to the atrophy.