Utilizing research from the Age-Related Eye Disease Study 2, researchers found that MA and GA may be part of the same disease process affecting the visual acuity of patients with AMD.
A report utilizing research from the Age-Related Eye Disease Study 2 (AREDS2) suggests that macular atrophy and geographic atrophy (GA) may be part of a continuum of the same disease process affecting the visual acuity (VA) of patients with age-related macular degeneration (AMD).
The report, from lead author Amithia Domalpally, MD, research director of the Fundus Photograph Reading Center at the University of Wisconsin, argued that GA and neovascular AMD are not without overlap, but that the development of atrophy may be "the final common pathway of AMD, with the neovascular process intercepting the process in some eyes."
Domalpally and colleagues intended to shed further light on whether MA could be a late sequela of disease process in AMD, or whether MA combined in AMD eyes with pre-existing GA during the exudative process of the disease.
To help clarify interplay, overlap, and association between MA, GA, AMD and VA, researchers used data collected from the five-year multicenter AREDS2 study, a National Eye Institute sponsored study on the prophylactic effects of nutritional supplements on AMD progression which took place between 2007-2013. The AREDS2 study collected clinical data of more than 3500 participants with intermediate or advanced AMD between the ages of 50-85 (median age = 74).
Domalpally stated that data from 1 of the AREDS2 ancillary studies—in which fundus autoflorescence (FAF) images were collected from 2509 study participants (4328 eyes) at risk for advanced AMD, GA, or choroidal neovascularization CNV development—provides a “unique opportunity to assess the development of macular atrophy in eyes with incident CNV."
Researchers assessed AREDS2 color and FAF images for features of atrophy at the annual visit where CNV was first identified, the previous visit, and all follow up visits. All retinal photographs were given an AREDS severity score to determine associated risk values for advanced AMD development.
After analysis, Domalpally and colleagues determined that out of 4328 eyes, 9.2% (n= 334) developed CNV over the course of the study. Of those eyes, 41% (n = 137) showed signs of hypoautoflorescence, a sign of MA.
In looking back on FAFs in visits preceding diagnosis of CNV development, Domalpally and colleagues discovered that 20.6% (n= 69) of eyes showing signs of MA upon CNV diagnosis had visible GA prior to MA and CNV. In patients without atrophy at CNV diagnosis, 11.3% (n = 38) developed atrophy by the end of 2 years, and 14.6% (n= 49) developed atrophy by 4 years.
Data from the study showed that eyes with pre-existing GA reported the largest areas of atrophy at event visits and follow-up periods.
There were also differences in VA over time in eyes with CNV with and without atrophy. Although there was only minimal difference between eyes with CNV and MA and CNV without MA by 2-year follow up (-3.2 letters versus -2.4 letters, respectively), the difference had increased significantly (-10.9 letters versus -3.7 letters, respectively) by the 3-year follow up.
Researchers determined that what may be regarded as macular atrophy is “not necessarily a late sequelae of CNV because GA is present at the onset of disease in approximately 40% of eyes when assessed with FAF imaging in the AREDS2 data set."
Domalpally suggested that the 40% approximation could in fact be an underestimate given the fact that some areas of atrophy can be obscured due to the exudative process of CNV, and that presence of atrophy at baseline has been shown to be a significant predictor of development of atrophy and poor VA over time, with eyes with atrophy showing a more pronounced decline in VA after 2 years.
The study, "Atrophy in Neovascular Age-Related Macular Degeneration: Age-Related Eye Disease Study 2 Report Number 15,” was published online in Ophthalmology Retina.