Geographic Atrophy and Choroidal Neovascularization in the Same Eye: A Review

Abstract

Geographic atrophy (GA) and choroidal neovascularization (CNV), the two late forms of age-related macular degeneration, are generally considered two distinct entities. However, GA and CNV can occur simultaneously in the same eye, with GA usually occurring first. The prevalence of this combined entity is higher in histological studies than in clinical studies. No distinct systemic or genetic risk characteristics are associated with the combined GA/CNV entity, although on clinical examination and retinal imaging it can feature drusen or subretinal drusenoid deposits. GA and CNV may exist within the spectrum of a single disease, or they may be two very different diseases. Therapy with antivascular endothelial growth factor (anti-VEGF) is often successful for CNV, but some evidence suggests increased rates of GA development in eyes treated with anti-VEGF. In this article, we review the current literature regarding the epidemiology, clinical presentation, and treatment options for patients with the combined GA/CNV entity.

A Revised Hemodynamic Theory of Age-Related Macular Degeneration

“…Friedman’s hypothesis that AMD manifests due to vascular resistance imbalances in larger arteries does not itself explain the exquisitely focal nature of drusen deposits, or AMD pathologies overall. Both GA and CNV have been observed concomitantly in the same eye in humans [26], which is difficult to reconcile with Friedman’s model of ophthalmic artery disturbances as being the discriminating factor between these pathologies. Similarly, choroidal hypoperfusion and atrophy have been reported in both neovascular and atrophic AMD [21], suggesting that at a macro-scale, hemodynamic changes might be insufficient to discriminate between AMD outcomes.…”

Risk of geographic atrophy in age-related macular degeneration patients treated with intravitreal anti-VEGF agents

“…1 Retrospective data analysed from multicentre clinical trials demonstrate the necessity of long term followup of patients treated with anti-vascular endothelial growth factor (anti-VEGF) agents, both to monitor long-term visual outcomes and also to evaluate safety of this therapy with respect to the risk of developing GA. [2][3][4] Recently, phase III clinical trials have begun to evaluate treatment for geographic atrophy (the parallel CHROMA and SPECTRI studies, ClinicalTrials.gov Identifier: NCT02247479 and NCT02247531, respectively).…”

Next-generation sequencing analysis of the ARMS2 gene in Turkish exudative age-related macular degeneration patients

“…Mitochondrial dysfunction resulting from aging may lead to compromised energy metabolism, accumulation of mitochondrial DNA mutations, and subsequent activation of apoptotic pathways (Lin and Beal, 2006;McBride et al, 2006). Compared to healthy individuals, in the retinas AMD patients, mitochondrial number and size are decreased, cristae are lost, and mitochondrial DNA mutations accumulate (Veritti et al, 2012;Kaszubski et al, 2016).…”

“…The former is characterized by a thickening of Bruch's membrane, accumulation of drusen beneath the retinal pigment epithelium (RPE), and geographic atrophy, with loss of the RPE and photoreceptors in the macula. Exudative AMD, by contrast, is characterized by choroidal neovascularization (CNV), defined by the growth of new, fragile choroidal blood vessels, which penetrate Bruch's membrane, resulting in invasion of the retina with leaking vasculature (Ambati and Fowler, 2012;Veritti et al, 2012;van Lookeren Campagne et al, 2014;Kaszubski et al, 2016). The prevalence of AMD is 2.1% among individuals aged 40-49 years, increasing to 35% for those >80 years old.…”