Stenting may help treat previously inoperable lesions

Common findings in ocular ischemic syndrome are rubeosis, peripheral retinal hemorrhages, and venous dilation without tortuosity. The syndrome is usually secondary to atherosclerotic coronary artery stenosis of greater than 90%, which results in a reduction of the ipsilateral perfusion pressure of about 50%, Dr. Marx said. He is clinical assistant professor of ophthalmology, Tufts University School of Medicine, and vice chairman and director of vitreoretinal surgery, department of ophthalmology, Lahey Clinic, Burlington, MA.

Fluorescein angiography findings common to ocular ischemic syndrome are delayed and patchy choroidal filling with prolonged arterial venous time.

The treatments available for ocular ischemic syndrome include panretinal photocoagulation for proliferative disease, carotid endarterectomy for lesions below the second cervical vertebra when stenosis is less than 100%, and angioplasty and stenting for lesions above the second cervical vertebra.

To date, only one reported case of ocular ischemic syndrome has been treated with stenting for a lesion in the cervical carotid artery, but no cases of stenting to treat ocular ischemic syndrome in the intracranial circulation have been reported.

Dr. Marx and colleagues conducted a retrospective chart review in which three patients were treated with percutaneous carotid artery stenting for ocular ischemic syndrome. All patients underwent fluorescein angiography and a full carotid artery evaluation by a neurologist; two interventional neuroradiologists then performed carotid angioplasty and stenting.

"All patients had a significant improvement in intracerebral perfusion," Dr. Marx said. "Patient 1, who had a precavernous carotid artery lesion, had improved fluorescein angiographic filling and antegrade flow through his ophthalmic artery, which is a correction from the retrograde flow observed before the stenting procedure. Patient 2, who had a cavernous lesion, had improved fluorescein angiographic filling and the flow in the ophthalmic artery remained retrograde. We speculate that the improved fluorescein angiographic filling is related to improved collateral flow.

"Patient 3 had a duplex lesion in the cervical and precavernous artery, with no change in the fluorescein angiographic filling and the flow remained retrograde," Dr. Marx said. "There was markedly improved intracerebral perfusion."

The clinical course of Patient 2 underscores the value of imaging. Patient 2 was a 71-year-old male with bilateral nonproliferative diabetic retinopathy, in whom there had been no progression over 2.5 years. The patient had decreased vision in the left eye with clinically significant macular edema 2.5 years after initial presentation. On fluorescein angiography, there was mildly delayed arterial filling with normal venous fill. The patient underwent photocoagulation for this macular edema.

He returned in 6 months with persistent macular edema, and there was markedly delayed arterial venous filling and delayed and patchy choroidal filling on fluorescein angiography. Carotid ultrasound did not reveal any abnormality on the left side and there was 50% to 75% stenosis on the right side.

After additional laser treatment, a similar delay in arterial venous transit time was found 6 months later along with persistent macular edema. Transcranial Doppler imaging showed reversal of flow in the ophthalmic artery, and cerebral angiography showed a 90% stenosis in the cavernous carotid. After angioplasty and stenting were performed, there was marked improvement in the cerebral perfusion and no change in the ophthalmic flow. However, fluorescein angiography showed marked improvement in the arterial venous time, which has persisted over the last year. The patient's vision has improved by one line and the macular edema has resolved.

Diabetic complications Dr. Marx noted that diabetic complications can include either microangiopathy or macroangiopathy.