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Editors Selection IGR 11-1
Medical Therapy: Intervisit IOP variation
Comment by Kuldev Singh on:
46468 Intraocular pressure: Modulation as treatment for glaucoma, Caprioli J; Varma R, American Journal of Ophthalmology, 2011; 152: 340-344
Caprioli and Varma (1497) provide their thought-provoking perspectives on the much debated and complex topic of intervisit intraocular pressure (IOP) variation as an independent risk factor for glaucomatous disease. They nicely summarize the disparate results of post-hoc analyses on data sets from large randomized clinical trials including the Advanced Glaucoma Interventions Study, (AGIS) Collaborative Initial Glaucoma Treatment Study, (CIGTS) Early Manifest Glaucoma Trial, (EMGT) European Glaucoma Prevention Study (EGPS) and the Diagnostic Innovations in Glaucoma Study (DIGS). They correctly point out that these studies differ with regard to patient populations including IOP levels, and propose that the impact of IOP variation may be dependent upon the mean level of IOP with a greater impact of variation when the mean is low versus when it is high.
Continuous 24 hour IOP monitoring in the clinical and research settings will go a long way towards determining whether the postulated impact of long-term IOP variation on the lamina cribrosa and other proposed pathophysiologic mechanisms hypothesized to result from such variation are confirmed or refuted
This review nicely complements a recent editorial in the August, 2011 issue of Archives of Ophthalmology entitled 'Intraocular Pressure Variability and Glaucoma Risk: Complex and Controversial.' In the absence of a continuous 24-hour IOP monitoring device, glaucoma investigators have sometimes relied on long-term IOP variability as a partial surrogate for risk related to short-term IOP fluctuation over 24 hours. Most glaucoma trials referenced above have measured IOP at several month intervals with the interval being six months, for example, in the Advanced Glaucoma Intervention Study. While longterm variability in such studies may partially reflect short-term fluctuation, an alternate hypothesis is that greater long-term variability largely reflects periods of time when the mean IOP is too high for the patient. Thus a patient's eye with a mean long-term IOP of 12 mmHg over an almost decade-long course of a large clinical trial, with an equal number of months spent at 18 mmHg and 6 mmHg may be more likely to show rapid progression, all other things being equal, than another patient's eye that also has a long-term mean IOP of 12 mmHg with the range always being between 11 and 13 mmHg, due to the former eye having a high mean IOP and thus being inadequately controlled for several years within the follow up period and not necessarily as a result of IOP fluctuation during the follow-up period. One can make a case for long-term IOP variability simply reflecting periods of inadequate mean IOP lowering during which mean IOP is above a threshold such that there is accelerated glaucomatous damage. Continuous 24-hour IOP monitoring in the clinical and research settings will go a long way towards determining whether the postulated impact of long-term IOP variation on the lamina cribrosa and other proposed pathophysiologic mechanisms hypothesized to result from such variation are confirmed or refuted.
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