PurposeTo assess OCT angiography (OCTA) effectiveness at detecting choroidal neovascularization (CNV) in cases of suspected neovascular age related macular degeneration (nAMD), chronic central serous retinopathy (cCSR) and pathological myopia compared to FFA and how it compares to a multimodal approach (OCT, FFA and ICGA) for detecting the vascular network.MethodsThis was a retrospective observational cohort study of patients who had clinical and/or OCT findings suggestive of CNV, having further investigation with FFA, with or without ICG, and had same day OCTA using the Heidelberg Spectralis OCT2 beta angiography module. Multimodal imaging interpretation was compared to OCTA images. OCTA images were also analysed for inter-rater reliability (using kappa statistic). The diagnostic accuracy of OCTA was compared to FFA (using Cochran's Q, p<0.05). OCTA was also compared to a multimodal approach in defining a vascular network.ResultsOverall sensitivity of OCTA compared to FFA was 71% and specificity of 81% (p=0.108). Subgroup analysis for OCTA vs FFA for detecting classic nAMD/type II CNV sensitivity was 100% and specificity of 76% (p<0.05). OCTA vs FFA for detecting occult nAMD/type-I CNV sensitivity was 47% and specificity of 76%, (p=0.248). OCTA was better than FFA at defining a vascular network overall, when OCT was suspicious (59% vs 49%).ConclusionsOCTA was better at detecting classic nAMD/type II CNV compared to FFA and for defining a vascular network in nAMD compared to FFA and ICGA. It was able to aid in making the diagnosis in cases where evidence of CNV was uncertain following FFA/ICGA.
Endothelial insulin receptors (Insr) promote sprouting angiogenesis, although the underpinning cellular and molecular mechanisms are unknown. Comparing mice with whole body insulin receptor haploinsufficiency (Insr +/-) against littermate controls, we found impaired limb perfusion and muscle capillary density after inducing hind-limb ischemia; this was in spite of increased expression of the pro-angiogenic growth factor Vegfa. Insr +/- neonatal retinas exhibited reduced tip cell number and branching complexity during developmental angiogenesis, which was also found in separate studies of mice with endothelium-restricted Insr haploinsufficiency. Functional responses to VEGF-A, including in vitro angiogenesis, were also impaired in aortic rings and pulmonary endothelial cells from Insr +/- mice. Human umbilical vein endothelial cells (HUVEC) with shRNA-mediated knockdown of Insr also demonstrated impaired functional angiogenic responses to VEGF-A. VEGF-A signaling to Akt and eNOS was intact, but downstream signaling to ERK1/2 was impaired, as was VEGF receptor-2 (VEGFR-2) internalization, which is required specifically for signaling to ERK1/2. Hence, endothelial insulin receptors facilitate the functional response to VEGF-A during angiogenic sprouting and are required for appropriate signal transduction from VEGFR-2 to ERK1/2.
BACKGROUND AND OBJECTIVE:
Retinovascular anomalies in the fellow eyes of patients with Coats’ disease have been described, but the clinical significance is unknown, as well as whether these lesions progress over time.
PATIENTS AND METHODS:
This is an international, multi center, retrospective, observational cohort study of fellow-eye abnormalities on widefield fluorescein angiography in patients with Coats’ disease.
RESULTS:
Three hundred fifty eyes of 175 patients with Coats’ disease were analyzed. A total of 33 patients (18.8%) demonstrated abnormal fellow-eye findings: 14 (42.4%) telangiectasias, 18 (54.5%) aneurysms, six (18.2%) segmental non-perfusion, six (18.2%) leakage, and two (6.0%) vascular tortuosity. All eyes were asymptomatic, and none of the lesions progressed over time. There was no association between fellow-eye findings with severity of Coats’ disease (P = .16), patient age (P = .16), or presence of systemic vascular disease (P = .16).
CONCLUSIONS:
The vascular abnormalities in fellow eyes of patients with Coats’ disease did not progress over time. Observation is a reasonable initial management strategy.
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