Elsevier

Ophthalmology

Volume 115, Issue 6, June 2008, Pages 934-940
Ophthalmology

Original article
Long-term Intraocular Pressure Fluctuations and Risk of Conversion from Ocular Hypertension to Glaucoma

https://doi.org/10.1016/j.ophtha.2007.08.012Get rights and content

Purpose

To investigate whether long-term intraocular pressure (IOP) fluctuations are a risk factor for conversion from ocular hypertension to glaucoma.

Design

Observational cohort study.

Participants

The study included 252 eyes of 126 patients with ocular hypertension observed untreated as part of the Diagnostic Innovations in Glaucoma Study. At baseline, ocular hypertensive eyes had elevated IOP, normal visual fields (VFs) on standard automated perimetry, and normal optic discs as evaluated by stereophotograph assessment.

Methods

Glaucoma conversion was defined as development of reproducible VF loss or optic disc damage. Analyses included all IOP measurements from the baseline visit to time of progression (for converters) and last follow-up (for nonconverters). Mean IOP and IOP fluctuation were calculated as the arithmetic mean and standard deviation (SD), respectively, of all available IOP measurements per eye.

Main Outcome Measures

Univariable and multivariable Cox regression analyses were used to evaluate the association between IOP fluctuation and time to progression. Multivariable models adjusted for age, mean IOP, central corneal thickness, vertical cup-to-disc ratio, and pattern SD.

Results

Forty eyes of 31 subjects developed glaucoma during follow-up. Mean IOPs during follow-up were 25.4±4.2 mmHg for the eyes that converted to glaucoma and 24.1±3.5 mmHg for the eyes that did not. Corresponding values for IOP fluctuation were 3.16±1.35 mmHg and 2.77±1.11 mmHg, respectively. Intraocular pressure fluctuation was not a risk factor for conversion to glaucoma both in univariable analysis (hazard ratio [HR], 1.30 per 1 mmHg higher; 95% confidence interval [CI], 0.76–1.96; P = 0.092) and in multivariable analysis (adjusted HR, 1.08 per 1 mmHg higher; 95% CI, 0.79–1.48; P = 0.620). Mean IOP during follow-up was a significant risk factor for progression both in univariable analysis (HR = 1.16 per 1 mmHg higher; 95% CI, 1.04–1.31; P = 0.010) and in multivariable analysis (adjusted HR, 1.20 per 1 mmHg higher; 95% CI, 1.06–1.36; P = 0.005).

Conclusion

Long-term IOP fluctuations do not appear to be significantly associated with the risk of developing glaucoma in untreated ocular hypertensive subjects.

Section snippets

Participants

This observational cohort study included 252 eyes of 126 ocular hypertensive patients who were observed without receiving ocular hypotensive treatment during follow-up. All patients were observed at the Hamilton Glaucoma Center, University of California San Diego as part of an ongoing prospective longitudinal study (Diagnostic Innovations in Glaucoma Study) designed to evaluate optic nerve structure, visual function, and risk factors in glaucoma. Patients in the Diagnostic Innovations in

Results

Demographic and clinical characteristics of the 252 eyes of 126 ocular hypertensive patients included in the study are shown in Table 1. Forty eyes of 31 subjects developed POAG during follow-up. Figure 1 shows the cumulative probability of developing glaucoma in at least one eye during the study. Mean follow-up time until conversion to glaucoma was 82.8 months (median, 70.4; first quartile, 56.9; third quartile, 106.7). Mean follow-up time for nonconverters was 86.3 months (median, 78.9; first

Discussion

In the current study, we investigated the association between long-term IOP fluctuation and mean IOP with risk of developing glaucoma among ocular hypertensive eyes. Although higher mean IOP levels were consistently associated with increased likelihood of developing glaucoma, IOP fluctuation was not associated with the study end points, in both univariable and multivariable models that adjusted for other clinically important variables.

The results of our study agree with those reported with the

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  • Cited by (0)

    Manuscript no. 2007-285.

    Supported in part by an independent research grant from Pfizer, Inc., New York, New York (FAM), and the National Eye Institute, Bethesda, Maryland (grant nos. EY11008 [LMZ], EY08208 [PAS]).

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