Travoprost- and Tafluprost-induced Changes in Intraocular Pressure and Ocular Pulse Amplitude

Purpose: To compare the intraocular pressure reduction and changes in ocular pulse amplitude of travoprost 0.003% and tafluprost 0.0015%. Methods: We assessed patients who were diagnosed with open-angle glaucoma from January 2017 to July 2019 for the first time at our hospital. Forty-two eyes were assigned to the travoprost group (23 patients) and 26 eyes were assigned to the tafluprost group (14 patients). Changes in intraocular pressure were measured by Goldmann applanation tonometry (GAT), and corrected ocular pulse amplitude (cOPA) was measured using dynamic contour tonometry. Changes in these parameters were observed and compared for 1 year. Results: No significant differences were observed between the GAT measurements and the cOPA of patients treated with travoprost and tafluprost for 1 year (p = 0.512, p = 0.105). The change in initial intraocular pressure on GAT observed after 1 week was -5.32 ± 2.63 mmHg for travoprost and -3.79 ± 3.19 mmHg for tafluprost (p = 0.0457). The initial change in cOPA was +0.04 ± 0.9 mmHg in the travoprost group and -0.76 ± 0.97 mmHg in the tafluprost group (p = 0.0028). Conclusions: Travoprost and tafluprost reached the targeted intraocular pressure with no difference in the long-term effects of reduced intraocular pressure. However, travoprost was initially better at lowering intraocular pressure faster, and tafluprost had a greater effect on lowering OPA. Prostaglandin analogs can be selected individually by considering the aforementioned factors.

Changes in ocular pulse amplitude and choroidal thickness in childhood obesity patients with and without insulin resistance

Purpose: To compare choroidal thickness (CT) and ocular pulse amplitude (OPA) in childhood obesity with insulin resistance (IR) and without IR. Methods: Seventy-three childhood obesity and 62 healthy children, who were both age-matched and gender-matched, comprised the study population in this prospective study. Obesity was determined as having a body mass index (BMI) – standard deviation (SD) score that was > 2 SD. Intraocular pressure (IOP) and OPA were measured using a dynamic contour tonometer. The CT measurements were performed using enhanced depth imaging optical coherence tomography at three locations, comprising at the fovea, at a position 500 µm nasal, and also at a position 500 µm temporal to the fovea. Results: Mean BMI value was 28.72 ± 4.85 in the patients with childhood obesity and 21.47 ± 1.14 in the control group. The mean IOP and OPA values were determined 15.90 ± 2.30 and 14.10 ± 2.16 mm Hg, 1.50 ± 0.28 and 1.74 ± 0.32 mm Hg in the patients with childhood obesity and the control group, respectively ( p < 0.001, p < 0.001). The mean subfoveal CT value was 350.50 ± 81.51 μm in the eyes with childhood obesity and 390.02 ± 71.50 μm in those of the control group ( p = 0.003). When the patient groups with and without IR were compared, no significant difference was found between CT, OPA and IOP values ( p > 0.005). Conclusions: Our results showed that both OPA and CT values were significantly decreased in childhood obesity patients. We suggest further studies to verify longitudinal changes in OPA and CT, as also the evaluation of these parameters in other populations.

The Ocular Pulse Decreases Aqueous Humour Outflow Resistance by Stimulating Nitric Oxide Production

Intraocular pressure (IOP) is not static, but rather oscillates by 2-3 mmHg due to cardiac pulsations in ocular blood volume known as the ocular pulse. The ocular pulse induces pulsatile shear stress in Schlemm's canal (SC). We hypothesize that the ocular pulse modulates outflow facility by stimulating shear-induced nitric oxide (NO) production by SC cells. We confirmed that living mice exhibit an ocular pulse with a peak-to-peak (pk-pk) amplitude of 0.5 mmHg under anaesthesia. Using iPerfusion, we measured outflow facility (flow/pressure) during alternating periods of steady or pulsatile IOP in both eyes of 16 cadaveric C57BL/6 mice (13-14 weeks). Eyes were retained in situ, with an applied mean pressure of 8 mmHg and 1.0 mmHg pk-pk pressure amplitude at 10 Hz to mimic the murine heart rate. One eye of each cadaver was perfused with 100 µM L-NAME to inhibit nitric oxide synthase, while the contralateral eye was perfused with vehicle. During the pulsatile period in the vehicle-treated eye, outflow facility increased by 16 [12, 20] % (p<0.001) relative to the facility measured during the preceding and subsequent steady periods. This effect was partly inhibited by L-NAME, where pressure pulsations increased outflow facility by 8% [4, 12] (p < 0.001). Thus, the ocular pulse causes an immediate increase in outflow facility in mice, with roughly one-half of the facility increase attributable to NO production. These studies reveal a dynamic component to outflow function that responds instantly to the ocular pulse and may be important for outflow regulation and IOP homeostasis.

Effect of Changing Heart Rate on the Ocular Pulse and Dynamic Biomechanical Behavior of the Optic Nerve Head

ABSTRACTPurposeTo study the effect of changing heart rate on the ocular pulse and the dynamic biomechanical behaviour of the optic nerve head (ONH) using a comprehensive mathematical model.MethodsIn a finite element model of a healthy eye, a biphasic choroid consisted of a solid phase with connective tissues and a fluid phase with blood, and the lamina cribrosa (LC) was viscoelastic as characterized by a stress-relaxation test. We applied arterial pressures at 18 ocular entry sites (posterior ciliary arteries) and venous pressures at four exit sites (vortex veins). In the model, the heart rate was varied from 60 bpm to 120 bpm (increment: 20 bpm). We assessed the ocular pulse amplitude (OPA), pulse volume, ONH deformations and the dynamic modulus of the LC at different heart rates.ResultsWith an increasing heart rate, the OPA decreased by 0.04 mmHg for every 10 bpm increase in heart rate. The ocular pulse volume decreased linearly by 0.13 µL for every 10 bpm increase in heart rate. The storage modulus and the loss modulus of the LC increased by 0.014 MPa and 0.04 MPa, respectively, for every 10 bpm increase in heart rate.conclusionsIn our model, the OPA, pulse volume, and ONH deformations decreased with an increasing heart rate, while the LC became stiffer. The effects of blood pressure / heart rate changes on ONH stiffening may be of interest for glaucoma pathology.SupportSingapore Ministry of Education, Academic Research Fund, Tier 2 (R-397-000-280-112).Commercial relationshipNone