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Editors Selection IGR 10-4

Clinical forms of glaucoma: Flow mediated vasodilatation in NTG

Comment by Selim Orgül on:

14051 Abnormal flow-mediated vasodilation in normal-tension glaucoma using a noninvasive determination for peripheral endothelial dysfunction, Su WW; Cheng ST; Hsu TS et al., Investigative Ophthalmology and Visual Science, 2006; 47: 3390-3394

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While the unique generally accept mean for glaucoma treatment is restricted to the lowering of intraocular pressure, ophthalmologists are still confronted with many patients who continue to deteriorate despite proper implementation of this concept. Although formal prove may not be there yet, there is a large consensus that blood flow alteration has a bearing on the faith of glaucomatous eyes. In this regard, many questions remain without good answers, including the characteristics of blood flow alteration in these patients, the aetiology of the harming pathway, the mechanisms preventing such changes from leading to a local damage, and the therapeutic options. One option for the pathway leading to altered blood flow response in various conditions could be the endothelial dysregulation.

In a case control study Su et al. (787) investigated this possibility by using a non-invasive method: endothelium-dependent flow-mediated vasodilation (FMD). Applying high-resolution vascular ultrasound technology, brachial artery responses to reactive hyperaemia (with increased flow causing endothelium dependent dilation) and to sublingual nitroglycerine (causing endothelium-independent dilation), can be assessed and has been widely used in investigations of systemic vascular diseases. FMD does not only decrease with aging, but even further in diseases such as systemic hypertension, diabetes mellitus, carotid artery disease, just to cite a few. Comparing the results in 40 normal tension glaucoma patients, the authors found a decreased flow mediated dilatory response, a result agreeing with earlier findings published by the group of Colm O'Brien. Similar approaches

Normal tension glaucoma patients have a decreased flow mediated dilatory response

in other diseases have shown, that such an altered response is correlated with increased intima thickness of the carotid artery, suggesting a link to arteriosclerotic vascular diseases. However, larger studies have called into question whether arteriosclerosis is really relevant in glaucoma and the question remains whether the vascular alterations seen in glaucoma patients would not be of a completely different nature. Consequently, the findings of the authors may raise hope that therapeutic options could arise since certain drugs, such as calcium channel blockers which have also been discussed in the treatment of glaucoma can improve FMD.

Some caution is, however, warranted when considering the applicability of the published results to daily practice. Indeed, the authors selected for good reasons only completely healthy glaucoma patients which, at least in our hospital, are rather rare. At younger age, some patients may indeed not have developed sizeable harm to other organs and systems and the age group of the presented sample of patients may well fit into such a group. However, these patients will relatively often have some signs of vascular dysregulation such as migraine or altered thermoregulation of the hands and feet. This characteristic seems not to be present in the population analysed in this study. Finally, normal tension glaucoma patients seem to be more often of the female gender, but here, the majority of the patients are male subjects. This may be explained by the fact, that subjects with a history of migraine and vascular dysregulation have been excluded. Consequently the presented population of normal tension glaucoma patients seems to be rather of an unusual type and the applicability of the findings may accordingly be relatively restricted. The question why at this stage altered systemic FMD does not affect any organ besides the eye remains also unclear (although the high concentration of mitochondria in the optic nerve head may render the latter more sensitive to ischemia/reperfusion damage) and one may be tempted to suggest an approach involving an ocular flow mediated vasodilation. A possibility would be to apply a suction cup and measure the vascular response of the retinal vasculature of the transient ischemia with the Retinal Vessel Analyzer, but this may not be without risk in glaucoma patients, especially considering the fact that this group of patients shows a higher propensity to develop retinal venous occlusion.

The therapeutical options which may ensue from this study have been addressed in earlier publications with inconsistent findings and still remain controversial. Furthermore, the rather unusual type of glaucoma patients recruited here for good reasons, i.e. not to impede the measured parameter, also restricts the applicability to patients seen in daily practice.

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