Position of Central Retinal Vascular Trunk and Preferential Location of Glaucomatous Damage in Myopic Normal-Tension Glaucoma.

PURPOSE

To investigate the spatial correlation between the central retinal vascular trunk and the preferential location of glaucomatous damage in myopic normal-tension glaucoma (NTG) eyes.

DESIGN

Cross-sectional study.

PARTICIPANTS

One hundred thirty-seven subjects with myopic NTG (137 eyes).

METHODS

The position of the vascular trunk was measured from the center of the Bruch membrane opening (BMO), which was delineated by optical coherence tomography imaging. The angular deviation was measured, with the horizontal nasal midline as 0° and the superior location as a positive value. The shift index was calculated as the distance of the vascular trunk from the BMO center relative to that of the BMO margin. The angular location of the midpoint of the retinal nerve fiber layer (RNFL) defect was measured from the BMO center. In cases with bi-hemispheric RNFL defects, the angular location was measured for the RNFL defect of larger width. For categorical analysis, hemispheric dominancy was determined if the RNFL defect in one hemisphere was larger than twofold that in the opposite hemisphere. In cases with no dominant hemisphere, the eye was classified as bi-equivalent involvement.

MAIN OUTCOME MEASURES

The vascular trunk position within the BMO and the location of glaucomatous damage.

RESULTS

The moderate- and severe-shift groups (shift index ≥ 0.5) were associated with younger age, longer axial length, smaller angular deviation, and lesser incidence of focal lamina cribrosa (LC) defect. A multiple regression analysis showed a significant correlation between the vascular trunk position and the RNFL defect location (P < 0.001). A logistic regression analysis revealed that the dominant RNFL defect occurred in the opposite hemisphere of the vascular trunk (P < 0.001), and bi-equivalent involvement in both hemispheres was associated with a larger shift index (P = 0.001). A conditional inference tree analysis showed that both the angular deviation (P < 0.001) and the extent of vascular trunk shift (P < 0.001) determined the RNFL defect location.

CONCLUSIONS

In myopic NTG eyes, the vascular trunk is located in the direction opposite of the RNFL defect with reference to the BMO. Because the vascular trunk is embedded in the LC, this implies that LC shift during axial elongation is associated with greater vulnerability of myopic eyes to glaucomatous damage.