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Results for “Retinal Neovascularization”

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PubMed2005

Nature and risk of neovascularization in the fellow eye of patients with unilateral retinal angiomatous proliferation.

PURPOSE: To determine the nature and risk of neovascularization in the fellow eyes of patients with unilateral retinal angiomatous proliferation (RAP), a neovascular form of age-related macular degeneration (AMD). METHODS: A consecutive series of 52 patients diagnosed with unilateral RAP were studied retrospectively. Clinical biomicroscopic examination, fluorescein angiography, and indocyanine green angiography were used to evaluate all patients for the development of neovascular manifestations in the fellow eye. RESULTS: Neovascularization developed in the fellow eye in 52 patients over the follow-up period (range, 2-36 months). All patients developed neovascular manifestations of RAP in the fellow eye. Twenty-one patients (40%) developed a RAP lesion within 1 year; 29 (56%), within 2 years; and 52 (100%), within 3 years. At the time of diagnosis of neovascularization in the fellow eye, 8 patients (15%) had a stage I RAP lesion, 36 (70%) had a stage II RAP lesion, and 8 (15%) had a stage III RAP lesion. Other characteristic findings in these patients included the presence of preretinal, intraretinal, and subretinal hemorrhages in 49 patients (94%) and pigment epithelial detachments in 41 patients (79%). CONCLUSIONS: In patients diagnosed with unilateral RAP lesions, the form of neovascularization that develops in the fellow eye is virtually always RAP. The annual and accumulative risk of neovascularization in the fellow eye is higher in patients with RAP than in those with other forms of neovascular AMD. These new findings enhance our understanding of the clinical spectrum of RAP in terms of its natural course and visual prognosis and may possibly offer useful information to establish future treatment options.

Aged↗
PubMed1999

Antioxidant enzymes in the macular retinal pigment epithelium of eyes with neovascular age-related macular degeneration.

PURPOSE: To test the hypothesis that neovascular age-related macular degeneration is related to oxidative stress involving the macular retinal pigment epithelium. This study investigated, as a function of age, levels of enzymes that defend tissues against oxidative stress in the macular retinal pigment epithelium of human eyes with this disease. METHODS: Surgical specimens of macular choroidal neovascular membranes from eyes with age-related macular degeneration and the macular regions of whole donor eyes with neovascular age-related macular degeneration or without evident ocular disease were studied by quantitative electron microscopic immunocytochemistry with colloidal gold-labeled second antibodies. Relative levels in retinal pigment epithelium cell cytoplasm and lysosomes were determined of five enzymes believed to protect cells from oxidative stress, as well as levels of the retinal pigment epithelium marker cytoplasmic retinaldehyde-binding protein, for comparison with the enzymes. RESULTS: Copper, zinc superoxide dismutase immunoreactivity increased and catalase immunoreactivity decreased with age in cytoplasm and lysosomes from macular retinal pigment epithelium cells of normal eyes and eyes with age-related macular degeneration. Cytoplasmic retinaldehyde-binding protein immunoreactivity showed no significant relationship to age or the presence of neovascular age-related macular degeneration. Glutathione peroxidase immunoreactivity was absent from human retinal pigment epithelium cells. Both heme oxygenase-1 and heme oxygenase-2 had highly significantly greater immunoreactivity in retinal pigment epithelium cell lysosomes than in cytoplasm, differing from the much greater cytoplasmic immunoreactivity of the other proteins studied. This immunoreactivity decreased with age, particularly in the lysosomes of retinal pigment epithelium cells from eyes with neovascular age-related macular degeneration. These decreases were of borderline significance (P = .067 for heme oxygenase-1; P = .12 for heme oxygenase-2) when eyes with age-related macular degeneration were compared with normal eyes by multivariable logistic regression. CONCLUSIONS: The high heme oxygenase-1 and heme oxygenase-2 lysosomal antigen levels in macular retinal pigment epithelium cells of eyes with neovascular age-related macular degeneration suggest that oxidative stress causes a pathologic upregulation of these enzymes. Increased lysosomal disposal may indicate that the reparative functions of these enzymes are accompanied by deleterious effects, necessitating their rapid removal from the cell. The much higher heme oxygenase-1 and heme oxygenase-2 antigen levels in macular retinal pigment epithelium cells from younger individuals suggest that protective mechanisms against oxidation and, hence, presumably to the development of age-related macular degeneration, decrease with age.

Adult↗
PubMed2001

[Pre- and postoperative ICGA exploration in neovascular membrane surgery].

INTRODUCTION: We performed a retrospective analysis of the use of indocyanine green angiography (ICGA) pre- and postoperatively in the surgery of neovascular membranes. MATERIALS AND METHODS: 81 membranes with retrofovealar extension visible on fluoresceine angiography were operated by vitrectomy and membrane removal from May 1994 to December 1998. Fifty-three had age-related macular degeneration (ARMD), 13 were due to high myopia, and 16 were complications of various inflammatory pathologies. Preoperative evaluation included ICGA, fluoresceine angiography, scanning laser ophthalmoscopy with the study of fixation by microperimetry, and, in recent cases, ocular coherence tomography. RESULTS: ICGA was a definite help in the indication to operate in all cases of ARMD. For 8 cases of inflammatory pathologies, ICGA identified the neovascular membrane within the inflammatory site. ICGA has definite prognostic value in membranes complicating high myopia. Postoperatively, ICGA confirmed the disappearance of neovascularization in ARMD and in the inflammatory group. CONCLUSIONS: ICGA is indispensable in the preoperative evaluation of choroidal subretinal neovascular membranes. Postoperatively, ICGA can identify relapses.

Adult↗
PubMed1996

[Late vision loss after focal hemorrhagic chorioretinopathy].

Prospective clinical studies about photocoagulation of extrafoveolar choroidal neovascularizations in focal hemorrhagic chorioretinopathy (CR) have demonstrated that the risk of visual loss years after successful treatment is related to the development of retinal pigment epithelium (RPE) atrophy around the laser scar. The reason for this event was thought to be late damage of RPE cells due to the laser treatment. However, because RPE atrophy can also be seen in untreated patients, a prospective study was started to test this pathogenetic hypothesis and to analyze the pathogenetic factors and prognostic importance of RPE atrophy in focal hemorrhagic CR. Eighty-eight patients (52 women, 36 men, 15-45 years old; mean follow-up 62 months; 26 patients treated by photocoagulation) with focal hemorrhagic CR were reexamined. Fifty-two patients (15 treated by photocoagulation and 37 untreated) showed clinically visible RPE atrophy. In these 52 patients the initial and final visual acuity, the amount of initial subretinal fluid (34.6% < 500 microns, 50% 500-750 microns, 15.4% > 750 microns) and the amount RPE atrophy (23.2% < 500 microns, 53.6% 500-750 microns, 23.2% > 750 microns) were analyzed. The development of RPE atrophy was dependent on the time of follow-up (36 patients without RPE atrophy, mean follow-up 29 months; 52 patients with RPE atrophy, mean 84 months, P < 0.001). Of the 52 patients with RPE atrophy, 15 were treated by photocoagulation. The distribution of RPE atrophy was similar to what was found in the 37 untreated patients (P = 0.4). With pronounced RPE atrophy, a decrease in final visual acuity was seen (RPE atrophy < 500 microns, mean visual acuity 0.5; 500-750 microns mean visual acuity 0.3; > 750 microns, mean visual acuity 0.1; P = 0.005). Increased RPE atrophy was also associated with a higher incidence of visual loss (p = 0.009). The amount of RPE atrophy was not dependent on the time of follow-up (P = 0.3), but only correlated with the initial amount of subretinal fluid (atrophy < 500 microns: subretinal fluid < 500 microns 15.4%, 500-750 microns 7.7%, > 750 microns 0%; atrophy 500-750 microns: subretinal fluid < 500 microns 19.2%, 500-750 microns 32.7%, < 750 microns 1.9%; atrophy > 750 microns: subretinal fluid < 500 microns 0%, 500-750 microns 9.6%, > 750 microns 13.5%; P < 0.0001). Because RPE atrophy in focal hemorrhagic CR was seen in patients both with and without photocoagulation therapy, laser treatment cannot be the causative factor. With increased follow-up the risk of the development of RPE atrophy increases in all patients. The resulting amount of RPE atrophy was only dependent on the initial amount of subretinal fluid. If the fovea is included in the exudative detachment, there is a higher risk of long-term visual loss.

Adolescent↗
PubMed1998

Optic nerve head neovascularization in a patient with inactive cytomegalovirus retinitis and immune recovery.

PURPOSE: To report a case of optic nerve head neovascularization in a patient with acquired immunodeficiency syndrome (AIDS) associated with inactive cytomegalovirus retinitis and immune recovery. METHOD: Case report. RESULTS: We examined a 29-year-old man with AIDS and inactive cytomegalovirus retinitis and found vitritis and prominent optic nerve head neovascularization. The patient had been treated with reverse transcriptase and protease inhibitors, resulting in a notable rise in CD4+ lymphocyte count and an undetectable human immunodeficiency virus (HIV)-RNA viral load. No cause of neovascularization other than intraocular inflammation was detected. CONCLUSION: Immune recovery in a setting of inactive cytomegalovirus retinitis can result in optic nerve head neovascularization, as seen in our patient.

AIDS-Related Opportunistic Infections↗
PubMed1992

Acute onset of rubeosis iridis after diabetic vitrectomy can indicate peripheral traction retinal detachment.

Acute onset or exacerbation of rubeosis iridis associated with peripheral retinal detachment after vitrectomy represents a rare but serious complication of advanced diabetic retinopathy that indicates a poor prognosis. The clinical features, surgical procedures, and anatomical and functional results for a series of 13 eyes presenting with this complication are reported. In addition to rubeosis iridis and peripheral retinal detachment, anterior hyaloidal fibrovascular proliferation (APH) was also present in 10 eyes. All eyes had undergone one or more previous vitrectomies for diabetic complications such as nonclearing vitreous hemorrhage and traction retinal detachment. Treatment modalities for iris neovascularization and peripheral retinal detachment included reattachment procedures with an encircling band, peripheral membrane peeling, and, if necessary, peripheral retinectomy. Peripheral coagulation therapy was performed in all eyes. Eight eyes received an intraocular silicone-oil tamponade. Early results (4 weeks post-surgery) showed regression or stabilization of rubeosis iridis in all eyes. Later results (mean, 9 months post-surgery) revealed nine eyes with stabilized anterior ocular neovascularization and reattachment of the retina. Four eyes were anatomic failures due to recurrent rubeosis iridis/AHP or traction retinal detachment, and three of them also developed ocular hypotony. None of the eyes has thus far been lost as a result of neovascular glaucoma or painful phthisis. Ambulatory vision was retained in ten eyes, but function was limited to a low level as a result of the underlying ischemic disease. Immediate reattachment surgery in combination with anterior/peripheral coagulation therapy was shown to be an effective measure for controlling iris neovascular activity in eyes afflicted with acute anterior ocular neovascularization.

Acute Disease↗
PubMed2002

Pathologic features of vascular endothelial growth factor-induced retinopathy in the nonhuman primate.

PURPOSE: Vascular endothelial growth factor (VEGF) is a potent ischemia-upregulated angiogenic protein that has been implicated in diabetic retinopathy. Intravitreal VEGF injections have not previously been shown to produce preretinal neovascularization. The purpose of this study was to further characterize the angiopathic changes that occur after intravitreal injections in a nonhuman primate and determine if preretinal neovascularization develops. DESIGN: Experimental animal study. METHODS: Vascular endothelial growth factor 165 was injected into the eyes of normal cynomolgus monkeys at regular intervals. As a control, normal eyes were injected with phosphate buffered saline. Color photography and fluorescein angiography were performed at regular intervals. The retinas were incubated for adenosine diphosphatase (ADPase) activity to visualize retinal vessels. The retinas were flat-embedded and areas of potential preretinal neovascularization were identified en bloc and serially sectioned. RESULTS: Areas of capillary nonperfusion and vessel dilation and tortuousity were seen by angiography. In serial sections, the nonperfused areas were found to be associated with endothelial cell hyperplasia in vessel lumens. Preretinal neovascularization originating only from superficial veins and venules was observed throughout peripheral retina, but was not seen in the posterior pole. Lacunae-like veins were subdivided by the process of intussusception and endothelial cell bridging. Arterioles demonstrated endothelial cell hyperplasia and microaneurysms. CONCLUSION: Intraocular injections of VEGF were sufficient to produce preretinal neovascularization in the nonhuman primate. Most vasculopathic structures were associated with endothelial cell hyperplasia. These results demonstrate that VEGF alone can produce many features of both nonproliferative and proliferative diabetic retinopathy including the previously undescribed development of preretinal neovascularization. This well-characterized VEGF-induced primate model of retinal neovascularization may be useful as a means of testing new treatments for retinal neovascularization.

Animals↗
PubMed2001

Retinal pigment epithelial tear after photodynamic therapy for choroidal neovascularization.

PURPOSE: To report a case of retinal pigment epithelial tear after photodynamic therapy for choroidal neovascularization. METHODS: Case report. A 74-year-old woman with exudative age-related macular degeneration and classic subfoveal choroidal neovascularization RE underwent photodynamic therapy with verteporfin. RESULTS: Ophthalmoscopy and fluorescein angiography RE disclosed a retinal pigment epithelial tear in the area of photodynamic therapy. CONCLUSION: This case presents the first report of a retinal pigment epithelial tear after photodynamic therapy with verteporfin for subfoveal choroidal neovascularization in age-related macular degeneration.

Aged↗
PubMed2000

Retinal choroidal anastomoses and occult choroidal neovascularization in age-related macular degeneration.

OBJECTIVE: This study was designed to identify the incidence of retinal choroidal anastomoses in patients with occult choroidal neovascularization (CNV) and focal hot spots on indocyanine green (ICG) angiography, to identify the clinical and angiographic features that would assist in their identification, and to determine if the presence of these anastomotic lesions affect the outcome of laser therapy. DESIGN: Combined prospective and retrospective cross-sectional study. PARTICIPANTS: One hundred fifty consecutive patients with newly diagnosed occult CNV secondary to exudative age-related macular degeneration and focal hot spots on ICG angiography were evaluated prospectively. In addition, a retrospective review was performed on 79 eyes previously reported to have undergone laser photocoagulation treatment with ICG guidance. METHODS AND TESTING: In all cases, stereo color and red-free photographs, and stereo fluorescein and digital ICG angiograms were obtained for evaluation. MAIN OUTCOME MEASURES: Images obtained by all four techniques were evaluated for the presence of a retinal choroidal anastomosis. Associated clinical and angiographic findings were noted. In the retrospective review, the success rate of laser treatment was correlated with the presence or absence of a retinal choroidal anastomosis. RESULTS: Of the 150 eyes evaluated prospectively, 31 (21%) were found to have a retinal choroidal anastomosis. Retinal choroidal anastomoses were found in 27% of patients with associated serous pigment epithelial detachment (PED), whereas 13% were found in those without an associated elevation of the retinal pigment epithelium. Seventy-one percent of eyes had multiple anastomotic connections. Ninety percent of eyes had at least one retinal vein involved in the anastomotic connection. Clinical evidence of preretinal and intraretinal hemorrhage and cystic edema coupled with angiographic evidence of intraretinal dye leakage were key features of retinal choroidal anastomoses. In the retrospective review, seven patients were found to have retinal choroidal anastomoses with associated serous PED and demonstrated a very low (14%) success rate for laser treatment. CONCLUSIONS: Retinal choroidal anastomoses can present as a primary manifestation of the exudative process in age-related macular degeneration. They may be seen in eyes with and without detachment of the retinal pigment epithelium. Specific clinical and angiographic features have been identified that can aid in the diagnosis of these vascular anomalies. Their presence represents a poor prognostic sign for successful ICG-guided laser treatment.

Arteriovenous Anastomosis↗
PubMed2006

Trans-scleral delivery of polyamine analogs for ocular neovascularization.

Periocular injections of the polyamine analog CGC-11144 three times a week causes regression of choroidal neovascularization. This regimen was selected to maximize chances of success for proof of concept, but is not ideal for clinical application. In this study we explored other regimens for periocular delivery of CGC-11144, and 2 other polyamine analogs, CGC-11047 and CGC-11093. A single periocular injection of 200 microg of CGC-11144, 2 mg of CGC-11047, or 1.5 mg of CGC-11093 caused significant suppression and regression of laser-induced choroidal neovascularization. An injection of 2 mg of CGC-11047 or 1.5 mg of CGC-11093 one or two weeks before, but not 3 weeks before, rupture of Bruch's membrane also caused significant suppression. Periocular injection of polyamine analogs also caused strong inhibition of retinal or subretinal neovascularization in mice with oxygen-induced ischemic retinopathy or Rhodopsin promoter/VEGF transgenic mice, respectively. These data suggest that periocular injection of one of 3 different polyamine analogs inhibits retinal or choroidal neovascularization and a single injection provides inhibitory activity for at least 2 to 3 weeks, which could provide the basis for a feasible treatment regimen for clinical trials.

Animals↗
PubMed2003

Mouse model of subretinal neovascularization with choroidal anastomosis.

PURPOSE: To characterize the phenotype and report a reliable genetic model of retinal angiogenesis and subretinal neovascularization in the mouse. METHODS: The mouse phenotype was characterized using ophthalmoscopy, fundus photography, fluorescein angiography, electroretinography, histology, gene sequencing, and linkage analysis. RESULTS: Scattered pink-gray retinal lesions were found on ophthalmoscopy and were confirmed to be subretinal neovascularization on fluorescein angiography. On histologic examination, outer plexiform retinal neovascularization with growth into the subretinal space was found as early as postnatal Day 15. On genetic analysis, homozygosity of the Vldlr mutation always segregated with the retinal angiogenesis, whereas normal and heterozygous mice had no neovascularization. The histologic studies 15 to 18 days consistently showed new outer plexiform neovascular vessels drawn to the subretinal space by 20 days, and by 30 to 50 days, subretinal hemorrhages and choroidal anastomoses were common. Mice by 8 months had increased vascularity of the iris and ciliary body. CONCLUSIONS: The Vldlr mutation in the mouse provides a good model for retinal angiogenesis and subretinal neovascularization. Finding a strong association between retinal angiogenesis and a very low density lipid receptor mutation is new, and study of lipid receptor physiology may broaden the understanding of retinal angiogenesis.

Animals↗