Lowering Intraocular Pressure in Myopic Maculopathy? The Evidence for IOP as a Modifiable Risk Factor

Myopic maculopathy is the leading cause of irreversible vision loss in highly myopic patients. No treatment has been proven to slow atrophic progression in myopic maculopathy. Could something as simple as lowering intraocular pressure (IOP) slow its progression?

Mechanisms of IOP driven effect in myopic maculopathy

Laplace law

Laplace law shows that wall stress is proportional to both radius and internal pressure within a thin-walled sphere. Applying this to the eye, internal pressure is measured by IOP, and radius is given by axial length. An increase in axial length, in the case of high myopia, will result in greater wall stress at a given IOP. Furthermore, in patients with high myopia, scleral thickness is decreased with remodelling of the scleral collagen fibres as the axial length increases. This leads to a decrease in the tensile strength of the sclera making it less resistant to the expansile force, which in turn leads to further expansion. Essentially, given a constant IOP, the weakened sclera can continue to expand like a balloon, leading to ongoing axial length increase in adulthood and posterior staphyloma in myopic maculopathy.

Scleral response to IOP in highly myopic eye

In response to the ongoing stretching, the scleral fibroblast can produce metalloproteinases (MMPs) that break down collagen fibres, and decrease production of tissue inhibitors of metalloproteinases (TIMPs) leading to thinning. A decrease in IOP can downregulate the above process.

Choroidal response to IOP in highly myopic eye

Choroidal thinning is universally observed in highly myopic eyes, with around 5 µm of thinning per dioptre of myopia, and choroidal thickness is negatively correlated with axial length. Lowering IOP has been shown to improve choroidal blood flow. After trabeculectomy, every 1 mmHg decrease in IOP corresponds to a mean increase in choroidal thickness of 3.4 µm. Topical anti-ocular hypertensive medications have also been shown to increase choroidal blood flow and choroidal thickness. Conversely, IOP-induced reduction in choroidal perfusion can promote scleral hypoxia in these highly myopic eyes.

If these mechanisms are correct, we would expect higher IOP to be associated with worse maculopathy outcomes, and this is what the clinical data show.

Evidence so far

What caught my eye in a recent paper published in Ophthalmology (April 2026) was that higher IOP independently predicted atrophy progression in myopic maculopathy. This paper examined the risk factors for progression in myopic maculopathy following posterior scleral contraction in 892 patients with high myopia, defined as -6 dioptres or more. In this cohort, every 1mmHg increase in IOP confers a 13.8% risk of myopic atrophy progression.

The association between IOP and atrophy progression in myopic maculopathy has been documented in a number of other studies. A German paper (Ophthalmology 2022) based on the Gutenberg Health Study analysed outcomes from 494 eyes of 323 participants without myopic maculopathy at baseline and 34 eyes of 27 subjects with myopic maculopathy, all with -6 dioptres or more of refractive error. It showed that high IOP was associated with progression of myopic maculopathy, with an odds ratio of 1.62 per mmHg.

In a Singaporean study published in Ophthalmology Science 2025, analysis of 988 eyes from 518 highly myopic multiethnic patients with a minimum follow-up time of 5 years showed that baseline glaucoma medication use was significantly associated with reduced AXL elongation over time (β = –0.077, P = 0.036), independent of IOP. However, IOP on its own was not significantly associated with the presence or progression of myopic macular degeneration, staphyloma, or axial length elongation in non-glaucomatous eyes.

Another study in Ophthalmology Science 2026 showed that cataract surgery was associated with both lower IOP and significantly slower axial elongation. The authors postulated that the effect of cataract surgery on slower axial elongation was driven by lower IOP, consistent with the above findings.

In a seemingly contradictory result published in Ophthalmology Retina 2025, 1228 eyes from 781 highly myopic patients from a European cohort, with a minimum follow-up time of 5 years, were examined for longitudinal progression of myopic maculopathy. IOP was not reported, but IOP-lowering therapies, both medications and glaucoma surgery, were associated with worse visual acuity outcome. However, instead of interpreting that IOP-lowering therapy was detrimental in this cohort, the more likely explanation is that those receiving IOP-lowering therapy had higher IOP to start with, which contributed to progression.

What are the implications to our treatment of myopic maculopathy

The following represents my approach based on the current evidence, recognising that no randomised trial has yet tested IOP lowering specifically for myopic maculopathy prevention.

Monitor axial length in the highly myopic eye

In contrast to the non-myopic eye, eyes with high myopia will have ongoing expansion of the axial length during adulthood due to the mechanisms discussed above. It is imperative to monitor the axial length in patients with myopic maculopathy once a year to document if there is any progression over time. The expansion rate is documented to be 0.031 +/- 0.030 mm per year. Within an ophthalmology practice, this can simply be performed using a biometry machine, such as the IOL master (Zeiss).

However, most patients with high myopia without maculopathy are managed by optometry practices without access to biometry. In these patients, assessment of refractive error for increasing myopia can serve as a surrogate for axial length measurement. As a rule of thumb, every 1 dioptre of refractive change corresponds to 0.3mm of axial length difference, so the average yearly expansion rate of 0.031mm corresponds only to -0.1 dioptre in refraction, making this a much less sensitive measure, though acceptable in this lower risk group. Once there are signs of early maculopathy, a referral to an ophthalmologist with expertise in medical retinal diseases should be considered.

Treat ocular hypertension in high myopia

Because of the evidence presented above, treatment for ocular hypertension (IOP of 21 mmHg or more) should be offered for all patients with myopic maculopathy or those with documented axial length expansion. The aim of the treatment should be returning IOP to the normal range. In most cases, this is achievable by drops. Such treatments are of low systemic and ocular risk, and are justifiable given the elevated risk of glaucoma and the plausible benefit in reducing axial length expansion within this group.

It is important to continue to monitor for glaucoma development and for axial length changes at least yearly after initiation of treatment, in order to assess for a therapeutic effect and to adjust treatment accordingly.

On the other hand, for those with high myopia with no evidence of axial length expansion, I will discuss the benefit of IOP lowering treatment and let the patient decide whether to proceed with treatment. I continue to monitor this group yearly and offer treatment if progression develops.

High myopia or myopic maculopathy without ocular hypertension

The indication for treatment within this group is weaker than the above. Myopic maculopathy is an irreversible condition. In the setting of normal IOP, the potential benefit of IOP lowering should still be discussed with this group of patients, especially those with ongoing axial length expansion. For patients who elect to proceed, topical treatment can be offered given the minimal risk involved.

In contrast, for those with high myopia but without maculopathy, the evidence is too weak to justify any IOP treatment in the setting of normal IOP. This group can be monitored yearly.

About Dr Leo Sheck

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Dr Sheck is a RANZCO-qualified, internationally trained ophthalmologist and runs a popular and respected practice in Auckland. He combined his initial training in New Zealand with a two-year advanced fellowship in Moorfields Eye Hospital, London. He also holds a Doctorate in Ocular Genetics from the University of Auckland and a Master of Business Administration from the University of Cambridge. He specialises in medical retina diseases (injection therapy), cataract surgery, ocular genetics, uveitis and electrodiagnostics.