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3 th primary PED presenting as the hallmark of neovascular activity and was induced by secondary format
4 long-term outcome of bevacizumab therapy for neovascular age related macular degeneration (NVAMD) in
5 variant of choroidal neovascularization and neovascular age related macular degeneration presenting
7 bizumab and bevacizumab for the treatment of neovascular age-related macular degeneration (AMD) among
8 trophy due to late-stage non-neovascular and neovascular age-related macular degeneration (AMD) and t
9 nce tomography (OCT) images of patients with neovascular age-related macular degeneration (AMD) and t
10 39.7% of eyes; retinal tear in 8.9% of eyes; neovascular age-related macular degeneration (AMD) in 7.
12 using a treat-and-extend (TREX) regimen for neovascular age-related macular degeneration (AMD) or fe
14 ss (CMT) and visual outcome in patients with neovascular age-related macular degeneration (AMD) treat
15 lop predictive models of anatomic outcome in neovascular age-related macular degeneration (AMD) treat
16 rospective clinical trials for management of neovascular age-related macular degeneration (AMD), diab
17 inal degenerative diseases including dry and neovascular age-related macular degeneration (AMD), reti
19 tinal angiomatous proliferation, a subset of neovascular age-related macular degeneration (AMD), whic
25 nsisted of 1200 OCT volumes of patients with neovascular age-related macular degeneration (AMD, n = 4
26 Novartis Pharma AG, Basel, Switzerland) for neovascular age-related macular degeneration (nAMD) afte
27 (OCT) with alternative tests for monitoring neovascular age-related macular degeneration (nAMD) and
28 ocks all isoforms of VEGF-A in patients with neovascular age-related macular degeneration (nAMD) demo
29 d long-term visual outcomes in patients with neovascular age-related macular degeneration (nAMD) duri
30 to investigate preferences of patients with neovascular age-related macular degeneration (nAMD) for
31 &E) versus monthly regimens in patients with neovascular age-related macular degeneration (nAMD) from
32 t outcomes with intravitreal aflibercept for neovascular age-related macular degeneration (nAMD) in r
36 sion of geographic atrophy (GA) in eyes with neovascular age-related macular degeneration (nAMD) trea
37 al-world visual acuity (VA) in patients with neovascular age-related macular degeneration (nAMD) trea
38 us adverse events (SAEs) among patients with neovascular age-related macular degeneration (nAMD) who
39 the outcomes over 12 months in patients with neovascular age-related macular degeneration (nAMD) with
40 anti-VEGF injections in patients treated for neovascular age-related macular degeneration (nAMD), dia
41 rolled patients treated with ranibizumab for neovascular age-related macular degeneration (nAMD), dia
42 using anti-VEGF therapy for the treatment of neovascular age-related macular degeneration (nAMD), oph
43 ith ranibizumab monotherapy in patients with neovascular age-related macular degeneration (nAMD).
44 Aflibercept in treatment-naive patients with neovascular age-related macular degeneration (nvAMD) in
46 ence tomography (OCT) in guiding therapy for neovascular age-related macular degeneration (nvAMD) to
47 (HE) and all other eyes among patients with neovascular age-related macular degeneration (NVAMD) tre
48 used in a treat-and-extend (TAE) regimen for neovascular age-related macular degeneration (NVAMD).
49 has changed the prognosis for patients with neovascular age-related macular degeneration (nvAMD).
50 afety of rAAV.sFlt-1 subretinal injection in neovascular age-related macular degeneration (wet AMD) o
53 helial growth factor agents for treatment of neovascular age-related macular degeneration or diabetic
55 helial growth factor agents for treatment of neovascular age-related macular degeneration or diabetic
63 ) had diabetic macular edema, 32 (25.8%) had neovascular age-related macular degeneration, and 32 (25
65 ch as proliferative diabetic retinopathy and neovascular age-related macular degeneration, uncontroll
75 athy (DR), retinal vein occlusion (RVO), and neovascular-age related macular degeneration (nvAMD).
76 variants more frequently than patients with neovascular AMD (11 of 93 [11.8%] vs 40 of 835 [4.8%]; P
78 ion, patients with MPNs had a higher risk of neovascular AMD (adjusted HR, 1.4; 95% CI, 1.2-1.6).
80 e age-related macular degeneration (AMD) and neovascular AMD (nvAMD) with serum 25-hydroxy vitamin D
81 nce of late AMD, geographic atrophy (GA) and neovascular AMD (NVAMD), year of recruitment, AMD gradin
82 gment epithelial (RPE) hemorrhage related to neovascular AMD (odds ratio 1.55 [95% confidence interva
86 ng 4 risk alleles in CFH and ARMS2 developed neovascular AMD 12.2 (95% CI, 6.2-18.3) years earlier th
87 the complement factor H (CFH) gene developed neovascular AMD 2.8 (95% CI, 0.5-5.0) years earlier (P =
89 izumab vs ranibizumab as initial therapy for neovascular AMD among US Medicare beneficiaries varied s
91 MD, 85.7% (95% CI, 57.2%-98.2%; n = 12) were neovascular AMD and 14.3% (95% CI, 2.0%-42.8%; n = 2) we
92 hat included 106 referral eyes for suspected neovascular AMD and 63 eyes with stable neovascular AMD.
93 l, 275 patients with a known age at onset of neovascular AMD and a genetic risk analysis were include
94 VEGF treatment for subfoveal and juxtafoveal neovascular AMD and a minimum follow-up of 24 months wer
95 ular, 384 geographic atrophy, and 192 mixed [neovascular AMD and geographic atrophy]) and 1153 contro
96 se, 47 met inclusion criteria; most targeted neovascular AMD and investigated anti-vascular endotheli
99 New referrals for patients with suspected neovascular AMD and patients with stable neovascular AMD
100 patients (n = 115 eyes) with treatment-naive neovascular AMD and PED (>150 mum), who were treated wit
103 recall of 0.81, with superior performance in neovascular AMD and RVO compared with DME, which was rep
104 ation included 101 eyes of 101 patients with neovascular AMD and thick submacular hemorrhage who unde
107 196 patients diagnosed with treatment-naive neovascular AMD between January 2009 and March 2013; the
108 iaries (N = 195 812) with an index claim for neovascular AMD between July 1, 2006, and June 30, 2009,
110 As a follow-up validation, we evaluate 3,772 neovascular AMD cases and 6,942 controls from five indep
111 ficant decrease of the RGCL in patients with neovascular AMD compared to the fellow (untreated) eye.
112 oint increase in sFlt-1, the odds for having neovascular AMD compared with non-AMD and neovascular AM
113 ng neovascular AMD compared with non-AMD and neovascular AMD decrease by 27.8%, odds ratio (OR) = 0.7
115 terns in anti-VEGF therapy for patients with neovascular AMD do not reflect optimal treatment strateg
116 intravitreal bevacizumab for treatment-naive neovascular AMD does not increase initial fluid-free int
118 um sFlt-1 differentiates those patients with neovascular AMD from both early AMD and non-AMD particip
119 Rim area was significantly thinner in the neovascular AMD group compared with controls (P = .047);
120 = .047); cup-to-disc ratio was higher in the neovascular AMD group compared with the control group (P
121 e log-rank test indicated that subjects with neovascular AMD had a significantly lower 3-year Parkins
122 ular endothelial growth factor therapies for neovascular AMD had decreased mortality compared with th
123 ts (7.0%) and 2 of 40 donor eyes (5.0%) with neovascular AMD had layered, hyperreflective sub-RPE lin
124 of these SNPs with angiographic features of neovascular AMD has been inconsistent in previous studie
128 fellow eye have focused on the incidence of neovascular AMD in the fellow eye of participants with n
130 g first-generation offspring of parents with neovascular AMD in the LIMPIA trial, MPOD as measured wi
132 onsecutive patients with iAMD in one eye and neovascular AMD in their fellow eye were imaged with FA,
133 The efficacy of antiangiogenic therapy in neovascular AMD is strongly determined by morphologic fe
139 Past smokers and current smokers developed neovascular AMD on average 4.9 (95% CI, 3.0-6.8) and 7.7
143 participants, 53 early AMD patients, and 97 neovascular AMD patients from Belfast in Northern Irelan
150 he 3-year follow-up period for subjects with neovascular AMD was 2.57 (95% CI: 1.42-4.64) that of com
151 iciaries that first received ranibizumab for neovascular AMD was 35%, and varied significantly (0.9%-
154 t-1 concentration of non-AMD, early AMD, and neovascular AMD were 90.8 +/- 2.9 pg/mL (+/- standard er
155 dvanced AMD, drusen, geographic atrophy, and neovascular AMD were determined by using a modified Wisc
159 ted neovascular AMD and patients with stable neovascular AMD were randomized into either routine or t
162 g teleophthalmologic screening for suspected neovascular AMD with retinal specialist-based screening.
164 diate and 1356 advanced AMD cases (primarily neovascular AMD) were confirmed by medical record review
165 diate and 1118 advanced AMD cases (primarily neovascular AMD) with a visual acuity of 20/30 or worse
166 diate and 1356 advanced AMD cases (primarily neovascular AMD) with a visual acuity of 20/30 or worse,
167 category 2, 26 for AREDS category 3, 26 for neovascular AMD, 26 with atrophic AMD, and 26 controls.
169 may better guide evaluation and treatment of neovascular AMD, and may contribute to the development o
171 RN effectively treated PEDs in patients with neovascular AMD, and significant vision gains resulted r
172 ome use of a monitoring device for detecting neovascular AMD, and the proportion who established a ba
173 line and the various components of late AMD (neovascular AMD, central GA, or any GA) also showed no s
174 ry RNFL thickness was significantly lower in neovascular AMD, compared to controls (P = .004); peripa
176 T specifically images RPE-related changes in neovascular AMD, contrary to conventional imaging method
182 influence on new MA development in eyes with neovascular AMD, whether dosed monthly or per TREX regim
208 t and quantify atrophy due to late-stage non-neovascular and neovascular age-related macular degenera
210 yes revealed a significant reduction in both neovascular and non-neovascular areas from baseline to m
211 mab injections, overall in the macula and in neovascular and non-neovascular areas, from baseline to
213 ficant reduction in both neovascular and non-neovascular areas from baseline to month 3 and month 6 (
214 all in the macula and in neovascular and non-neovascular areas, from baseline to month 3 (loading pha
218 erapy, indicating a more mature longstanding neovascular complex resistant to anti-VEGF therapy.
220 t voltage from aberrantly located preretinal neovascular complexes is transmitted into the intraretin
221 in occlusion (CRVO) and stratify the risk of neovascular complication based on wider areas of visible
225 ded good visual gains without progression of neovascular disease or increased need for intravitreal a
226 tors may be a useful therapeutic strategy in neovascular disease to reduce VEGF165-induced edema with
227 I, 32.1%-45.4%; P < .001), and 38.2% loss in neovascular disease where RPE remained intact (95% CI, 2
238 or (VEGF) is a common treatment strategy for neovascular eye disease, a major cause of vision loss in
241 s open-angle (2/26), exfoliative (2/26), and neovascular following central retinal vein occlusion fro
242 cts can be used for studying the dynamics of neovascular formation in-vitro by a combination of live
243 .048 [Kaplan-Meier], respectively) and less neovascular glaucoma (11.6% and 21.3% after 5 years, P =
249 ucleation were tumor recurrence in 60 (61%), neovascular glaucoma in 21 (21%), and tumor nonresponse
252 ts that in larger tumors the enucleation and neovascular glaucoma rates might be reduced by adjuvant
253 set cataract was noted in 22 patients (44%), neovascular glaucoma was noted in 1 patient (2%), and th
262 erited blinding disorder, autosomal dominant neovascular inflammatory vitreoretinopathy (ADNIV, OMIM
264 epth-resolved identification of nonexudative neovascular lesions in eyes with iAMD suggests the need
265 , retinal pigment epithelial depigmentation, neovascular lesions, and geographic atrophy using the mo
267 allowing 2 monthly visits for patients with neovascular macular degeneration (nAMD) compared with mo
268 treatment for patients with newly diagnosed neovascular macular degeneration: monthly or as-needed b
271 nitis (n = 5), hemangioma (n = 1), choroidal neovascular membrane (n = 1), or nerve fiber layer infar
273 is cohort of patients had advanced choroidal neovascular membrane upon enrollment (recurrent or resis
274 e the characteristics of pediatric choroidal neovascular membranes (CNVs) associated with retinochoro
275 ts affected by C3 glomerulopathy can develop neovascular membranes as retinal complications of pigmen
276 ity to study the morphology of occult type 1 neovascular membranes in AMD and allows precise structur
277 ic patterns and quantifiable features of the neovascular membranes were studied on en face projection
278 namic therapy for the treatment of choroidal neovascular membranes, has also been shown to be an effe
285 as a novel therapeutic agent to treat ocular neovascular pathologies and may complement current anti-
289 f AMD (2 with nonneovascular DPED and 2 with neovascular pigment epithelium detachment [PED]) and 49
291 hage dysfunction plays a pivotal role during neovascular proliferation in diseases of ageing includin
292 -induced retinal changes in animal models of neovascular retinal disease approximately 3-4-fold longe
293 o measure vascular voltages in human retinal neovascular specimens and rodent models of retinal neova
294 tor for the early detection of the choroidal neovascular stage before substantial vision loss has occ
297 of pathologic retinal angiogenesis, reducing neovascular tuft formation and increased avascular area,
298 ecule resulted in a significant reduction of neovascular tufts in oxygen-induced retinopathy, support
299 ed a high level of Cavin-2 expression in the neovascular tufts in the mouse model of oxygen-induced r
300 ovascularization (CNV), is a hallmark of the neovascular (wet) form of advanced AMD and leads to sign
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