Research Article
No Evidence for Retinal Damage Evolving from Reduced Retinal
Blood Flow in Carotid Artery Disease
Henning Heßler,
1
Hanna Zimmermann,
1
Timm Oberwahrenbrock,
1
Ella Maria Kadas,
1
Janine Mikolajczak,
1
Alexander U. Brandt,
1
Andreas Kauert,
2
Friedemann Paul,
1,3
and Stephan J. Schreiber
3
1
NeuroCure Clinical Research Center, Charit´ e-Universit¨ atsmedizin Berlin, 10117 Berlin, Germany
2
Department of Neurology, K¨ onigin-Elisabeth-Herzberge Hospital, 10365 Berlin, Germany
3
Department of Neurology, Charit´ e-Universit¨ atsmedizin Berlin, 10117 Berlin, Germany
Correspondence should be addressed to Henning Heßler; henning.hessler@charite.de
Received 22 May 2015; Revised 24 June 2015; Accepted 25 June 2015
Academic Editor: Goji Tomita
Copyright © 2015 Henning Heßler et al. Tis is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Introduction. Carotid artery disease (CAD) comprising high-grade internal carotid artery stenosis (CAS) or carotid artery occlusion
(CAO) may lead to ipsilateral impaired cerebral blood fow and reduced retinal blood supply. Objective. To examine the infuence of
chronic CAD on retinal blood fow, retinal morphology, and visual function. Methods. Patients with unilateral CAS ≥ 50% (ECST
criteria) or CAO were grouped according to the grade of the stenosis and to the fow direction of the ophthalmic artery (OA).
Retinal perfusion was measured by transorbital duplex ultrasound, assessing central retinal artery (CRA) blood fow velocities.
In addition, optic nerve and optic nerve sheath diameter were measured. Optical coherence tomography (OCT) was performed
to study retinal morphology. Visual function was assessed using high- and low-contrast visual paradigms. Results. Twenty-seven
patients were enrolled. Eyes with CAS ≥ 80%/CAO and retrograde OA blood fow showed a signifcant reduction in CRA peak
systolic velocity (no-CAD side: 0.130 ± 0.035 m/s, CAS/CAO side: 0.098 ± 0.028; = 0.005; = 12). OCT, optic nerve thicknesses,
and visual functional parameters did not show a signifcant diference. Conclusion. Despite assessable hemodynamic efects, chronic
high-grade CAD does not lead to gaugeable morphological or functional changes of the retina.
1. Introduction
Carotid artery disease (CAD) comprising high-grade carotid
artery stenosis (CAS) or carotid artery occlusion (CAO) of
the internal carotid artery (ICA) was shown to be associated
with restricted ocular blood fow as measured by Doppler
sonography [1–5]. Te higher the grade of CAS, the more
relevant the impairment of the retinal blood fow, especially
if the ophthalmic artery (OA) shows a retrograde blood fow
[6]. A common carotid artery occlusion (CCA-O) impedes
the blood fow of the ipsilateral internal and external carotid
artery (ECA) and is another risk factor for limited orbital
perfusion [7, 8]. Ocular manifestations of CAD are a common
fnding, for instance, occurring as amaurosis fugax caused by
acute embolic central retinal artery occlusion or as a chronic
retinal ischemia in the form of ocular ischemic syndrome
(OIS). Retinal examination in CAD patients is generally
performed in direct time relation to the occurrence of clinical
symptoms like sudden or progressive visual loss. However,
it remains unclear whether subclinical retinal abnormalities
or visual impairment occurs. Ultrasound allows reliable
dynamic assessment of orbital blood fow, measured as
central retinal artery (CRA) fow velocity. It can also be used
for structural analysis of optic nerve sheath diameter (ONSD)
and is a proven diagnostic tool to evaluate papilledema in
intracranial pressure with comparable results to MRI exam-
inations [9]. Optical coherence tomography (OCT) allows
reliable quantifcation of retinal layers and is able to detect
retinal axonal and neuronal loss even in the absence of clinical
visual symptoms in multiple sclerosis and other CNS diseases
[10–12]. In this pilot study, we analyze the efects of CAD-
induced chronic reduced retinal blood fow on optic nerve
thickness and retinal morphology and function.
Hindawi Publishing Corporation
BioMed Research International
Volume 2015, Article ID 604028, 8 pages
http://dx.doi.org/10.1155/2015/604028