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Editors Selection IGR 21-4

Clinical Forms of Glaucoma: Perfusion and Microvascular Changes in NTG II

Tae-Woo Kim

Comment by Tae-Woo Kim on:

91824 Nocturnal blood pressure dip and parapapillary choroidal microvasculature dropout in normal-tension glaucoma, Shin JW; Jo YH; Song MK et al., Scientific reports, 2021; 11: 206


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The choroidal microvascular dropout (CMvD) is a newly described phenomenon using optical coherence tomography angiography (OCTA). The CMvD is preferentially or exclusively found in the area of beta-zone parapapillary atrophy (PPA) either with (conventional beta-zone) or without Bruch's membrane (gamma-zone). The perfusion is impaired in the area of CMvD as assessed by indocyanine green angiography (ICG), which indicates that CMvD is a true perfusion defect rather than an imaging artifact. Much is unveiled regarding this newly described phenomenon. Particularly the pathogenesis of CMvD remains to be elucidated. Shin et al., described that NTG eyes with CMvD had nighttime diastolic BP (DBP) dip of greater magnitude and longer duration than eyes without CMvD. This finding is in line with previous observations that the presence of CMvD is associated with diastolic BP or mean arterial pressure. Shin et al's study has a strength in that they used 24-h ambulatory BP monitoring data.

The development of CMvD is probably associated with many factors. One thing to be considered is that CMvD is mostly found in the area of PPA and its inner border is adjacent to the disc margin. This preferential location indicates that localized factors in the parapapillary region may also play an important role as well as systemic factors. In addition, it has been recently demonstrated that CMvD is also found in patients with compressive optic neuropathy (CON). This finding indicates that CMvD may occur as a secondary phenomenon to retinal nerve fiber layer loss. The possibility of secondar development of MvD does not necessarily understate the importance of CMvD. The presence of CMvD in patients with CON indicates that prefusion to the prelaminar and laminar tissue is directly connected or related to the juxtapapillary perfusion. Under this condition, the decrease of metabolic demand in the prelaminar tissue may trigger or induce the development of CMvD. Taking this into account, the primary development of CMvD by a certain mechanism (vessel wall damage due to mechanical stress, or occlusion of capillaries due to vascular stasis or whatever) may promote the damage of axons passing the nearby prelaminar and laminar tissue.

Shin et al. nicely demonstrated that the development of CMvD may be associated with systemic vascular factors but there is still a long way to go before the pathogenesis of CMvD is fully understood. Given its potential importance in the pathogenesis of glaucomatous optic nerve damage, understanding how CMvD develops may contribute to improving the management of glaucoma patients which is solely dependent on the IOP lowering.



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