Ocular findings in patients with carotid stenosis undergoing carotid endarterectomy

Purpose: To assess the partly unknown ocular findings in carotid stenosis (CS) patients and the effect of carotid endarterectomy (CEA) on these findings, we studied CS patients before and 6 months after CEA, in comparison to healthy non-medicated controls. Methods: A total of 70 CS patients (mean 68 years, 81% male), and 41 controls (69, 76%) entered our prospective non-randomized clinical trial; 49 (70%) had cerebrovascular symptoms, most commonly transient monocular blindness— ocular TIA or amaurosis fugax— in 28 patients (57%) and hemispheric TIA in 17 (35%). After our anterior and posterior bio-microscopical examination with fundus photographs, we graded retinal microvascular abnormalities objectively and evaluated central retinal arterial and venular equivalent (CRAE and CRVE) semiautomatically. Dynamic Vessel Analyzer served to assess flicker-induced vascular reactions, and optical coherence tomography to measure subfoveal choroidal thickness (SFCT). Results: We found ocular signs of CS in 17 patients (24%, 95% CI 16-36), of whom, 4 (6%) had embolic Hollenhorst plaques and 13 (19%), hypoperfusion-related signs. The latter included ocular ischemic syndrome (OIS) with typical mid-peripheral hemorrhages requiring ocular treatment in 4 (6%), mild OIS in 6 (9%), and de novo findings in 3 (4%). One patient had an irreversible neovascular glaucoma with poor visual acuity, one had reversible iris neovascularization, and one developed ocular hyperperfusion with macular edema one week after CEA. Among microvascular abnormalities, the patients showed more severe grades in arteriolar and venular tortuosity in the macula than did the controls at baseline. CRAE was similar in laterality and in patients compared to controls. At baseline, we detected higher CRVE in the patients´ ipsilateral eye. Ipsilateral arteriolar and venular flicker-induced dilation appeared lower in patients than in controls at baseline. After CEA, ipsilateral venular dilation increased, and a trend toward the same was evident in arteriolar dilation. SFCT was lower in patients than in controls, with no difference in laterality. Symptomatic patients showed lower CRAE before CEA than did their counterparts. Patients with ipsilateral ocular signs of CS showed lower SFCT than those without these signs. Conclusions: In addition to midperipheral hemorrhages, emboli, and visual disturbances, potential ocular biomarkers of CS include dilated venules, higher grades in vessel tortuosity in the macula, reduced flicker-induced dilatations, and low SFCT. Ocular signs of CS should be detected before irreversible changes occur. Those patients with reduced visual acuity or ocular pain or both before or after CEA need prompt ophthalmological examination. Symptoms seem to relate to thinner arterioles and ocular signs of CS to thinner choroid. CEA seems to influence the retinal blood flow in a positive way.