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Editors Selection IGR 22-1

Anatomical structures: Peripapillary Choroid and RNFL

Linda Zangwill

Comment by Linda Zangwill on:

81115 Evaluation of Parapapillary Choroidal Microvasculature Dropout and Progressive Retinal Nerve Fiber Layer Thinning in Patients With Glaucoma, Kim JA; Lee EJ; Kim TW, JAMA ophthalmology, 2019; 137: 810-816


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Optical coherence tomography angiography (OCTA) has facilitated the three-dimensional visualization of retinal vasculature architecture of the optic nerve head and macula. Most glaucoma studies to date have focused on the microvasculature of the radial peripapillary capillaries layer of optic nerve head and the superficial vascular complex of the macula, as these layers have been shown to be associated with severity of glaucomatous visual field damage. Given that the short posterior ciliary arteries that perfuse the optic nerve head are located in the choroid, assessing the microvasculature in the choroid may be of particular importance for improving of understanding of the pathophysiology of the disease, and for developing predictive models of POAG progression. In the first longitudinal study quantifying parapalliary choroidal vascular dropout (MvD) over time, Kim and colleagues1 report that an enlargement in choroidal MvD area measured from enface Triton swept-source OCT angiogrpahy images is associated with progressive RNFL thinning in 68 POAG patients. In contrast, baseline and follow-up MvD area by itself was not associated with the rate of RNFL loss over time. Global and sectoral MvD changes were also documented. Other factors associated with faster RNFL thinning include larger beta zone parapapillary atrophy, and disc hemorrhage during follow-up.

This study adds to the growing literature suggesting that vascular insufficiency is associated with faster glaucomatous progression

The study is well designed, with appropriate masking, good interobserver agreement in the manual assessment of MvD area, and appropriate statistical analysis. This study adds to the growing literature suggesting that vascular insufficiency is associated with faster glaucomatous progression by measuring microvascular dropout in the parapapillary choroid. As the authors mention, caution should be exercised when evaluating the microvascular of the deeper layers as projection artifacts from the superficial layers are often not completely removed. Moreover, as only patients with MvD at baseline were included, the relative importance of MvD area enlargement in terms its prevalence and role in glaucoma pathophysiology remains to be determined. Further investigation is also necessary to assess the temporal relationship between MvD and the development of glaucoma to determine whether MvD enlargement is a cause or result of glaucomatous progression.



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