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This paper explores the role of autonomic dysfunction in primary open-angle glaucoma (POAG, n = 18), normal tension glaucoma (NTG, n = 19) and 36 age-matched controls. The exact IOP profile of the glaucoma patients was not provided. All patients fasted overnight and the following morning they underwent continuous electrocardiogram and measures of finger blood pressure while lying down. These measures were repeated after five minutes of passive standing. Subsequently, they consumed a 600 kilocalorie, carbohydrate-rich meal. This was followed by repeat physiological measures in both the supine and standing position at 30-minute intervals over a two-hour period. In this experimental paradigm, the effect of two perturbations are assessed: passive positional change and a vasovagal response whereby a meal induces a shift in blood flow to the gut.
A major concern is that a myriad of derived outcomes are generated and numerous comparisons between these outcomes are made. While the authors recognize this issue, I do not believe they fully correct for the multiple comparison problem that this work presentsIn addition to heart rate and blood pressure, the investigators derive the spectral power of the variability of these parameters at low frequency and high frequency bands to assess the intrinsic sympathovagal function of the heart. A major concern is that a myriad of derived outcomes are generated and numerous comparisons between these outcomes are made. While the authors recognize this issue, I do not believe they fully correct for the multiple comparison problem that this work presents. With that said, I would highlight the following outcome. Thirty minutes after the meal, the mean arterial pressure decreased in POAG versus control subjects by approximately ten mmHg both in the supine and standing position. This did not happen in the NTG group. The authors suggest this postprandial hypotensive response represents a form of autonomic failure after an essential normal activity that might de-stabilize ocular perfusion and contribute to optic nerve degeneration in POAG. The subject of dynamic autonomic function in POAG most certainly deserves further study.
The authors suggest this postprandial hypotensive response represents a form of autonomic failure after an essential normal activity that might de-stabilize ocular perfusion and contribute to optic nerve degeneration in POAG