Evaluation of Outflow Structures In Vivo after the Phacocanaloplasty.

Purpose. To evaluate the in vivo changes in Schlemm's canal (SC) and the trabecular meshwork (TM) in patients with primary open-angle glaucoma (POAG) after phacocanaloplasty using anterior segment optical coherence tomography (AS-OCT). Methods. Ten eyes of nine patients with POAG (6 men and 3 women) who underwent phacocanaloplasty. Preoperative and postoperative visual acuity (VA), intraocular pressure (IOP), and use of glaucoma medications were evaluated. The main outcome measures were the area of SC and TM thickness assessed using AS-OCT before and 12 months after surgery. Results. We found statistically significant reduction in IOP (from 26.4 (8.6) mmHg to 12.9 (2.5) (p < 0.05) mmHg), increase in VA from 0.7 (0.4) to 0.9 (0.2), and decrease in glaucoma medication from 2.6 (1.2) to 1.1 (1.3) at 12 months postoperatively. There was a significant increase in the SC area (3081.7 (842.8) µm(2) versus 5098.8 (1190.5) µm(2), p < 0.001) and a decrease in mean TM thickness (91.2 (18.6) µm versus 81.3 (15.1) µm, p = 0.001) after surgery. We found negative correlations between SC area and IOP before surgery (r = -0.67, p = 0.03) and also between SC area before and IOP reduction 12 months after the phacocanaloplasty (r = -0.80, p = 0.005). Conclusions. Our results showed statistically significant dilation of SC area and reduction of TM thickness after phacocanaloplasty in POAG patients. The degree of SC expansion was related to the IOP decrease.

New insights into pathophysiological mechanisms regulating conventional aqueous humor outflow.

The aim of the article was to overview the pathophysiology of the conventional outflow pathway, trabecular meshwork, and intraocular pressure and to discuss the options of future glaucoma treatment directed to improvement in aqueous outflow. The literature search in the Medline, Embase, and Cochrane databases from April to May 2012 was performed; a total of 47 articles analyzed. The diminished conventional pathway may be altered by several pathophysiological mechanisms like TM obstruction caused by transforming growth factor-ß2, clastic nondeformable cells, macrophages leaking from hypermature cataract, iris pigment, lens capsular fragments after YAG-laser posterior capsulotomy, proteins and their subfragments. It is known that trabecular meshwork contraction reduces outflow, and the actomyosin system is directly linked to this mechanism. New glaucoma drugs are still under investigation, but it is already proven that agents such as latranculin-B are effective in improving aqueous drainage. Selective Rho-associated coiled coilforming protein kinase inhibitors have been shown to cause a significant improvement in outflow facility and may become a new option for glaucoma treatment. Caldesmon negatively regulates actin-myosin interactions and thus increases outflow. Stem cells may replace missing or nonfunctional trabecular meshwork cells and hopefully will bring a new treatment solution. Pathophysiological mechanisms regulating conventional aqueous humor outflow are still not fully understood and require further investigations. Future treatment decisions should be directed to a specific mechanism regulating an elevation in intraocular pressure.

Comparison of intraocular pressure, blood pressure, ocular perfusion pressure and blood flow fluctuations during dorzolamide versus timolol add-on therapy in prostaglandin analogue treated glaucoma subjects.

OBJECTIVE: To compare the effects of dorzolamide and timolol add-on therapy in open-angle glaucoma (OAG) patients previously treated with prostaglandin analogue (Pg), by evaluating fluctuations in the intraocular (IOP), blood (BP), ocular perfusion pressures (OPP) and retrobulbar blood flow (RBF) parameters. METHODS: 35 OAG patients (35 eyes), 31 women (88.6%) age 63.3 (8.9) years were evaluated in a 3 month randomized, cross-over, single-masked study. During the experiments BP, heart rate, IOP and OPP were assessed 4 times per day (8-12-16-20 h). RBF was measured twice per day (8-20 h) using Color Doppler imaging in the ophthalmic (OA), central retinal (CRA), nasal (nSPCA) and temporal (tSPCA) posterior ciliary arteries. In each vessel, peak systolic velocity (PSV) and end-diastolic velocity (EDV) were assessed and vascular resistance (RI) calculated. RESULTS: Both add-on therapies lowered IOP in a statistically significant manner from 15.7 ± 2.4 mmHg at latanoprost baseline to 14.9 ± 2.2 mmHg using dorzolamide (p < 0.001) and 14.2 ± 1.9 mmHg using timolol (p < 0.001). The IOP lowering effect was statistically significant at 20 h, favoring timolol as compared to dorzolamide (1.4 ± 2.4 vs. 0.2 ± 2.1 mmHg), (p < 0.05). Dorzolamide add-on therapy showed smaller IOP (2.0 ± 1.4), SPP (13.3 ± 7.9), systolic BP (13.5 ± 8.7) and diastolic BP (8.4 ± 5.4) fluctuations as compared to both latanoprost baseline or timolol add-on therapies. Higher difference between morning and evening BP was correlated to decreased evening CRA EDV in the timolol group (c = -0.41; p = 0.01). With increased MAP in the morning or evening hours, we found increased evening OA RI in timolol add-on group (c = 0.400, p = 0.02; c = 0.513, p = 0.002 accordingly). Higher MAP fluctuations were related to impaired RBF parameters during evening hours-decreased CRA EDV (c = -0.408; p = 0.01), increased CRA RI (c = 0.576; p < 0.001) and tSPCA RI (c = 0.356; p = 0.04) in the dorzolamide group and increased nSPCA RI (c = 0.351; p = 0.04) in the timolol add-on group. OPP fluctuations correlated with increased nSPCA RI (c = 0.453; p = 0.006) in the timolol group. OPP fluctuations were not related to IOP fluctuations in both add-on therapies (p < 0.05). CONCLUSIONS: Both dorzolamide and timolol add-on therapies lowered IOP in a statistically significant fashion dorzolamide add-on therapy showed lower fluctuations in IOP, SPP and BP. Higher variability of daytime OPP led to impaired RBF parameters in the evening.