advertisement
Impaired ocular blood flow has long been implicated in the pathogenesis of glaucoma, and enhancement of ocular perfusion is an attractive potential treatment target. Ocular pulse amplitude (OPA), which is calculated as the difference between systolic and diastolic IOP, has been suggested as a possible, easily measured, marker for ocular perfusion. Using OPA, Park et al. performed a study to compare the effects of tafluprost and latanoprost on ocular perfusion.
The study population consisted of 27 normal-tension glaucoma (NTG) and 14 primary openangle glaucoma (POAG) patients divided into two groups: one treated with tafluprost, and the other treated with latanoprost. OPA was measured using the dynamic contour tonometer (DCT) and IOP measured using Goldmann applanation tonometry. Baseline IOP was 17.1 ± 3.8 mmHg in the taftuprost group, and 17.5 ± 2.9 mmHg in the latanoprost group. Baseline OPA measured by DCT was 2.3 ± 0.6 mmHg in the taftuprost group and 2.6 ± 0.4 mmHg in the latanoprost group. After three months of treatment, the mean decrease in IOP from baseline was 4.1 mmHg in the taftuprost group compared with 2.1 mmHg in the latanoprost group. Although there was a significant difference between the two groups in mean OPA at one week and three months, there was no significant difference in the reduction of OPA from baseline (P = 0.17).
Reduction of OPA may be an indication of improved ocular blood flow. However, contrary to the conclusion in this study, the results in this study were largely inconclusive with no clear difference between tafluprost and latanoprost. A significant difference between the two groups in mean OPA was only found at some time points, and no significant difference in OPA reduction from baseline detected. Even if OPA were clearly different between the two groups, extrapolation to a difference in ocular blood flow would be difficult since it is not a specific marker for ocular perfusion. OPA is strongly influenced by IOP, and in this study, the tafluprost group had a greater IOP lowering effect than the latanoprost group. The authors also calculated a corrected OPA, which supposedly compensates for the effect of IOP, but it is not clear how this model was validated. As well, OPA is strongly influenced by ocular rigidity (which itself is strongly affected by IOP).1 Ocular rigidity was not assessed in this study, and a difference between the two groups may result in a difference in OPA.
Despite these limitations, the results are interesting and warrant further investigation using more objective methods for assessing ocular perfusion. If a therapy were identified as having a superior beneficial effect on ocular blood flow, it may be particularly useful for NTG patients, in whom impaired ocular blood flow may be especially important.