Ocular pulse amplitude and Doppler waveform analysis in glaucoma patients.
OBJECTIVE
To determine the correlation between ocular blood flow velocities and ocular pulse amplitude (OPA) in glaucoma patients using colour Doppler imaging (CDI) waveform analysis.


METHODS
A prospective, observer-masked, case-control study was performed. OPA and blood flow variables from central retinal artery and vein (CRA, CRV), nasal and temporal short posterior ciliary arteries (NPCA, TPCA) and ophthalmic artery (OA) were obtained through dynamic contour tonometry and CDI, respectively. Univariate and multiple regression analyses were performed to explore the correlations between OPA and retrobulbar CDI waveform and systemic cardiovascular parameters (blood pressure, blood pressure amplitude, mean ocular perfusion pressure and peripheral pulse).


RESULTS
One hundred and ninety-two patients were included [healthy controls: 55; primary open-angle glaucoma (POAG): 74; normal-tension glaucoma (NTG): 63]. OPA was statistically different between groups (Healthy: 3.17 ± 1.2 mmHg; NTG: 2.58 ± 1.2 mmHg; POAG: 2.60 ± 1.1 mmHg; p < 0.01), but not between the glaucoma groups (p = 0.60). Multiple regression models to explain OPA variance were made for each cohort (healthy: p < 0.001, r = 0.605; NTG: p = 0.003, r = 0.372; POAG: p < 0.001, r = 0.412). OPA was independently associated with retrobulbar CDI parameters in the healthy subjects and POAG patients (healthy CRV resistance index: β = 3.37, CI: 0.16-6.59; healthy NPCA mean systolic/diastolic velocity ratio: β = 1.34, CI: 0.52-2.15; POAG TPCA mean systolic velocity: β = 0.14, CI 0.05-0.23). OPA in the NTG group was associated with diastolic blood pressure and pulse rate (β = -0.04, CI: -0.06 to -0.01; β = -0.04, CI: -0.06 to -0.001, respectively).


CONCLUSIONS
Vascular-related models provide a better explanation to OPA variance in healthy individuals than in glaucoma patients. The variables that influence OPA seem to be different in healthy, POAG and NTG patients.
Department of Ophthalmology, Centro Hospitalar Lisboa Central, Lisbon, Portugal; Department of Pharmacology and Neurosciences, Faculty of Medicine, Lisbon University, Lisbon, Portugal.
Luís
L
Abegão Pinto
Evelien
E
Vandewalle
Koen
K
Willekens
Carlos
C
Marques-Neves
Ingeborg
I
Stalmans
D000368:Aged; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000502:physiology; D016022:Case-Control Studies; D019842:Ciliary Arteries / Q000502:physiology*; D005260:Female; D005902:Glaucoma, Open-Angle / Q000503:physiopathology*; D006801:Humans; D007429:Intraocular Pressure / Q000502:physiology; D017078:Laser-Doppler Flowmetry; D057066:Low Tension Glaucoma / Q000503:physiopathology*; D008297:Male; D011446:Prospective Studies; D063177:Pulse Wave Analysis; D012161:Retinal Artery / Q000502:physiology*; D012169:Retinal Vein / Q000502:physiology*; D016037:Single-Blind Method; D014065:Tonometry, Ocular
colour Doppler imaging; normal-tension glaucoma; ocular pulse amplitude; primary open-angle glaucoma; vascular dysregulation