title: [Ischemic or non-ischemic central artery occlusion. An explanation for the development or lack of development of neovascularization].
abstract: In a retrospective study we analyzed 29 central retinal artery occlusions (CRAO) with reference to the findings of ophthalmodynamometry (ODM) and fluorescein angiograms (FLA). We tried to find explanations for the relatively low rate of neovascularization in CRAO and predictive constellations for CRAO that will develop neovascularization. In 5 eyes the pathologic findings were classed as ischemic ophthalmopathy because of carotid or ophthalmic artery stenosis: 2 of these 5 eyes showed iris neovascularization (rubeosis iridis), while the other 3 "only" showed a CRAO with no clinical signs of ischemic ophthalmopathy. Of the remaining 24 eyes with CRAO there were 2 eyes with rubeosis iridis, which could be attributed to the CRAO itself (8.3%). FLA revealed ischemic perfusion of the retina in these 2 cases. ODM revealed reperfusion of the central artery (CRA) in 17 of 25 eyes with CRAO (71%) within the first 2 weeks. In 2 blind eyes that were re-examined 3 and 5 months after CRAO no iris or retinal neovascularization was found despite persisting malperfusion of CRA. In these 2 cases the minimal retinal perfusion needed because of complete retinal necrosis was sufficient explanation for the nonevolution of neovascularization. If ischemia is the essential condition for neovascularization, we can propose two explanations for non-development of neovascularization after CRAO: either there is adequate recanalization (majority of cases) or the need for perfusion is minimal or zero. Only in cases of persisting malperfusion and partially surviving retinal tissue (function!) will neovascularization perhaps develop. ODM is an adequate method of estimating the perfusion of CRA.
authors.affiliation: Universitäts-Augenklinik Bochum.
authors.forename: R
authors.initials: R
authors.lastname: Meyer-Schwickerath
authors.forename: A
authors.initials: A
authors.lastname: Hagel
authors.forename: D
authors.initials: D
authors.lastname: Nahberger
authors.forename: U
authors.initials: U
authors.lastname: Gronemeyer
mesh_terms: D001783:Blood Flow Velocity / Q000502:physiology; D002343:Carotid Artery, Internal / Q000473:pathology; D016893:Carotid Stenosis / Q000175:diagnosis / Q000473:pathology; D005451:Fluorescein Angiography; D006801:Humans; D007429:Intraocular Pressure / Q000502:physiology; D007498:Iris / Q000098:blood supply; D009389:Neovascularization, Pathologic / Q000175:diagnosis / Q000473:pathology; D009884:Ophthalmodynamometry; D012161:Retinal Artery / Q000473:pathology; D015356:Retinal Artery Occlusion / Q000175:diagnosis* / Q000473:pathology; D015861:Retinal Neovascularization / Q000175:diagnosis* / Q000473:pathology; D012189:Retrospective Studies