Damage resulting from open-angle glaucoma (OAG) was recently studied in association with choroidal microvasculature dropout (CMvD), a localized complete loss of microvasculature within the beta-zone parapapillary atrophy of the choroidal layer. Researchers believe that the presence of CMvD may indicate compromised optic nerve head perfusion, as the parapapillary choroid and optic nerve head share blood supply with and are in proximity to the short posterior ciliary artery. A recent study examined the potential prognostic significance CMvD may have for OAG and found that it’s an independent predictor of subsequent VF progression in OAG eyes.

The retrospective, observational study included 80 OAG eyes with and without CMvD (n=40 for each group), matched for age and baseline VF severity. The researchers defined VF progression according to the Early Manifest Glaucoma Trial criteria. All subjects underwent OCT angiography scanning with en-face images of the retinal pigment epithelium to confirm presence of CMvD.

They found that during a mean follow-up of 35.91 months, there was a significant difference in VF progression rates between the CMvD(-) and CMvD(+) groups (22.5% vs. 70%). They identified baseline CMvD and higher visit-to-visit IOP fluctuation as significant predictors of VF progression. Additionally, they reported a significant difference between VF mean sensitivity at the central and superior central VF regions after two years of follow-up.

 “To date, the pathogenic significance of CMvD with respect to glaucoma prognosis has remained unclear,” the researchers wrote. “The parapapillary choroid receives its blood supply via short posterior ciliary arteries (SPCAs) and is located anatomically next to the prelaminar tissue and lamina cribrosa. It’s thus conceivable that SPCAs may provide microvasculature circulation to the deep optic nerve head structures such as the prelaminar tissue and lamina cribrosa by way of centripetal branches. Hence, the presence of CmvD may indicate a compromised or lack of perfusion to deep-layer structures of the optic nerve head.” They surmise that hypoxic damage induced by hypo-perfusion in this region may restrict axonal transport of neurotrophic factors by releasing toxic agents.

The researchers concluded, “A detected CMvD at baseline may provide an important clue to future progressive VF loss in OAG eyes, particularly in the central VF region, that requires more aggressive clinical treatment.”