The vitreous in AMD A new study finds that vitreomacular adhesion (VMA) is a risk factor for exudative age-related macular degeneration (AMD), and posterior vitreous detachment (PVD) may protect against exudative AMD.

The cause of choroidal neovascularization (CNV) in exudative AMD is not fully understood, especially regarding the role of vitreous. Previous studies have described the relationship between the posterior vitreous and the macula in AMD and have suggested that vitreomacular adhesion is important in the development of exudative changes. Whether genetic and environmental factors specifically affect this relationship is yet to be described.

PVD is a common condition which occurs in about 75% of people over the age of 65. The vitreous is a clear jelly-like substance within the eye which takes up the space behind the lens and in front of the retina. It is 99 per cent water. The other 1 per cent consists of collagen protein which is important in maintaining the shape of the vitreous. At birth the vitreous is attached to the retina. The firm jelly-like substance of the vitreous changes with age. The central part of the vitreous becomes more liquid and the outer part (cortex) peels away from the retina. As it comes away from the retina it can cause the symptoms of posterior vitreous detachment - flashes of light and floaters.

Vitreomacular adhesion is when the vitreous cortex is adherent to the macula, as it is at birth. Occasionally, the vitreous may remains adherent to the macula after it has detached from the rest of the posterior retina. Under such circumstances it is prone to exterting tractional force upon the macula. Vitreomacular traction may be evident on optical coherence tomography as a steep slope of the inner macular surface, or a sharp angulation and localized deformation of the retinal profile, at the adhesion site of the vitreous.

Methods and Results

This was a multicenter retrospective, observational study consisting of 29 previously untreated subjects with active exudative (wet) AMD in one eye and active nonexudative (dry) AMD in the fellow eye who were compared with 10 previously untreated subjects with end-stage geographic atrophy in one eye and an end-stage fibrotic (disciform) scar in the fellow eye. This study aimed to mitigate any influence of genetics and environmental factors by studying patients with exudative AMD in one eye and nonexudative AMD in the fellow eye. All subjects were studied with ultrasonography to identify the presence of PVD and by optical coherence tomography to detect VMA.

The incidence of PVD in eyes with nonexudative AMD was 69% (20 of 29), compared with 21% (6 of 29) with active exudative AMD (P = .002). VMA was present in 38% (11 of 29) of eyes with exudative AMD and in only 10% (3 of 29) eyes with nonexudative AMD (P = .008).

The incidence of PVD in geographic atrophy was 70% (7 of 10), compared with 40% (4 of 10) with disciform scar (P = .44). VMA was present in 20% (2 of 10) eyes with disciform scars and in 0% (0 of 10) eyes with geographic atrophy (P = .48).

Discussion and Conclusions

The results of this study demonstrate that in active AMD, PVD is highly associated with nonexudative AMD, whereas VMA is related strongly to exudative AMD.

These results compare favorably with the results of a study of 551 subjects that determined that for a group of individuals with a mean age of 80 years, the incidence of PVD was 73%, very close to the 69% incidence observed in the present study for the eyes with dry AMD and very different from the 21% incidence of PVD detected in the eyes with wet AMD. Thus, it seems that for active AMD, the findings in previous studies are confirmed and the observations regarding the potential role of vitreous in AMD are not influenced by genetic and environmental factors.

The possible mechanisms by which VMA may promote exudative AMD are as follows:

• Anomalous PVD with VMA can cause chronic traction on the macula and can induce low-grade inflammation. The effects of inflammation on AMD have previously been established.
• The presence of the posterior vitreous cortex attached to the macula may prevent oxygen and perhaps nutrients from diffusing from the ciliary body into the macula. The resulting state of relative ischemia may promote CNV via the action of vascular endothelial growth factor.
• An adherent posterior vitreous cortex may trap proangiogenic cytokines such as vascular endothelial growth factor within the macula, contributing to neovascularization.
• Vitreomacular traction may impact the chorioretinal interface and may disrupt the normal interactions between the RPE and its junctional proteins.
• It is also possible that as soon as the CNV begins in exudative AMD, an attached posterior vitreous promotes further vessel proliferation, similar to how it contributes to retinal and optic disc neovascularization in diabetic retinopathy, that is, via traction.

In conclusion, ultrasonography and OCT were used to determine the incidence of PVD and VMA in previously untreated patients with active AMD, as well as in patients with end-stage AMD. Vitreous is more likely to be attached in exudative AMD than in nonexudative AMD, and thus anomalous PVD may be an important risk factor for progression of nonexudative AMD to exudative AMD. If future prospective studies confirm these findings, then it may be valuable to consider vitrectomy or pharmacologic vitreolysis as prophylaxis in preventing exudative AMD.

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Am J Ophthalmol. 2009 Jul;148(1):79-82.e2