Treatment Options for Macular Edema Following Retinal Vein Occlusion

EP: 1.An Overview of Retinal Vein Occlusion

EP: 2.Retinal Vein Occlusion: Practical Advice on Work-up and Diagnosis

EP: 3.Diagnosing Retinal Vein Occlusion During the COVID-19 Pandemic

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EP: 4.Treatment Options for Macular Edema Following Retinal Vein Occlusion

EP: 5.VEGF Inhibitor Trial Data in Macular Edema Following Retinal Vein Occlusionanti-VEGF therapy

EP: 6.Macular Edema Following Retinal Vein Occlusion: Comparing Anti-VEGF Therapies

EP: 7.Practical Advice on Treating Macular Edema Following Retinal Vein Occlusion

EP: 8.Treating MEfRVO: Considerations for Steroids and Combination Therapy

EP: 9.Unmet Needs in Treating Macular Edema Following Retinal Vein Occlusion

Transcript:

Jayanth Sridhar, MD: The standard of care for a patient with retinal vein occlusion and macular edema is intravitreal anti-VEGFtherapy. But even if a patient presents with a retinal vein occlusion without macular edema, I do talk to them about injection therapy because they may need it down the line. What I talk to them about is that we have therapy that’s been proven over a decade to be efficacious. It has been proven to be safe, given for many years. It does work. I do temper the goal slightly, you referenced that 2- to 3-line vision improvement. I don’t tell them to expect perfection, but I do tell them that this is a disease process where VEGF is upregulated tremendously. With retinal vein occlusion, if you look at the levels of VEGF, there are much higher levels of VEGF when you compare it to macular degeneration, diabetic retinopathy, diabetic macular edema, the other conditions we use these drugs for. It’s a very VEGF-mediated disease, and a very VEGF-responsive disease. I tell them, “Oftentimes, you’ll see a substantial improvement after initial therapy, and continued improvement usually will happen after that.” We can talk about what you tell patients about the number of injections and how you time those out. But I do start talking about, “Our goal is to maximize your vision. Our goal is to get you to a point where we max it out. It may not be all the way back to your baseline, but we’re going to get as close as possible, and the study data show us that we can achieve substantial improvements.”

Rishi P. Singh, MD: Now we have laser treatment. We’ve used it for vein occlusions, for branch retinal vein occlusions. Maybe we could summarize the CVOS and VIVA studies. Basically, when those studies came out back in the early 1990s, they showed that the central retinal vein study had really no benefit with additional focal laser applied to the retina and the macula. While in branch retinal veins, it showed it could stabilize vision, not necessarily improve vision but stabilize vision, in those with some amount of vision loss or macular edema. We have applied that to our regimens now as well as the fact that we have obviously anti-VEGF therapy approved since about the 2007 or 2008 timeframe. Then lastly, we also have steroids, which are available to us in both an intraocular off-label format but also sustained-delivery format, and the format of a dexamethasone implant. We have those as well to bolster our ability to treat patients. Walk me through why the mechanism of action of anti-VEGFmakes sense in retinal vein occlusion.

Jayanth Sridhar, MD: That’s a phenomenal question, Rishi, and to understand why anti-VEGFmakes sense, you have to think about what the pathophysiology of macular edema and retinal neovascularization is in vein occlusion. A common question I get from patients is, “My vein occlusion was 12 months ago, but I am still having issues. Why is that?” The vein occlusion may have been a transient or temporary event, but it initiates a cascade that has permanent effects. It causes capillary hyperperfusion at the retinal level. That results in upregulation in production of angiogenic factors, such as vascular endothelial growth factor. That will in turn aggravate this cycle, this vicious cycle where that will worsen hyperperfusion and cause further production of this molecule, which is why it’s so upregulated in this condition. Anti-VEGFmakes a lot of sense because it steps right in the middle of that cascade, it blocks one of the primary factors, not the only factor but one of the primary factors for this process, and allows the retina to experience reduction in inflammation, reduction in edema. With reductions in edema, you allow the retina—we really are talking about the macula, the fovea—you allow that tissue to restore to more normal anatomy. And that allows for more normal function in terms of vision.

Rishi P. Singh, MD: Thank you all for watching this HCPLive® Peers & Perspectives. If you enjoyed this content, please subscribe to our e-newsletter to receive upcoming Peers & Perspectives and other great content right in your inbox. Thank you for watching.

Transcript edited for clarity.