Retinal hemodynamics using scanning laser ophthalmoscopy and hemorheology in chronic open-angle glaucoma.
OBJECTIVE
Recent studies suggest that elevated intraocular pressure is not the only causative factor for the development of visual field loss and optic nerve damage in glaucomatous eyes. The authors determine whether retinal hemodynamics or blood fluidity are alternated in eyes of patients with open-angle glaucoma compared with those of age- and sex-matched healthy subjects.


METHODS
High-quality video fluorescein angiograms were obtained from single eyes of 51 patients with chronic open-angle glaucoma. From these angiograms, the arm-retina time, mean dye velocity, and arteriovenous passage time were quantified. The data from patients were compared with those of an age- and sex-matched group of healthy subjects.


RESULTS
In patients with chronic open-angle glaucoma, an 11% reduction of the mean dye velocity (P < 0.05) and a 41% prolongation of the arteriovenous passage time (P < 0.01) was observed relative to the values obtained among the control subjects. Among hematocrit values, plasma viscosity, and erythrocyte aggregation, only plasma viscosity showed a significant increase (4%; P < 0.01) in patients with chronic open-angle glaucoma.


CONCLUSIONS
These results indicate that a pronounced circulatory deficit exists within the retinal vasculature of glaucomatous eyes, which may coexist with, but cannot be fully attributed to, an increase in plasma viscosity.
Wolf
S
S
Augenklinik der Medizinische Fakultät, Rheinisch-Westfälischen Technischen Hochschule Aachen, Germany.
Arend
O
O
Sponsel
W E
WE
Schulte
K
K
Cantor
L B
LB
Reim
M
M
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002908:Chronic Disease; D005260:Female; D005451:Fluorescein Angiography; D005654:Fundus Oculi; D005902:Glaucoma, Open-Angle / Q000503:physiopathology* / Q000628:therapy; D006439:Hemodynamics; D018056:Hemorheology; D006801:Humans; D007834:Lasers; D008297:Male; D008875:Middle Aged; D009887:Ophthalmoscopy; D012171:Retinal Vessels / Q000503:physiopathology*