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July 1994

Color Doppler Hemodynamics of Giant Cell Arteritis

Author Affiliations

From the Vascular Studies Laboratory and Neuro-ophthalmology Service (Drs Ho, Sergott, Savino, and Bosley) and Retina Service (Dr Regillo), Wills Eye Hospital, Philadelphia, Pa; the Retinal Service, Manhattan Eye, Ear, and Throat Hospital, New York, NY (Dr Ho); the Department of Ophthalmology, Klinikum der Johannes Gutenberg-Universität, Mainz, Germany (Dr Lieb); and Eye Centers of Florida, Fort Myers (Dr Flaharty). Dr Ho is now with the Scheie Eye Institute, University of Pennsylvania, Philadelphia. The authors have no proprietary interest in the development or marketing of any device or material described.

Arch Ophthalmol. 1994;112(7):938-945. doi:10.1001/archopht.1994.01090190086026

Objectives:  To determine quantitative and qualitative hemodynamic alterations within the ophthalmic, central retinal, and short posterior ciliary arteries in patients with giant cell arteritis (GCA) proved by biopsy specimen.

Design, Patients, and Setting:  A consecutive case series of patients with GCA referred to an urban eye hospital who were evaluated with color Doppler imaging that was used to analyze orbital blood flow velocities and vascular resistance in 22 consecutive patients with GCA compared with age and sex-matched controls.

Results:  Patients with GCA all demonstrated significantly reduced central retinal and short posterior ciliary arterial mean flow velocities as well as significantly increased vascular resistance compared with matched controls. Ophthalmic artery mean flow velocity demonstrated marked variation depending on the anatomic location studied. Other color Doppler imaging characteristics of GCA included the following: ophthalmic artery aliasing (high velocity and turbulent flow at presumed focal vasculitic stenoses), reversal of flow within the ophthalmic artery, reduced and truncated timevelocity waveforms of the central retinal and short posterior ciliary arteries, and absolute deficits of flow within the central retinal and short posterior ciliary arteries. Aliasing of flow velocity within the ophthalmic artery (two patients) was associated with clinical progression of GCA.

Conclusions:  These data support the concept that quantitative and qualitative alterations in blood flow are pathophysiologic mechanisms of visual loss in GCA. This technique may be useful in the diagnosis and management of GCA since some of the color Doppler waveforms observed in GCA have not been seen in nonarteritic optic neuropathy. Treatment with corticosteroids often appears to stop the progression of these hemodynamic abnormalities but generally does not improve preexisting vascular abnormalities.

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