Purpose. To study the involvement of vascular and vegetative factors in the pathogenesis of glaucoma attack. Material and methods. 12 patients (24 eyes) aged 49 to 82 — 5 men and 7 women, including 3 patients with acute glaucoma and 9 patients with subacute glaucoma were subjected to an ophthalmological examination that included visometry, tonometry, automated static perimetry, OCT and OCT angiography. They were also tested for heart rate variability (HRV) using a Polar heart rate monitor, and for plasminogen content and products of fibrin/fibrinogen degradation in the tear. For comparison, the contralateral eyes of these patients were examined. Results. In the eyes with an acute glaucoma attack, the vascular network was noticeably weakened, especially in the area of the deep peripapillary vascular plexus at the lamina cribrosa level, and focal capillary loss was observed. The peripapillary density of the deep vascular plexus in the eyes with an acute attack was 33.0 ± 5.6 % (М ± m), which was significantly (p < 0.01) lower as compared to 50.0 ± 4.7 % in the unaffected eyes. This indicator correlated with the thickness of the ganglion cell complex (GCC) (p < 0.01). In unaffected eyes, no correlations were found between these glaucoma-related parameters. A significant amount of fibrin/fibrinogen degradation products was found in the tear of glaucoma patients, which may point to a violation of blood circulation in the optic nerve vessels. It has been established that glaucoma attack occurs with increased activity of sympathetic regulation of blood flow. Conclusion. When monitoring this contingent of patients, it is essential to determine the sympathetic-parasympathetic status of the patient. Taking into account the vascular component of the condition, it is expedient to introduce the necessary additions into its treatment plans
Acute Glaucoma cured by Escrine
